Open AccessDownregulation of miR‑106b‑3p increases sensitivity to cisplatin in esophageal cancer cells by targeting TGM3
Author(s) -
Yiwei Zhu,
Yun Zhang,
Xiaohua Li,
Yuntao Su,
Na Wang,
Minli Chen,
Zhe Yang
Publication year - 2021
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2021.12110
Subject(s) - cisplatin , downregulation and upregulation , microrna , cancer research , apoptosis , cell cycle , oncogene , flow cytometry , biology , viability assay , cell , cell culture , microbiology and biotechnology , chemotherapy , biochemistry , genetics , gene
Esophageal cancer (EC) is one of the most malignant and lethal digestive‑related tumors worldwide. However, acquired drug resistance is a major obstacle concerning anticancer chemotherapy. An increasing number of studies have reported that microRNAs (miRNAs/miRs) are implicated in regulating the sensitivity of drug resistance in esophageal squamous cell carcinoma (ESCC). The aim of the present study was to investigate the role of miR‑106b‑3p in the sensitivity of cisplatin for ESCC. Initially, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was performed to analyze miR‑106b‑3p and protein‑glutamine γ‑glutamyltransferase E (TGM3) expression levels in ESCC and non‑tumor adjacent tissues. By using bioinformatics software TargetScan, TGM3 was predicted to be a potential downstream target of miR‑106‑3p. Following verification that TGM3 was a downstream target of miR‑106b‑3p by the dual‑luciferase reporter assay, the effects of miR‑106b‑3p transfection on KYSE30 cell viability and apoptosis following treatment with cisplatin were confirmed using Cell Counting Kit‑8 and flow cytometry assays, respectively. The results revealed that miR‑106b‑3p levels were upregulated, whereas TMG3 levels were downregulated in ESCC tissues. Dual‑luciferase reporter assays confirmed that miR‑106b‑3p negatively regulated TGM3 expression by binding to its 3'UTR sequence. It was also shown that inhibition of miR‑106b‑3p could enhance the anti‑proliferative effects, while promoting the apoptotic effects of cisplatin in the KYSE30 cell line by targeting TGM3. In conclusion, the present study demonstrated that downregulation of miR‑106b‑3p may increase the sensitivity of KYSE30 cell to cisplatin by targeting TGM3.