Up-regulation of microRNA-136 induces apoptosis and radiosensitivity of esophageal squamous cell carcinoma cells by inhibiting the expression of MUC1

This present study is performed to figure out the role of microRNA-136 (miR-136) in radiosensitivity of esophageal squamous cell carcinoma (ESCC) cells through the regulation of MUC1. Seventy-four ESCC patients were divided into radiotherapy sensitive group and radiotherapy resistance group. Colony...

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Bibliographic Details
Published in:Experimental and molecular pathology 2019-10, Vol.110, p.104278-104278, Article 104278
Main Authors: Huang, Hua-Zhong, Yin, Yi-Fa, Wan, Wen-Jun, Xia, Dan, Wang, Rui, Shen, Xue-Min
Format: Article
Language:English
Subjects:
Apoptosis
Apoptosis - genetics
Apoptosis - radiation effects
Cell Line, Tumor
Cell Proliferation - genetics
Cell Proliferation - radiation effects
Cell Survival - genetics
Cell Survival - radiation effects
Esophageal Neoplasms - genetics
Esophageal Neoplasms - radiotherapy
Esophageal squamous cell carcinoma
Esophageal Squamous Cell Carcinoma - genetics
Esophageal Squamous Cell Carcinoma - radiotherapy
Female
Gene Expression Regulation, Neoplastic - radiation effects
Humans
Male
microRNA-136
MicroRNAs - genetics
Middle Aged
MUC1
Mucin-1 - genetics
Radiation Tolerance - genetics
Radiosensitivity
Up-Regulation
X-Rays
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Summary:This present study is performed to figure out the role of microRNA-136 (miR-136) in radiosensitivity of esophageal squamous cell carcinoma (ESCC) cells through the regulation of MUC1. Seventy-four ESCC patients were divided into radiotherapy sensitive group and radiotherapy resistance group. Colony formation assay and flow cytometry were used to test the radiosensitivity of radiotherapy resistant strain and parent strain. The expression of miR-136 between radiotherapy resistant strain and parent strain was detected by RT-qPCR, and the expression of miR-136 in Eca109 and TE-1 cells as well as Eca109-R and TE-1-R cells was detected after different doses of X-ray irradiation. Eca109 and TE-1 cells as well as Eca109-R and TE-1-R cells with overexpression of miR-136 or co-overexpression of miR-136 and MUC1 were constructed. Cell proliferation, colony formation and apoptosis was detected by CCK-8 assay, colony formation assay, and flow cytometry, respectively. The expression of miR-136 in ESCC tissues was lower and MUC1 mRNA and protein expression was higher than that in adjacent normal tissues. The expression of miR-136 was negatively correlated with the expression of MUC1 mRNA in ESCC. Low expression of miR-136 and high expression of MUC1 were associated with tumor size, lymph node metastasis and distant metastasis. The expression of miR-136 increased while the expression of MUC1 decreased in the radiotherapy sensitive group of ESCC patients relative to the radiotherapy resistant group. The colony formation ability of radiation resistant cell line was stronger than that of parent cell line, and the apoptosis rate showed an opposite trend. Up-regulation of miR-136 reduced the survival rate, suppressed colony formation ability and induced apoptosis of ESCC cells under irradiation, which was reversed by upregulated MUC1. This study demonstrates that up-regulation of miR-136 induces apoptosis and radiosensitivity of ESCC cells by inhibiting the expression of MUC1.
ISSN:0014-4800
1096-0945
DOI:10.1016/j.yexmp.2019.104278