BACKGROUND: It has been shown that circular RNA (circRNA) is associated with human cancers, however, few studies have been reported in hepatocellular carcinoma (HCC). OBJECTIVE: To estimate clinical values of a circular RNA, Hsa_circ_0001649, in HCC. METHODS: Expression level of hsa_circ_0001649 was detected in HCC and paired adjacent liver tissues by real-time quantitative reverse transcription-polymerase chain reactions (qRT-PCRs). Differences in expression level of hsa_circ_0001649 were analyzed using the paired t-test. Tests were performed between clinical information and hsa_circ_0001649 expression level by analysis of variance (ANOVA) or welch t-test and a receiver operating characteristics (ROC) curve was established to estimate the value of hsa_circ_0001649 expression as a biomarker in HCC. RESULTS: hsa_circ_0001649 expression was significantly downregulated in HCC tissues (p = 0.0014) based on an analysis of 89 paired samples of HCC and adjacent liver tissues and the area under the ROC curve (AUC) was 0.63. Furthermore, hsa_circ_0001649 expression was correlated with tumor size (p = 0.045) and the occurrence of tumor embolus (p = 0.017) in HCC. CONCLUSIONS: We first found hsa_circ_0001649 was significantly downregulated in HCC. Our findings indicate hsa_circ_0001649 might serve as a novel potential biomarker for HCC and may function in tumorigenesis and metastasis of HCC.
Renal Cell Carcinoma (RCC) has the highest mortality rate of the genitourinary cancers and the incidence of RCC has risen steadily. If detected early, RCC is curable by surgery although a minority are at risk of recurrence. Increasing incidental detection and an ageing population has led to active surveillance as an option for patients with small renal masses. RCC is heterogeneous and comprises several histological cell types with different genetics, biology and behavior. The identification of the genes predisposing to inherited syndromes with RCC has provided much of our knowledge of the molecular basis of early sporadic RCC. Many of the oncogenes and tumor suppressor genes that are mutated leading to pathway dysregulation in RCC remain to be elucidated. Global studies of copy number, gene sequencing, gene expression, miRNA expression and gene methylation in primary RCC will lead towards this goal. The natural history of RCC indicated by candidate precursor lesions, multifocal or bilateral disease, growth rate of small renal masses under surveillance, and high risk populations provide insight into the behavior of this disease. The use of molecular markers for early detection and prognosis merits more attention with ongoing advances in omics technologies. This review focuses on early RCC, that is disease confined within the renal capsule.
BACKGROUND: Circular RNAs (circRNAs) have been found playing important roles in regulating cancer progression. Human circRNA microarray was performed to screen for abnormally expressed circRNA in gastric cancer tissues. In this study, we are aimed to investigate the relationship between a new circular RNA named hsa_circ_0000520 and gastric cancer development. METHODS: The hsa_circ_0000520 levels were detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) in gastric tissue, cell and plasma levels, respectively. Then, the association between the expression level of hsa_circ_0000520 and the clinicopathological features of patients with gastric cancer was further analyzed. Finally, a network of hsa_circ_0000520-miRNA-mRNA interactions was predicated. RESULTS: In this study, hsa_circ_0000520 was first found to be significantly down-regulated in gastric cancer tissues, plasma and gastric cancer cell lines compared with control cases. Clinicopathological features showed that hsa_circ_0000520 level in GC tissues was negatively associated with TNM stage and in GC plasma linked with CEA expression. Finally, a total of 9 miRNAs and 9 candidate mRNA were predicted to have an interaction with hsa_circ_0000520. CONCLUSIONS: We first identified that hsa_circ_0000520 was significantly down-regulated in gastric cancer. Our study indicated hsa_circ_0000520 might serve as a novel biomarker for gastric cancer and is involved in gastric carcinoma development.
