scholarly journals Neuromedin U induces an invasive phenotype in CRC cells expressing the NMUR2 receptor

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Patrycja Przygodzka ◽  
Ewelina Sochacka ◽  
Kamila Soboska ◽  
Marcin Pacholczyk ◽  
Izabela Papiewska-Pająk ◽  
...  
Keyword(s):  
Protein Detection ◽  
Dna Demethylation ◽  
Receptor Expression ◽  
Protein Sequencing ◽  
The Cancer Genome Atlas ◽  
Migration And Invasion ◽  
Accurate Identification ◽  
Invasive Phenotype ◽  
Tissue Samples ◽  
Variable Expression

Abstract Background Successful colorectal cancer (CRC) therapy often depends on the accurate identification of primary tumours with invasive potential. There is still a lack of identified pathological factors associated with disease recurrence that could help in making treatment decisions. Neuromedin U (NMU) is a secretory neuropeptide that was first isolated from the porcine spinal cord, and it has emerged as a novel factor involved in the tumorigenesis and/or metastasis of many types of cancers. Previously associated with processes leading to CRC cell invasiveness, NMU has the potential to be a marker of poor outcome, but it has not been extensively studied in CRC. Methods Data from The Cancer Genome Atlas (TCGA) were used to analyse NMU and NMU receptor (NMUR1 and NMUR2) expression in CRC tissues vs. normal tissues, and real-time PCR was used for NMU and NMU receptor expression analysis. NMU protein detection was performed by immunoblotting. Secreted NMU was immunoprecipitated from cell culture-conditioned media and analysed by immunoblotting and protein sequencing. DNA demethylation by 5-aza-CdR was used to analyse the regulation of NMUR1 and NMUR2 expression. NMU receptor activity was monitored by detecting calcium mobilisation in cells loaded with fluo-4, and ERK1/2 kinase activation was detected after treatment with NMU or receptor agonist. Cell migration and invasion were investigated using membrane filters. Integrin expression was evaluated by flow cytometry. Results The obtained data revealed elevated expression of NMU and NMUR2 in CRC tissue samples and variable expression in the analysed CRC cell lines. We have shown, for the first time, that NMUR2 activation induces signalling in CRC cells and that NMU increases the motility and invasiveness of NMUR2-positive CRC cells and increases prometastatic integrin receptor subunit expression. Conclusions Our results show the ability of CRC cells to respond to NMU via activation of the NMUR2 receptor, which ultimately leads to a shift in the CRC phenotype towards a more invasive phenotype.

scholarly journals MiR-1301-3p Inhibits Epithelial to Mesenchymal Transition via Targeting RhoA in Pancreatic Cancer

2020 ◽  
Author(s):  
Xinxue Zhang ◽  
Xin Zhao ◽  
Junming Xu ◽  
Jun Ma ◽  
Zhe Liu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Epithelial To Mesenchymal Transition ◽  
Epithelial Mesenchymal Transition ◽  
The Cancer Genome Atlas ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Tissue Samples ◽  
Mesenchymal Transition ◽  
Pathological Differentiation

Abstract Background: Micro(mi)RNAs play an essential role in the epithelial-mesenchymal transition (EMT) process in human cancers. This study aimed to uncover the regulatory mechanism of miR-1301-3p on EMT in pancreatic cancer (PC).Methods: GEO database (GSE31568, GSE41372, and GSE32688) and the PC cohort of The Cancer Genome Atlas were applied to discover the expression and prognostic role of miR-1301-3p. In the validation cohort, qRT-PCR was performed in 72 paired PC tissue samples. CCK-8, wound healing, and transwell migration assays were used to detect miR-1301-3p function on PC cells. Luciferase reporter assays and western blotting were performed to discover the potential target of miR-1301-3p on EMT.Results: Our study revealed that miR-1301-3p was downregulated in PC tissues compared with normal samples. A low level of miR-1301-3p was associated with malignant pathological differentiation, lymphatic metastasis, tumor residual, and unsatisfactory overall survival. Gene Ontology analyses indicated that miR-1301-3p possibly regulated cell cycle and adheren junction. In vitro assays showed that miR-1301-3p suppressed proliferation, migration, and invasion ability of PC cells. Mechanically, miR-1301-3p inhibits RhoA expression, and knockdown of RhoA upregulated E-cadherin; however, downregulated N-cadherin and vimentin level.Conclusions: MiR-1301-3p acts as a prognostic biomarker for PC and inhibits PC progression by targeting RhoA induced EMT process.

