The regulation of miR-139-5p on the biological characteristics of breast cancer cells by targeting COL11A1

Shequn Gu; Jihui Luo; Wenxiu Yao; Shequn Gu; Jihui Luo; Wenxiu Yao

doi:10.3934/mbe.2020073

Mathematical Biosciences and Engineering

2020, Volume 17, Issue 2: 1428-1441. doi: 10.3934/mbe.2020073

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The regulation of miR-139-5p on the biological characteristics of breast cancer cells by targeting COL11A1

1.
The First Department of Medical Oncology, The First People's Hospital of Chenzhou, Southern Medical University, Chenzhou 423000, China
2.
The Second General Surgery Department for Carcinoma, The First People's Hospital of Chenzhou, Chenzhou 423000, China
3.
Department of Thoracic Oncology, The Cancer Hospital of Sichuan Province, Chengdu 610000, China

Received: 30 May 2019 Accepted: 12 November 2019 Published: 27 November 2019

ObjectiveThis study aimed to explore the regulatory mechanism of miR-139-5p on the biological characteristics of breast cancer cells by targeting Collagen type XI alpha 1 chain (COL11A1).

MethodGEO2R was used to identify the differentially expressed genes (DEGs) of breast cancer in GEO database. miRDB, miRanda and TargetScan databases were used to predict the miRNAs that regulate COL11A1. qRT-PCR was used to detect the expressions of COL11A1 and miR-139-5p in breast cancer cells, and western blot was used to detect the protein level of COL11A1. RNA binding protein immunoprecipitation assay was employed to test the targeted relationship between miR-139-5p and COL11A1, which was further verified by dual-luciferase reporter gene assay. CCK-8 assay was performed to detect the cell proliferation, and flow cytometry was carried out to examine the cell apoptosis. Moreover, western blot was used for the detection of caspase-3, Bax and Bcl-2 protein levels.

ResultsA total of five DEGs were screened from the GEO database, of which COL11A1 was the only highly expressed in breast cancer. According to the database analysis, we predicted that miR-139-5p was much likely to target the expression of COL11A1. MiR-139-5p was poorly expressed in breast cancer cells and targeted inhibited COL11A1. Silencing COL11A1 or overexpressing miR-139-5p both could inhibit the proliferation and promote the apoptosis, while overexpressing the two factors simultaneously could reverse such effect.

ConclusionOverexpression of miR-139-5p inhibits the proliferation and promotes the apoptosis of breast cancer cells by inhibiting the expression of COL11A1.
- miR-139-5p,
- COL11A1,
- breast cancer,
- proliferation,
- apoptosis,
- GEO2R
Citation: Shequn Gu, Jihui Luo, Wenxiu Yao. The regulation of miR-139-5p on the biological characteristics of breast cancer cells by targeting COL11A1[J]. Mathematical Biosciences and Engineering, 2020, 17(2): 1428-1441. doi: 10.3934/mbe.2020073

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Abstract

ObjectiveThis study aimed to explore the regulatory mechanism of miR-139-5p on the biological characteristics of breast cancer cells by targeting Collagen type XI alpha 1 chain (COL11A1).

MethodGEO2R was used to identify the differentially expressed genes (DEGs) of breast cancer in GEO database. miRDB, miRanda and TargetScan databases were used to predict the miRNAs that regulate COL11A1. qRT-PCR was used to detect the expressions of COL11A1 and miR-139-5p in breast cancer cells, and western blot was used to detect the protein level of COL11A1. RNA binding protein immunoprecipitation assay was employed to test the targeted relationship between miR-139-5p and COL11A1, which was further verified by dual-luciferase reporter gene assay. CCK-8 assay was performed to detect the cell proliferation, and flow cytometry was carried out to examine the cell apoptosis. Moreover, western blot was used for the detection of caspase-3, Bax and Bcl-2 protein levels.

ResultsA total of five DEGs were screened from the GEO database, of which COL11A1 was the only highly expressed in breast cancer. According to the database analysis, we predicted that miR-139-5p was much likely to target the expression of COL11A1. MiR-139-5p was poorly expressed in breast cancer cells and targeted inhibited COL11A1. Silencing COL11A1 or overexpressing miR-139-5p both could inhibit the proliferation and promote the apoptosis, while overexpressing the two factors simultaneously could reverse such effect.

ConclusionOverexpression of miR-139-5p inhibits the proliferation and promotes the apoptosis of breast cancer cells by inhibiting the expression of COL11A1.

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