4.5 Article

Analysis of differentially expressed long non-coding RNAs revealed a pro-tumor role of MIR205HG in cervical cancer

Journal

MOLECULAR MEDICINE REPORTS
Volume 25, Issue 2, Pages -

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2021.12558

Keywords

MIR205HG; cervical cancer; long non-coding RNAs

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Cervical cancer is a major threat to women's health and the role of long non-coding RNAs (lncRNAs) in this cancer type is largely unknown. In this study, researchers analyzed the expression of different lncRNAs in cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC) tissues and found that MIR205HG was overexpressed in CESC tissues. Further analysis revealed that genes related to MIR205HG were enriched in cancer-related pathways. Knockdown of MIR205HG significantly reduced the proliferation and migratory and invasive abilities of CESC cells. These findings identify potential lncRNA candidates for cervical cancer research and suggest a pro-tumor role of MIR205HG in CESC.
Cervical cancer is the fourth most common female malignancy for both incidence and mortality worldwide and is one of the major threats to women's health. The role of long non-coding RNAs (lncRNAs) in cervical cancer remains largely unknown. In the present study, the differentially expressed lncRNAs in cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC) tissues were retrieved form The Cancer Genome Atlas (TCGA) and were analyzed. The expression analysis of related genes was performed with GEPIA. The proliferation and migratory and invasive abilities of MIR205HG knockdown CESC cells were analyzed using Cell Counting Kit-8 and transwell assays. The expression of Ki-67 and p16 was detected by immunofluorescence. A total of 203 differentially expressed lncRNAs were identified. The results demonstrated that MIR205HG was overexpressed in CESC tissues. Furthermore, the genes related to MIR205HG were enriched in cancer-related pathways. MIR205HG knockdown significantly decreased the proliferation and migratory and invasive abilities of CESC cells. In addition, silencing of MIR205HG significantly decreased the expression of p16 in C-33 A cells. The expression of fibroblast growth factor receptor 3, thymidine phosphorylase and GTPase HRas was downregulated in MIR205HG knockdown CESC cells. These findings revealed some potential lncRNA candidates for cervical cancer research and suggested that MIR205HG may have a pro-tumor role in CESC.

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