scholarly journals Thymosin β 10 is overexpressed and associated with unfavorable prognosis in hepatocellular carcinoma

2019 ◽  
Vol 39 (3) ◽  
Author(s):  
Chunrong Song ◽  
Zhong Su ◽  
Jing Guo
Keyword(s):  
Hepatocellular Carcinoma ◽  
Human Cancer ◽  
Normal Liver ◽  
The Cancer Genome Atlas ◽  
Migration And Invasion ◽  
Tumor Biomarker ◽  
Advanced Tumor Stage ◽  
Poor Overall Survival ◽  
Tissue Samples ◽  
Advanced Tumor

Abstract Thymosin β 10 (TMSB10) has been demonstrated to be overexpressed and function as an oncogene in most types of human cancer including hepatocellular carcinoma (HCC). In our study, we present more evidence about the clinical significance and biological function of TMSB10 in HCC. First, we observed levels of TMSB10 expression were obviously increased in HCC tissues compared with normal liver tissues at The Cancer Genome Atlas (TCGA) datasets. Furthermore, we confirmed that TMSB10 mRNA and protein levels were also increased in HCC tissue samples compared with normal adjacent normal liver tissue samples. In addition, we found high TMSB10 expression was remarkably associated with the advanced tumor stage, large tumor size, distant metastasis, and poor prognosis, and acted as an independent factor for predicting poor overall survival in HCC patients. Loss-of-function studies suggested silencing of TMSB10 expression dramatically reduced cell proliferation, migration, and invasion in HCC. In conclusion, TMSB10 may hold promise as a tumor biomarker for predicting prognosis and a potential target for developing a novel therapeutic strategy.

scholarly journals MIR100HG: a credible prognostic biomarker and an oncogenic lncRNA in gastric cancer

2019 ◽  
Vol 39 (4) ◽  
Author(s):  
Jun Li ◽  
Qingfeng Xu ◽  
Wen Wang ◽  
Shaojun Sun
Keyword(s):  
Gastric Cancer ◽  
Cancer Patients ◽  
Prognostic Biomarker ◽  
Human Cancer ◽  
The Cancer Genome Atlas ◽  
Migration And Invasion ◽  
Epithelial Cell Line ◽  
Tissue Samples ◽  
Poor Prognostic Factor ◽  
Gastric Cancer Patients

Abstract The MIR100HG expression was observed to be up-regulated or down-regulated in human cancer tissues depending on tumor types. However, there was no report about the role of MIR100HG in gastric cancer. In our study, we first found levels of MIR100HG expression were increased in gastric cancer cell lines and tissue samples compared with normal gastric epithelial cell line and adjacent normal gastric mucosa tissue samples, respectively. Moreover, high MIR100HG expression was positively associated with clinical stage, tumor invasion, lymph node metastasis, and distant metastasis in gastric cancer patients. Survival analysis showed MIR100HG expression was negative correlated with clinical outcome in gastric cancer patients from The Cancer Genome Atlas (TCGA) database or our study, and high MIR100HG expression served as an independent poor prognostic factor for gastric cancer patient’s overall survival. The study in vitro suggested down-regulation of MIR100HG expression inhibits cell proliferation, migration, and invasion in gastric cancer. In conclusion, MIR100HG is a credible prognostic biomarker and functions as an oncogenic lncRNA in gastric cancer.

scholarly journals Development and validation of a novel 3-gene prognostic model for pancreatic adenocarcinoma based on ferroptosis-related genes

2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Jihua Yang ◽  
XiaoHong Wei ◽  
Fang Hu ◽  
Wei Dong ◽  
Liao Sun
Keyword(s):  
Pancreatic Adenocarcinoma ◽  
Prognostic Model ◽  
Molecular Model ◽  
External Validation ◽  
Gene Signature ◽  
The Cancer Genome Atlas ◽  
Functional Enrichment ◽  
Migration And Invasion ◽  
Lasso Regression ◽  
Tissue Samples