BACKGROUND: Long non-coding RNA (lncRNA) H19 has been well studied playing an important role in breast cancer (BC) progress and the expression of H19 may service as a diagnostic target for BC. However, it is unclear if circulating IncRNA H19 could as a potential biomarker for BC diagnosis and monitor. OBJECTIVE: The objective of our study was to determine whether plasma lneRNA H19 could be used as biomarkers for the screening and early diagnosis of breast cancer. METHODS: In this study, we carried out a quantitative real-time PCR (qRT-PCR) method to examine the expression levels of lncRNA H19 in 24 pairs of BC tissues and 20 pairs of BC plasma. The differentially expressed of plasma H19 was further validated in another 102 BC patients and 96 healthy controls. The potential correlations between plasma H19 levels and clinicopathological characteristics were analyzed. Receiver operating characteristic (ROC) curve was performed to evaluate the diagnostic values of plasma H19 between 30 early stage BC patients and 30 healthy controls. 24 paired pre- and postoperative plasma samples were detected to assess the tumor monitoring values. RESULTS: The results revealed that the expression of H19 was significantly increased in BC tissues and plasma compared with healthy controls (P < 0.05), and plasma H19 levels were significantly correlated with estrogen receptor (ER) (P = 0.008), progesterone receptor (PR) (P = 0.025), c-erbB-2 (P = 0.043) and lymph node metastasis (P = 0.006). The area under the ROC curve (AUC) of plasma H19 was 0.81(sensitivity, 56.7%; specificity, 86.7%; P < 0.0001), which was higher than the values of carcinoembryonic antigen (CEA) and carbohydrate antigen 153 (CA153). Furthermore, plasma H19 levels were significantly decreased in postoperative samples than preoperative samples (P = 0.0006). CONCLUSION: Plasma H19 may serve as a potential biomarker for BC early screening and prognosis monitor.
This paper aimed to probe into the expression of long non-coding RNA (lncRNA) SNHG16 in human gastric cancer (GC) and its potential tumor biological functions. The expression of lncRNA SNHG16 was detected in GC and adjacent tissues and GC cell lines using qRT-PCR. GC MGC-803 cells were transfected with siRNA of lncRNA SNHG16, as well as blank and negative control. A series of experiments including CCK-8, flow cytometry, transwell, and wound healing assay were adopted to evaluate the effects of lncRNA SNHG16 on cell growth and metastasis. Besides, the nude mouse xenograft tumor model was established to draw tumor growth curve and measure tumor volume during treatments. TUNEL staining was used to determine the apoptosis rate of tissues. The expression of lncRNA SNHG16 in GC tissue, significantly associated with invasion depth, lymph node metastasis, TNM stage and histological differentiation (all P < 0.05), was upregulated compared with adjacent tissues. Transfected with siRNA of lncRNA SNHG16 inhibited GC MGC-803 cell proliferation, and arrested cells in the G0/G1 phase, and then promoted apoptosis rate with reduced cell invasion and shortened migration distance. Additionally, the nude mice xenograft presented lower tumor growth rate and weight loss alongside elevated apoptosis rate of tumor tissues. LncRNA SNHG16 is highly expressed in GC, while suppression of SNHG16 expression can inhibit proliferation, weaken invasion and migration of GC cells, and enhance apoptosis, to be a novel target for GC clinical treatment.
Long non-coding RNAs (lncRNAs) were playing critical roles in tumorigenesis. However, in prostate cancer, the roles and mechanisms of lncRNAs especially ANRIL were largely unknown. We investigated the effects of ANRIL on the proliferation and migration of prostate cancer cells using CCK-8 assay and Transwell migration assay. Real-time PCR and western blotting assays were used to analyze the levels of ANRIL, let-7a, TGF-beta 1, p-Smad2 and p-Smad7. Our results showed that ANRIL was significantly overexpressed in prostate cancer tissues compared with corresponding normal tissues. Knockdown of ANRIL significantly inhibited the proliferation and migration of prostate cancer LNCap, PC3 and DU145 cells. Knockdown of ANRIL significantly decreased the levels of TGF-beta 1 and p-Smad2, and increased the level of p-Smad7 in prostate cancer LNCap cells. We further found that knockdown of ANRIL significantly enhanced the expression of let-7a, and rescue experiment found that let7a inhibitor recovered the suppressive effects of ANRIL silencing on the proliferation and migration of prostate cancer LNCap, PC3 and DU145 cells. And let-7a inhibitor recovered the suppressive effects of ANRIL silencing on the activity of TGF-beta 1/Smad signaling pathway in prostate cancer LNCap cells. Taken together, our findings indicated that overexpression of lncRNA ANRIL promoted the proliferation and migration of prostate cancer cells via regulating let-7a/TGF-beta 1/Smad signaling pathway.
