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CiRS-7 promotes growth and metastasis of esophageal squamous cell carcinoma via regulation of miR-7/HOXB13.

ABSTRACT: The circular RNA ciRS-7 has been reported to be involved in the pathogenesis of various tumors, including gastric and colorectal cancer. However, the role of ciRS-7 in esophageal squamous cell carcinoma (ESCC) remains unsolved. In this study, we found that the ciRS-7 expression was significantly upregulated in ESCC cancer tissues compared with matched normal tissues and associated with poor patient survival. Overexpression of ciRS-7 abrogated the tumor-suppressive roles of miR-7 including cell proliferation, migration and invasion in vitro as well as tumor growth and lung metastasis in vivo. Mechanistically, ciRS-7 functioned as the sponge of miR-7 and reactivated its downstream HOXB13-mediated NF-?B/p65 pathway. Conclusively, our findings demonstrate how ciRS-7 induces malignant progression of ESCC and that ciRS-7 may act as a novel prognostic marker and therapeutic target for this lethal disease.

SUBMITTER: Li RC

PROVIDER: S-EPMC6079012 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature

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CiRS-7 promotes growth and metastasis of esophageal squamous cell carcinoma via regulation of miR-7/HOXB13.

Li Rui-Chao RC Ke Shun S Meng Fan-Kai FK Lu Jun J Zou Xiao-Jing XJ He Zhi-Gang ZG Wang Weng-Feng WF Fang Ming-Hao MH

Cell death & disease 20180806 8

The circular RNA ciRS-7 has been reported to be involved in the pathogenesis of various tumors, including gastric and colorectal cancer. However, the role of ciRS-7 in esophageal squamous cell carcinoma (ESCC) remains unsolved. In this study, we found that the ciRS-7 expression was significantly upregulated in ESCC cancer tissues compared with matched normal tissues and associated with poor patient survival. Overexpression of ciRS-7 abrogated the tumor-suppressive roles of miR-7 including cell p ...[more]

PMID: 30082829

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Project description:BackgroundEsophageal cancer (EC) is one of the most lethal cancers. Esophageal squamous cell carcinoma (ESCC) is the most common histological subtype in Asian people. Diverse microRNAs, such as miR-375, have been confirmed to be involved in the process of tumorigenesis and metastasis. However, the underlying mechanism through which miR-375 acts in ESCC patients remains unknown.MethodsWe used The Cancer Genome Atlas (TCGA) database to analyze the association between miR-375 and the survival rate in patients with esophageal squamous cell carcinoma. Real Time quantitative PCR (RT-qPCR) analysis was performed to evaluate the level of miR-375 in EC tissues and cells. A luciferase reporter assay was used to confirm the target gene of miR-375. A colony formation assay as well as flow cytometric and transwell invasion experiments were employed to examine the effects of miR-375 and peroxiredoxin 1 (PRDX1) on ESCC cells. A tumor xenograft mouse model was then used to investigate the role of miR-375 on tumor growth in vivo. Moreover, we performed rescue experiments to evaluate the effect of PRDX1 on ESCC progression.ResultsmiR-375 expression was significantly downregulated in both ESCC clinical tissues and serum, and the reduction of miR-375 was remarkably linked to a poor prognosis in ESCC. Further investigation illustrated that aberrant expression of miR-375 dampened the growth and infiltration of ESCC cells both in vitro and in vivo. Bioinformatics and luciferase reporter analysis verified that the transcript of PRDX1 is a direct target of miR-375 and its expression in ESCC cells was found to be inversely modulated by miR-375. Moreover, the tumor formation experiment in nude mice confirmed that miR-375 can effectively dampen tumor growth in xenograft tumor mice models. Notably, over-expression of PRDX1 effectively counteracted the tumor-suppressing capabilities of miR-375.ConclusionsWe demonstrated the antitumor effect of miR-375 on ESCC by targeting PRDX1 both in vitro and in vivo.