Abstract Background Molecular markers play an important role in predicting clinical outcomes in pancreatic adenocarcinoma (PAAD) patients. Analysis of the ferroptosis-related genes may provide novel potential targets for the prognosis and treatment of PAAD. Methods RNA-sequence and clinical data of PAAD was downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) public databases. The PAAD samples were clustered by a non-negative matrix factorization (NMF) algorithm. The differentially expressed genes (DEGs) between different subtypes were used by “limma_3.42.2” package. The R software package clusterProfiler was used for functional enrichment analysis. Then, a multivariate Cox proportional and LASSO regression were used to develop a ferroptosis-related gene signature for pancreatic adenocarcinoma. A nomogram and corrected curves were constructed. Finally, the expression and function of these signature genes were explored by qRT-PCR, immunohistochemistry (IHC) and proliferation, migration and invasion assays. Results The 173 samples were divided into 3 categories (C1, C2, and C3) and a 3-gene signature model (ALOX5, ALOX12, and CISD1) was constructed. The prognostic model showed good independent prognostic ability in PAAD. In the GSE62452 external validation set, the molecular model also showed good risk prediction. KM-curve analysis showed that there were significant differences between the high and low-risk groups, samples with a high-risk score had a worse prognosis. The predictive efficiency of the 3-gene signature-based nomogram was significantly better than that of traditional clinical features. For comparison with other models, that our model, with a reasonable number of genes, yields a more effective result. The results obtained with qPCR and IHC assays showed that ALOX5 was highly expressed, whether ALOX12 and CISD1 were expressed at low levels in tissue samples. Finally, function assays results suggested that ALOX5 may be an oncogene and ALOX12 and CISD1 may be tumor suppressor genes. Conclusions We present a novel prognostic molecular model for PAAD based on ferroptosis-related genes, which serves as a potentially effective tool for prognostic differentiation in pancreatic cancer patients.

scholarly journals Long Non-Coding RNA SH3PXD2A-AS1 Promotes Cell Progression Partly Through Epigenetic Silencing P57 and KLF2 in Colorectal Cancer

2018 ◽  
Vol 46 (6) ◽  
pp. 2197-2214 ◽  
Author(s):  
Zhonghua Ma ◽  
Peng Peng ◽  
Jing Zhou ◽  
Bingqing Hui ◽  
Hao Ji ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colorectal Cancer ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
The Cancer Genome Atlas ◽  
Current Evidence ◽  
Migration And Invasion ◽  
Mice Model ◽  
Tissue Samples

Background/Aims: Colorectal cancer (CRC) is one of the most commonly diagnosed malignancies worldwide. Current evidence has revealed the key roles of long non-coding RNAs (IncRNAs) in multiple cancers, including CRC. In this study we identified the lncRNA SH3PXD2A-AS1 as a novel molecule associated with CRC progression by analyzing the publicly available data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) assays were performed to examine the expression levels of SH3PXD2A-AS1 in CRC tissue samples and CRC cell lines. Cell viability examination, colony-formation experiments, ethynyl deoxyuridine (Edu) assays and flow cytometry were performed to investigate the roles of SH3PXD2A-AS1 in CRC proliferation, cell cycle regulation, and apoptosis. Transwell assays were used to explore the effects of SH3PXD2A-AS1 on CRC cells migration and invasion. A nude mice model was used to assess the effects of SH3PXD2A-AS1 on tumorigenesis in vivo. Subcellular fractionation, RNA immunoprecipitation (RIP), and chromatin immunoprecipitation (ChIP) assays were conducted to detect the molecular mechanisms of SH3PXD2A-ASl-mediated gene expression. Rescue assays were used to determine whether P57 and Kruppel-like factor 2 (KLF2) were involved in SH3PXD2A-ASl-dependent CRC proliferation. Results: We firstly found that SH3PXD2A-AS1 was significantly upregulated in CRC tissues and cell lines, and overexpression of SH3PXD2A-AS1 was correlated with tumor size, TNM stage, and lymph node metastasis in patients with CRC. Furthermore, SH3PXD2A-AS1 knockdown inhibited CRC cells proliferation, migration and invasion in vitro, and suppressed tumorigenesis in vivo. Mechanistic studies indicated that SH3PXD2A-AS1 could epiqenetically repress P57 and KLF2 expression through interaction with EZH2. Rescue experiments suggested that SH3PXD2A-ASl-mediated oncogenesis was impaired by overexpression of P57 or KLF2. Interestingly, the expression of SH3PXD2A-AS1 was inversely correlated with the expression of P57 and KLF2 in CRC tissue samples. Conclusion: Our research presents the first evidence that SH3PXD2A-AS1 acts as an oncogene in CRC, and may be a promising diagnostic or therapeutic target in patients with CRC.