Our study aimed to explore the effects of long noncoding RNA (lncRNA)-ANCR on the invasion and migration of colorectal cancer (CRC) cells by regulating enhancer of zeste homolog 2 (EZH2) expression. CRC tissues and adjacent normal tissues were collected and CRC SW620 cells line and normal human intestinal epithelial cells (HIECs) were incubated. CRC SW620 cells line was transfected with ANCR-siRNA. The expressions of ANCR and EZH2 mRNA were measured by real-time quantitative polymerase chain reaction (RT-qPCR). EZH2 and trimethylation of H3K27 (H3K27me3) protein expressions were detected using Western blotting. The relationship between ANCR and EZH2 was determined through RNA pull-down and co-immunoprecipitation (co-IP) assays. Cell invasion and migration were determined by Trans-well and cell scratch assays. ANCR, EZH2 and H3K27me3 expressions were up-regulated in CRC tissues and SW620 cells (all P < 0.05). After transfected with ANCR-siRNA, SW620 cells showed decreased ANCR expression and EZH2 mRNA and protein expressions (all P < 0.05). According to the results of RNA pull-down and co-IP assays, ANCR could specifically bind to EZH2. The results of Trans-well and cell scratch tests showed that when ANCR expression was decreased, the invasion and migration abilities of SW620 cells significantly declined (both P < 0.05). In conclusion, these results suggest that lncRNA-ANCR could influence the invasion and migration of CRC cells by specifically binding to EZH2.
OBJECTIVE: The purpose of this study was to explore serum PCAT-1 expression in multiple myeloma (MM) and examine the potential usefulness of this molecule as a biomarker for diagnosis in MM. METHODS: Serum samples were collected from 60 newly diagnosed untreated MM patients, and 48 healthy controls. Serum PCAT-1 expression levels were detected by RT-qPCR. In addition, correlations between the relative expression of serum PCAT-1 and the concentrations of lactic acid dehydrogenase (LDH), beta M-2, lambda light chain and. light chain were assessed. RESULTS: It was found that the relative expression of serum PCAT-1 in MM patients (81.02 +/- 136.9) was higher than that in healthy controls (3.17 +/- 5.75) (U = 307.0, P < 0.0001) and was significantly correlated with beta M-2 concentration (r = 0.461, P = 0.0002), but not with LDH, kappa light and lambda light chain concentration (r = 0.061, P = 0.641; r = 0.007, P = 0.956; r = -0.090, P = 0.499 respectively). Additionally, it was significantly correlated with different isotype of MM (H = 7.464, P = 0.024). The AUC of the ROC curve of serum PCAT-1 was 0.892 (95% CI 0.833-0.950), which was higher than other markers. Combining PCAT-1 and beta M-2 together, the sensitivity was highest compared with other markers alone, or combined. CONCLUSION: The expression levels of serum PCAT-1 in MM patients were significantly higher than that in healthy controls, suggesting that it may be useful in the auxiliary diagnosis of MM.
OBJECTIVE: To investigate the expression and role of long non-coding RNA (IncRNA) small nucleolar RNA host gene 12 (SNHG12) in papillary thyroid carcinoma (PTC). METHODS: The relative expression levels of IncRNA SNHG12 (hereinafter referred to as SNHG12) in 42 pairs of PTC tissues and para-carcinoma tissues were detected via quantitative reverse transcription polymerase chain reaction (qRT-PCR). SNHG12 specific interference sequences were designed and synthesized. The relative expression level and transfection efficiency of SNHG12 in PTC cells were detected via qRT-PCR. After the interference in SNHG12 expression, the change in cell proliferation capacity was detected via methyl thiazolyl tetrazolium (MTT) assay, the change in cell cycle distribution was detected via flow cytometry, the changes in cell migration and invasion capacities were detected via Transwell assay and wound healing assay, and the changes in expressions of molecular markers of Wnt/beta catenin pathway were detected via Western blotting. The pulmonary metastasis model of nude mice was established, and the changes in migration and invasion capacities of tumor cells were studied via the in-vivo experiment after the interference in SNHG12 expression. RESULTS: The results of qRT-PCR showed that the SNHG12 expression was up-regulated in 30 pairs of PTC tissues and cells. The results of MTT assay showed that the cell proliferation capacity was inhibited after the interference in SNHG12. The results of flow cytometry showed that the cell cycle progression was blocked in G1-G0 phase after the knockdown of SNHG12 expression. The results of Transwell assay and Western blotting showed that the interference in SNHG12 could inhibit the invasion and metastasis capacities of tumor cells through influencing the Wnt/beta-catenin signaling pathway. Metastatic tumor model of nude mice showed that SNHG12 could affect the invasion and metastasis of tumor cells in vivo. CONCLUSION: The SNHG12 expression is relatively high in PTC tissues and cells. In-vivolin-vitro experiments prove that SNHG12 can promote the proliferation and metastasis of PTC cells through influencing the Wnt/beta-catenin signaling pathway.