Project description:BackgroundEsophagus squamous cell carcinoma (ESCC) is a sort of cancer that occurs in the esophageal epithelial tissue. This study performed integrated bioinformatics analysis of Gene Expression Omnibus (GEO) datasets GSE32424, GSE29968, and GSE130078. Collagen type XI alpha 1 (COL11A1) was identified as the hub gene in ESCC progression. The involvement of COL11A1 in ESCC development was next determined using in vitro functional tests.MethodsHub genes were identified through integrated bioinformatics analysis. The real-time reverse transcription-polymerase chain reaction was implemented for detecting the expression of COL11A1 mRNA in esophageal cancer cells. KYSE-30 cells were transfected using a vector encoding COL11A1. The proliferation of cells was determined using the Cell Counting Kit-8 (CCK-8) assay. Detection of the cell migration and invasion was made through making use of the transwell test. The development of ESCC cells in vivo was evaluated in naked mice. The interplay among COL11A1 and microRNA-335-5p (miR-335-5p) was discovered using a luciferase reporter experiment.ResultsIn vitro studies showed the upregulation of COL11A1 in ESCC cell lines obtained from ESCC patients and upregulation of COL11A1 was correlated with poor disease-free survival of ESCC patients, thereby implying an oncogenic involvement of COL11A1 in ESCC. Overexpression of COL11A1 enhanced the proliferation of ESCC cells, invasion, and migration; whereas COL11A1 knockdown impeded the proliferation of ESCC cells, invasion, and migration. Additionally, miRNA pathway analysis in combination with TargetScan's online prediction and the luciferase reporter assay suggested miR-335-5p targeting and negatively regulating the COL11A1 3' untranslated region (3'UTR) within ESCC cells. MiR-335-5p overexpression diminished the development of ESCC cells. Additionally, co-expression of COL11A1 ameliorated the repressive influence of miR-335-5p overexpression on the growth and metastasis of ESCC cells.ConclusionsUsing comprehensive bioinformatics analysis, the current study identified COL11A1 as an oncogene in ESCC. The mechanistic studies indicated that COL11A1 promoted ESCC cell progression and that miR-335-5p negatively regulated the expression of COL11A1 in ESCC.

Project description:BackgroundThe human ether a-go-go-related gene 1 (HERG1) is involved in tumor progression; however, its role in esophageal squamous cell carcinoma (ESCC) is not well studied. This study investigated HERG1 function in ESCC progression and elucidated the underlying mechanisms.MethodsThe prognostic value of HERG1 was determined by immunohistochemistry in ESCC biopsies. Cell growth and proliferation were analyzed by colony formation and methyl thiazolyl tetrazolium assays. Cell migration and invasion were analyzed by wound healing and Boyden transwell assays. Epithelial-mesenchymal transition (EMT) was evaluated by immunoblotting and quantitative polymerase chain reaction (qPCR). A xenograft mouse model was used to validate the tumorigenic and metastatic roles of HERG1 in vivo.ResultsHERG1 expression was overall higher in ESCC tissues compared to adjacent non-tumor tissues. A retrospective analysis of 349 patients with ESCC (stages I-IV) confirmed increased HERG1 expression was associated with disease progression and higher mortality rate. The overall survival of the patients was significantly worse when their tumors displayed higher HERG1 expression. HERG1 knockdown reduced tumor growth and metastasis in athymic mice. HERG1 affected the proliferation, migration, and invasion of two ESCC cell lines (TE-1 and KYSE-30). Changes in HERG1 expression affected the expression of cell cycle- and EMT-related proteins; these effects were reversed by altering the expression of thioredoxin domain-containing protein 5 (TXNDC5), which is also associated with the clinicopathological characteristics of patients with ESCC and is relevant to HERG1 in pathological biopsies. Additionally, HERG1 expression altered phosphoinositide 3-kinase (PI3K) and AKT phosphorylation, thereby affecting TXNDC5 expression.ConclusionsHERG1 contributes to poor prognosis in patients with ESCC by promoting ESCC cell proliferation, migration, and invasion via TXNDC5 through the PI3K/AKT signaling pathway. Our findings provided novel insights into the pathology of ESCC and role of HERG1 in tumor progression, suggesting that targeting HERG1 has potential diagnostic and therapeutic value for ESCC treatment.

Dataset Information

CiRS-7 promotes growth and metastasis of esophageal squamous cell carcinoma via regulation of miR-7/HOXB13.

Publications

CiRS-7 promotes growth and metastasis of esophageal squamous cell carcinoma via regulation of miR-7/HOXB13.

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