scholarly journals Novel LncRNA OXCT1-AS1 Indicates Poor Prognosis and Contributes to Tumorigenesis by Regulating miR-195/CDC25A Axis in Glioblastoma

2020 ◽  
Author(s):  
Chen Zhong ◽  
Qian Yu ◽  
Shengjun Zhou ◽  
Yucong Peng ◽  
Zhendong Liu ◽  
...  
Keyword(s):  
Therapeutic Target ◽  
Poor Prognosis ◽  
Cell Clone ◽  
Glioma Cells ◽  
The Cancer Genome Atlas ◽  
Migration And Invasion ◽  
Potential Mechanism ◽  
Potential Therapeutic Target ◽  
Tissue Samples

Abstract BackgroundIt’s well known that long noncoding RNAs (lncRNAs) contribute to multiple biological processes of human glioblastoma (GBM). However, identifying a specific lncRNA target is still the major difficulty. In this study, bioinformatics methods and competing endogenous RNA network (ceRNA) regulatory rules was used to identify GBM related lncRNAs, and found OXCT1 antisense RNA 1 (OXCT1-AS1) may acted as a potential therapeutic target for treatment of glioma.MethodsBased on the Gene Expression Omnibus (GEO) date set, we identified differential lncRNAs, microRNAs and mRNAs and constructed a lncRNA associated ceRNA network.Novel lncRNA OXCT1-AS1 was proposed to exercise its function as a ceRNA, and its potential targeted miRNAs was predicted through the database LncBase Predicted v.2. The expression pattern of OXCT1-AS1 was measured in glioma and normal tissue samples. Effect of OXCT1-AS1 on glioma cells were checked by cell count kit 8 assay, cell clone formation assay, transwell assay and flow cytometry in vitro, respectively. The dual-luciferase activity assay was performed to investigate the potential mechanism of ceRNA network. Finally, orthotopic mouse models of glioma was created to evaluate the influence of OXCT1-AS1 on tumor growth in vivo.ResultsIn this study, it was found that the expression of lncRNA OXCT1-AS1 is upregulated in both The Cancer Genome Atlas (TCGA) GBM cases and GBM tissue samples we collected, and a high expression of OXCT1-AS1 predicts poor prognosis of gliomas. Suppressing OXCT1-AS1 expression significantly decreased the proliferation of GBM cells and inhibited cell migration and invasion. We further investigated the potential mechanism and found OXCT1-AS1 may acted as a ceRNA of miR-195 to enhance CDC25A expression and attenuate glioma cells progression. Finally, knocking down of OXCT1-AS1 notably attenuated the severity of glioma in vivo.ConclusionOXCT1-AS1 inhibited glioma progression by regulating miR-195-5p/ CDC25A axis and can be a specific tumor marker and a novel potential therapeutic target for glioma treatment.

scholarly journals Long Noncoding RNA ASB16-AS1 Promotes Proliferation, Migration, and Invasion in Glioma Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Delong Zhang ◽  
Huanggui Zhou ◽  
Jun Liu ◽  
Jie Mao
Keyword(s):  
Differential Expression ◽  
Noncoding Rna ◽  
Expression Profiles ◽  
Tumor Staging ◽  
Quantitative Polymerase Chain Reaction ◽  
Differential Expression Analysis ◽  
Glioma Cells ◽  
The Cancer Genome Atlas ◽  
Migration And Invasion ◽  
Tissue Samples