BACKGROUND: Chronic hepatitis C (CHC) is a contagious liver disease that results from infection with the hepatitis C virus (HCV). The most serious consequence of CHC is HCV-related hepatocellular carcinoma (HCC). OBJECTIVE: To illustrate the clinical significance of lncRNA HEIH expression in serum and exosomes in the development of HCV-related HCC. METHODS: Thirty-five CHC, twenty-two HCV-induced cirrhosis and ten HCV-related HCC patients in Huzhou Central Hospital from January 2016 to September 2016 were recruited in the present study. Basic patient information, clinical serological indicators, and clinical imaging data were investigated and analyzed. Serum samples were collected from patients after receiving informed consent. Exosomes were extracted from the serum, and electron microscopy was used to observe the ultrastructure of exosomes. Quantitative PCR was used to detect lncRNA HEIH gene expression in serum and exosomes. RESULTS: The changes in the ALT, GGT, HDL, INR, Alb and AFP levels in the patients with HCV-induced cirrhosis and HCVrelated HCC were statistically significant. In patients with HCV-related HCC, lncRNA-HEIH expression in serum and exosomes was increased, but the ratio of lncRNA-HEIH expression in serum versus exosomes was decreased compared to patients with CHC.
BACKGROUND: Gastric cancer is the fourth most frequent cancer and the second cause of cancer-related deaths worldwide. China has a high incidence of gastric cancer. Inflammation is a critical component of tumor progression. It has been widely accepted that gastric cancer is an inflammation-driven cancer. In this study, we investigated the application value of systemic inflammatory response (SIR) markers, platelet to lymphocyte ratio (PLR) and neutrophil to lymphocyte ratio (NLR), in early diagnosis and prognostic prediction in patients with resectable gastric cancer. MATERIALS AND METHODS: One hundred and sixty-two patients with resectable gastric cancer were included and separated into groups according to median pre-operative PLR or NLR values (PLR low: = 208, and NLR low: = 4.02, respectively). To evaluate the changes in PLR or NLR values after operation, we introduced the concept of post-/pre-operative PLR or NLR ratios (= 1 suggested not decreased PLR or NLR values). RESULTS: Pre-operative PLR and NLR levels were significantly higher in gastric cancer patients compared with the healthy subjects. Low pre-operative PLR and NLR levels correlated with better clinicopathological features, including decreased depth of invasion, less lymph node metastasis and early tumor stage. Kaplan-Meier plots illustrated that higher pre-operative NLR and PLR had decreased overall survival (OS) and disease-free survival (DFS). Surgical tumor resection resulted in a significant decrease in both PLR and NLR levels. Patients whose post-/pre-operative PLR or NLR ratios < 1 had better OS. Multivariate Cox regression analysis revealed that tumor stage, pre-operative NLR level, and post/pre-operative NLR ratio are prognostic factors affecting DFS, while depth of invasion, lymph node metastasis, tumor stage, pre-operative PLR level, and post/pre-operative PLR ratio are prognostic factors affecting OS. CONCLUSIONS: PLR and NLR measurements can provide important diagnostic and prognostic results in patients with resectable gastric cancer.
