Jian Liu1, Yamei Pang2, Huangzhen Wang1, Yanbo Li3, Xin Sun1, Fei Xu4, Hong Ren5, Dapeng Liu6. 1. Department of Thoracic Surgery and Oncology, First Affiliated Hospital, Medical College, Xi'an Jiaotong University, Xi'an 710061, China. 2. Department of Respiration, First Affiliated Hospital, Medical College, Xi'an Jiaotong University, Xi'an 710061, China. 3. Department of Neurology, First Affiliated Hospital, Medical College, Xi'an Jiaotong University, Xi'an 710061, China. 4. Department of Radiation Oncology, Fudan University, Shanghai Cancer Center, Shanghai 200032, China. 5. Department of Thoracic Surgery and Oncology, First Affiliated Hospital, Medical College, Xi'an Jiaotong University, Xi'an 710061, China. *Corresponding authors, E-mail: kissable_liu@163.com. 6. Department of Thoracic Surgery and Oncology, First Affiliated Hospital, Medical College, Xi'an Jiaotong University, Xi'an 710061, China. *Corresponding authors, E-mail: renh_med@163.com.
Abstract
OBJECTIVE: To investigate the effect of microRNA-101 (miR-101) on the proliferation and migration of breast cancer cells and its possible mechanism. METHODS: The expressions of miR-101 and DNA methyltransferase 3a (DNMT3a) in breast cancer tissues, corresponding normal breast tissues, breast cancer cells and normal breast cells were detected by real-time quantitative PCR. The lentiviral vectors containing miR-101 and shRNA-DNMT3a sequences were transfected into MDA-MB-231 cells to regulate the expressions of miR-101 and DNMT3a. The expressions of DNMT3a and E-cadherin were determined by Western blotting. The proliferation and migration abilities of MDA-MB-231 cells were evaluated by MTT assay and wound healing assay, respectively. RESULTS: Breast cancer tissues and breast cancer cell lines (MCF-7, MDA-MB-231, MDA-MB-361, HCC70) showed lower miR-101 expression and higher DNMT3a expression than the adjacent normal breast tissues and normal breast cell line. The overexpression of miR-101 resulted in downregulation of DNMT3a and restoration of E-cadherin. Besides, knockdown of DNMT3a by shRNA increased E-cadherin expression. MTT assay and would healing assay showed that miR-101 overexpression significantly inhibited the proliferation and migration abilities of MDA-MB-231 cells. CONCLUSION: miR-101 may inhibit MDA-MB-231 cell proliferation and migration by repressing DNMT3a expression and up-regulating E-cadherin expression.
OBJECTIVE: To investigate the effect of microRNA-101 (miR-101) on the proliferation and migration of breast cancer cells and its possible mechanism. METHODS: The expressions of miR-101 and DNA methyltransferase 3a (DNMT3a) in breast cancer tissues, corresponding normal breast tissues, breast cancer cells and normal breast cells were detected by real-time quantitative PCR. The lentiviral vectors containing miR-101 and shRNA-DNMT3a sequences were transfected into MDA-MB-231 cells to regulate the expressions of miR-101 and DNMT3a. The expressions of DNMT3a and E-cadherin were determined by Western blotting. The proliferation and migration abilities of MDA-MB-231 cells were evaluated by MTT assay and wound healing assay, respectively. RESULTS:Breast cancer tissues and breast cancer cell lines (MCF-7, MDA-MB-231, MDA-MB-361, HCC70) showed lower miR-101 expression and higher DNMT3a expression than the adjacent normal breast tissues and normal breast cell line. The overexpression of miR-101 resulted in downregulation of DNMT3a and restoration of E-cadherin. Besides, knockdown of DNMT3a by shRNA increased E-cadherin expression. MTT assay and would healing assay showed that miR-101 overexpression significantly inhibited the proliferation and migration abilities of MDA-MB-231 cells. CONCLUSION:miR-101 may inhibit MDA-MB-231 cell proliferation and migration by repressing DNMT3a expression and up-regulating E-cadherin expression.
Authors: Fernanda Cardoso da Silva; Angelo Borges de Melo Neto; Christina Aparecida Martins; Thaís Cunha de Sousa Cardoso; Matheus de Souza Gomes; Thaise Gonçalves de Araújo; Cristina Ribas Fürstenau Journal: Purinergic Signal Date: 2021-11-05 Impact factor: 3.765