Glioma is a lethal, malignant intracranial tumor that becomes progressively common. It has been shown that long noncoding RNAs (lncRNAs) serve important roles in numerous diseases such as gliomas. lncRNAs can regulate the expression of targeted genes through various mechanisms. To identify a novel lncRNA that may be critical in glioma, the present study downloaded the RNA expression profiles of 171 glioma tissues and 5 normal tissues from The Cancer Genome Atlas (TCGA) database using the TCGAbiolinks package in R. Then, lncRNAs in the downloaded TCGA data were identified using the HUGO Gene Nomenclature Committee (HGNC). Based on the fragments per kilobase million value, differential expression analysis was conducted using the limma package in R. In addition, receiver operating characteristic (ROC) analysis was performed, and the area under the curve (AUC) was evaluated using the ROCR package in R. A total of 178 lncRNAs corresponding to differentially expressed genes with an AUC >0.85 were selected. Upon identifying the differential lncRNAs, ceRNA networks were constructed with these differential lncRNAs using the starbase database. From these networks, the top 10% hub genes were selected. In addition, the present study randomly selected 4 lncRNAs for quantitative polymerase chain reaction validation in tissue samples. The results revealed that lncRNA ASB16-AS1 exhibited significantly differential expression in tissue samples and was significantly associated with tumor staging and grading. Furthermore, the proliferation, invasion, and migration of U87MG and U251 glioblastoma stem-like cells (U87GS, U251GS) were significantly inhibited upon inhibition of ASB16-AS1, and the expression of key proteins in the EMT signaling pathway was affected by knocking down ASB16-AS1. Overall, the present study revealed that lncRNA ASB16-AS1 improves the proliferation, migration, and invasion of glioma cells.

scholarly journals AHA1 regulates cell migration and invasion via the EMT pathway in colorectal adenocarcinomas

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dasom Kim ◽  
Ji Wook Moon ◽  
Dong Hwa Min ◽  
Eun Sun Ko ◽  
Bokyung Ahn ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Lines ◽  
Fibroblast Cell ◽  
The Cancer Genome Atlas ◽  
Migration And Invasion ◽  
Specific Marker ◽  
Tissue Samples ◽  
Expression Levels ◽  
Cell Migration And Invasion ◽  
Normal Tissues

AbstractThe progression of colorectal cancer (CRC) has been well studied and understood with the development of molecular and genetic techniques. However, specific marker(s) that could be used to predict lymph node (LN) involvement, which is the most important prognostic factor for CRC, have not been identified so far. Our previous study, in which network analysis of LN(+) and LN(−) CRC gene expression was carried out with data obtained from the Cancer Genome Atlas, led to the identification of AHA1. AHA1 is a co-chaperone activator of the Hsp90 ATPase activity. However, the role of AHA1 expression in cancer cells is still unclear. To investigate how AHA1 expression regulates the cancer cell progression and/or metastasis of human CRC, the expression levels of AHA1 and Hsp90 were examined in 105 CRC tissue samples and compared with those in paired normal tissue. The RNA expression levels of AHA1 and Hsp90aa1, but not Hsp90ab, were significantly higher in cancer tissues than in adjacent paired normal tissues (p = 0.032 and p = 0.0002, respectively). In particular, AHA1, but not Hsp90aa1 and Hsp90ab, was closely associated with the TNM stage, LN stage, and tumor metastasis (p = 0.035, p = 0.012, and p = 0.0003, respectively). Moreover, the expression of AHA1 was not only higher in the CRC cell lines than in the normal colon fibroblast cell line but was also associated with the progression of these CRC cell lines. Overexpression of AHA1 in SW480 cells increased, whereas suppression of AHA1 expression in HCT116 cells reduced cell migration and invasion through the regulation of Snail, E-cadherin, pSRC, and pAKT, which are associated with EMT signaling. Taken together, our study suggests that AHA1 contributes to the metastatic advantage of human CRC.

scholarly journals TEAD4 modulated LncRNA MNX1-AS1 contributes to gastric cancer progression partly through suppressing BTG2 and activating BCL2