Volatile organic compounds (VOCs) biomarkers in breath provide a novel, noninvasive and quick approach to diagnosis lung cancer. The aim of the proposed study was to investigate the VOCs biomarkers in exhaled breath for lung cancer. The VOCs in exhaled breath of 88 lung cancer patients, 70 lung benign disease and 85 healthy people were analyzed by Solid Phase Micro Extraction - Gas Chromatography Mass Spectrometry (SPME-GCMS). Three types of lung cancer cells and 18 lung cancer patients' tissues were cultured in vitro. The VOCs in the headspace of these cultivations were analyzed as an evidence of production mechanism of the VOCs in breath. Three lung cancer diagnosis models were constructed respectively in exhaled breath samples using Linear Discriminant Analysis (LDA). Leave one out cross validation was employed to evaluate these models. 23 VOCs, whose areas under curve (AUC) of receiver operating characteristic (ROC) > 0.60 and p < 0.01, were confirmed as the VOCs biomarkers for lung cancer. Three diagnostic models based on 23 VOCs could easily discriminate lung cancer patients from controls with 96.47% sensitivity and 97.47% specificity. However, the discrimination between early stage and later stage lung cancer was not very obvious.
The aim of present study was to investigate the role of preoperative neutrophil to lymphocyte ratio (NLR) and platelet to lymphocyte ratio (PLR) used as prognostic markers for predicting chemotherapeutic response and survival outcomes in patients with epithelial ovarian cancer (EOC) who are receiving platinum-based chemotherapy. A total of 344 patients diagnosed with EOC who are receiving platinum-based chemotherapy from 2005 to 2010 in the hospital were enrolled. NLR and PLR were calculated from complete blood cell count taken before operation. The patients were divided into platinum-resistant (P-R) group and platinum-sensitive (P-S) group according to chemotherapeutic response. Clinicopathologic variables and outcomes were retrospectively collected and compared among groups. We used receiver operating characteristic (ROC) curves to calculate optimal cut-off values for NLR and PLR to predict chemotherapeutic response and prognosis. The AUC, sensitivity, specificity of NLR > 3.02 to predict platinum resistance were 0.819, 75.0% and 81.45%, respectively. The corresponding values of PLR > 207 were 0.727, 60.42% and 85.48%, respectively. Patients with lower value of NLR (NLR < 3.02) or PLR (PLR < 207) had a longer progression-free survival (PFS) and overall survival (OS). In multivariate analysis, NLR and PLR showed a significant association with PFS (hazard ratio [HR], 1.733; 95% CI, 1.225-2.453, P = 0.002 and HR, 1.952; 95% CI, 1.430-2.662, P < 0.001) and OS (HR, 1.616; 95% CI, 1.138-2.297, P = 0.007, and HR, 2.167; 95% CI, 1.565-3.000, P < 0.001). These results suggest that the assessment of NLR and PLR could assist the identification of patients with poor prognosis and had potential clinical value in predicting platinum resistance in patients with EOC.
BACKGROUND: LncRNA and microRNA play an important role in the development of human cancers; they can act as a tumor suppressor gene or an oncogene. LncRNA GAS5, originating from the separation from tumor suppressor gene cDNA subtractive library, is considered as an oncogene in several kinds of cancers. The expression of miR-221 affects tumorigenesis, invasion and metastasis in multiple types of human cancers. However, there's very little information on the role LncRNA GAS5 and miR-221 play in CRC. Therefore, we conducted this study in order to analyze the association of GAS5 and miR-221 with the prognosis of CRC and preliminary study was done on proliferation, metastasis and invasion of CRC cells. In the present study, we demonstrate the predictive value of long non-coding RNA GAS5 (lncRNA GAS5) and mircoRNA-221 (miR-221) in the prognosis of colorectal cancer (CRC) and their effects on CRC cell proliferation, migration and invasion. METHODS: One hundred and fifty-eight cases with CRC patients and 173 cases of healthy subjects that with no abnormalities, who've been diagnosed through colonoscopy between January 2012 and January 2014 were selected for the study. After the clinicopathological data of the subjects, tissue, plasma and exosomes were collected, lncRNA GAS5 and miR-221 expressions in tissues, plasma and exosomes were measured by reverse transcription quantitative polymerase chain reaction (RT-qPCR). The diagnostic values of lncRNA GAS5 and miR-221 expression in tissues, plasma and exosomes in patients with CRC were analyzed using receiver operating characteristic curve (ROC). Lentiviral vector was constructed for the overexpression of lncRNA GAS5, and SW480 cell line was used for the transfection of the experiment and assigned into an empty vector and GAS5 groups. The cell proliferation, migration and invasion were tested using a cell counting kit-8 assay and Transwell assay respectively. RESULTS: The results revealed that LncRNA GAS5 was upregulated while the miR-221 was downregulated in the tissues, plasma and exosomes of patients with CRC. The results of ROC showed that the expressions of both lncRNA GAS5 and miR-221 in the tissues, plasma and exosomes had diagnostic value in CRC. While the LncRNA GAS5 expression in tissues, plasma and exosomes were associated with the tumor node metastasis (TNM) stage, Dukes stage, lymph node metastasis (LNM), local recurrence rate and distant metastasis rate, the MiR-221 expression in tissues, plasma and exosomes were associated with tumor size, TNM stage, Dukes stage, LNM, local recurrence rate and distant metastasis rate. LncRNA GAS5 and miR-221 expression in tissues, plasma and exosomes were found to be independent prognostic factors for CRC. Following the overexpression of GAS5, the GAS5 expressions was up-regulated and miR-221 expression was down-regulated; the rate of cell proliferation, migration and invasion were decreased. CONCLUSION: The results obtained from the present study provide evidence on the roles of lncRNA GAS5 and miR-221 in the diagnosis and prognosis of CRC, and lncRNA GAS5 was found to inhibit CRC cell proliferation, migration and invasion by down-regulation of miR-221.
Semiconductor quantum dots are tiny light-emitting nanocrystals (2-10 nm) that have captivated researchers in the biomedical field in the last decade. Compared to organic dyes and fluorescent proteins, quantum dots (QDs) have unique optical properties such as tunable emission spectra, improved brightness, superior photostability, and simultaneous excitation of multiple fluorescence colors. Since the first successful reports on biological use of QDs a decade ago, QDs and their bioconjugates have been successfully applied in various imaging applications including fixed cell labeling, imaging of live cell dynamics, in situ tissue profiling, fluorescence detection, sensing and in vivo animal imaging. In this review, we will cover the optical properties of QDs, the biofunctionization strategies, their in vitro diagnostic applications and in vivo imaging applications. In addition, we will discuss the making of a new class of QDs - the self-illuminating QDs and their in vivo imaging and sensing applications. We will conclude with the issues and perspectives on QDs as in vivo imaging probes.
BACKGROUND: The long non-coding RNAs (lncRNAs) are emerging as important regulators in cancer progression. Clear cell renal cell carcinoma (ccRCC) is one of the most common urological cancers with poor prognosis. In this study, we examined the functional role of the lncRNA, nuclear enriched abundant transcript 1 (NEAT1) in ccRCC progression. METHODS: We performed quantitative real time PCR and western blotting assays to measure mRNA and protein expression levels, respectively. CCK-8 assay, cell invasion and migration assays were used to determine the cell proliferative, cell invasive and migratory ability. Flow cytometric analysis was performed to examine cell apoptosis. RESULTS: The expression levels of NEAT1 was up-regulated in ccRCC tissues and up-regulation of NETA1 was positively correlated with tumor size, higher Fuhrman grade, and lymph node metastasis, and also predicts worse 5-year survival rate of patients with ccRCC. NEAT1 knock-down by NEAT siRNAs transfection suppressed cell proliferation and induced cell apoptosis in ccRCC cell lines. In addition, NEAT1 knock-down suppressed cell invasion and migration and inhibited the mRNA and protein expression levels of epithelial-mesenchymal transition-related markers in ccRCC cell lines. CONCLUSIONS: In conclusion, NEAT1 may be an important mediator in the regulation of ccRCC progression and predicts the poor prognosis in patients with ccRCC.