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
You Shuai ◽  
Zhonghua Ma ◽  
Weitao Liu ◽  
Tao Yu ◽  
Changsheng Yan ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Mechanistic Model ◽  
Ectopic Expression ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Tissue Samples ◽  
Reporter Assays

Abstract Background Gastric cancer (GC) is the third leading cause of cancer-related mortality globally. Long noncoding RNAs (lncRNAs) are dysregulated in obvious malignancies including GC and exploring the regulatory mechanisms underlying their expression is an attractive research area. However, these molecular mechanisms require further clarification, especially upstream mechanisms. Methods LncRNA MNX1-AS1 expression in GC tissue samples was investigated via microarray analysis and further determined in a cohort of GC tissues via quantitative reverse transcription polymerase chain reaction (qRT-PCR) assays. Cell proliferation and flow cytometry assays were performed to confirm the roles of MNX1-AS1 in GC proliferation, cell cycle regulation, and apoptosis. The influence of MNX1-AS1 on GC cell migration and invasion was explored with Transwell assays. A xenograft tumour model was established to verify the effects of MNX1-AS1 on in vivo tumourigenesis. The TEAD4-involved upstream regulatory mechanism of MNX1-AS1 was explored through ChIP and luciferase reporter assays. The mechanistic model of MNX1-AS1 in regulating gene expression was further detected by subcellular fractionation, FISH, RIP, ChIP and luciferase reporter assays. Results It was found that MNX1-AS1 displayed obvious upregulation in GC tissue samples and cell lines, and ectopic expression of MNX1-AS1 predicted poor clinical outcomes for patients with GC. Overexpressed MNX1-AS1 expression promoted proliferation, migration and invasion of GC cells markedly, whereas decreased MNX1-AS1 expression elicited the opposite effects. Consistent with the in vitro results, MNX1-AS1 depletion effectively inhibited the growth of xenograft tumour in vivo. Mechanistically, TEAD4 directly bound the promoter region of MNX1-AS1 and stimulated the transcription of MNX1-AS1. Furthermore, MNX1-AS1 can sponge miR-6785-5p to upregulate the expression of BCL2 in GC cells. Meanwhile, MNX1-AS1 suppressed the transcription of BTG2 by recruiting polycomb repressive complex 2 to BTG2 promoter regions. Conclusions Our findings demonstrate that MNX1-AS1 may be able to serve as a prognostic indicator in GC patients and that TEAD4-activatd MNX1-AS1 can promote GC progression through EZH2/BTG2 and miR-6785-5p/BCL2 axes, implicating it as a novel and potent target for the treatment of GC.

scholarly journals Expression and clinical significance of miR-3615 in hepatocellular carcinoma

2021 ◽  
Vol 49 (1) ◽  
pp. 030006052098154
Author(s):  
Xin Yuan ◽  
Yize Zhang ◽  
Zujiang Yu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Survival Curve ◽  
Clinicopathological Characteristics ◽  
The Cancer Genome Atlas ◽  
Prognostic Information ◽  
Ki 67 ◽  
Tissue Samples ◽  
Expression Levels ◽  
Kaplan Meier ◽  
Serum Alpha Fetoprotein

Objective To investigate the association between microRNA-3615 (miR-3615) expression and the prognosis and clinicopathological features in patients with hepatocellular carcinoma (HCC). Methods We obtained clinicopathological and genomic data and prognostic information on HCC patients from The Cancer Genome Atlas (TCGA) database. We then analyzed differences in miR-3615 expression levels between HCC and adjacent tissues using SPSS software, and examined the relationships between miR-3615 expression levels and clinicopathological characteristics. We also explored the influence of miR-3615 expression levels on the prognosis of HCC patients using Kaplan–Meier survival curve analysis. Results Based on data for 345 HCC and 50 adjacent normal tissue samples, expression levels of miR-3615 were significantly higher in HCC tissues compared with adjacent tissues. MiR-3615 expression levels in HCC patients were negatively correlated with overall survival time and positively correlated with high TNM stage, serum Ki-67 expression level, and serum alpha-fetoprotein level. There were no significant correlations between miR-3615 expression and age, sex, and pathological grade. Conclusion MiR-3615 may be a promising new biomarker and prognostic factor for HCC.

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