In this paper we evaluate tissue elasticity as a longstanding but qualitative biomarker for prostate cancer and sonoelastography as an emerging imaging tool for providing qualitative and quantitative measurements of prostate tissue stiffness. A Kelvin-Voigt Fractional Derivative ( KVFD) viscoelastic model was used to characterize mechanical stress relaxation data measured from human prostate tissue samples. Mechanical testing results revealed that the viscosity parameter for cancerous prostate tissue is greater than that derived from normal tissue by a factor of approximately 2.4. It was also determined that a significant difference exists between normal and cancerous prostate tissue stiffness ( p < 0.01) yielding an average elastic contrast that increases from 2.1 at 0.1 Hz to 2.5 at 150 Hz. Qualitative sonoelastographic results show promise for cancer detection in prostate and may prove to be an effective adjunct imaging technique for biopsy guidance. Elasticity images obtained with quantitative sonoelastography agree with mechanical testing and histological results. Overall, results indicate tissue elasticity is a promising biomarker for prostate cancer.
BACKGROUND: Bladder cancer is the fourth most common malignancy among men urinary system and it is a complex disease caused by genetic and environmental factors. OBJECTIVE: This study aimed to evaluate the effects of hepatocellular carcinoma up-regulated long non-coding RNA ( lncRNA HULC) on bladder cancer and to reveal the potential mechanisms. METHODS: The expression level of HULC in 276 bladder cancer patients was detected. The association of HULC level with patient recurrence was performed by Kaplan-Meier and log-rank test. Moreover, T24 and RT4 cells were transfected with HULC and ZIC2 targeted siRNAs, HULC expressing vector and corresponding controls. Subsequently, cell viability, apoptosis and tumorigenesis were examined. RESULTS: The expression level of HULC was increased in bladder cancer tissues. High expression of HULC was correlated with advanced clinical stage and lower recurrence-free rate. HULC was remarkably promoted cell viability but inhibited apoptosis, meanwhile conspicuously increased the expression of Cyclin A/D1/E and Bcl-2. Xenograft tumor model showed that HULC promoted tumor weights in vivo. CONCLUSIONS: LncRNA HULC promoted bladder cancer cells proliferation and inhibited apoptosis.
BACKGROUND: MicroRNAs (miRNAs) emerge as important regulators involved in malignant progression in some tumors. MiR-181a has been found to function as a tumor suppressor in some tumors including non-small cell lung cancer (NSCLC). However, the functional role of miR-181a in NSCLC still needed to be investigated. METHODS: The expression of miR-181a were determined by qRT-PCR, the association between miR-181a and clinicopathological data were performed by chi-square test and survival analysis were evaluated by Kaplan-Meier curve and log rank test. Cell proliferation and invasion were assessed by CCK8, cell colony formation and transwell assays. Luciferase reporter assay demonstrated that CDK1 was a target of miR-181a. Western blot assay detected the relative protein expression. RESULTS: In the study, our results showed that miR-181a was significantly down-regulated in non-small cell lung cancer (NSCLC) tissues and cell lines. MiR-181 expression levels were significantly associated with histological grade, N status and TNM stage in the patients and lower miR-181a predicted a poor prognosis in NSCLC patients. Furthermore, upregulation of miR-181a significantly suppressed the NSCLC cell proliferation, colony formation, and cell invasion capacities. Moreover, upregulation of miR-181a inhibited CyclinB1 and CyclinD1 expression in NSCLC cells. Luciferase activity assay results demonstrated CDK1 was a direct target of miR-181a and miR-181a inhibited cell proliferation by regulating the mRNA and protein levels of CDK1 in NSCLC cells. CONCLUSION: These data suggested that miR-181a plays a tumor suppressor and may be a potential therapeutic target for NSCLC patients.
In China, hepatocellular carcinoma (HCC) is the most commonly diagnosed cancer and the leading cause of cancer death in men, followed by lung and stomach cancer. There was an urgent need to identify novel prognostic biomarkers for HCC. We explored the expression pattern of m6A related proteins in HCC tissues by using TCGA in this study. We found that the m6A 'reader' YTHDF1 was significantly upregulated in HCC and was positive correlated with pathology stage. Kaplan-Meier analysis showed that Lower YTHDF1 expression level was associated with better survival of HCC patients. Furthermore, we performed GO and KEGG pathway analysis of YTHDF1 co-expressed genes and found YTHDF1 played an important role in regulating HCC cell cycle progression and metabolism. We believed that this study will provide a potential new therapeutic and prognostic target for HCC.