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Effect of CBX4/miR-137/Notch1 signaling axis on the proliferation and migration of breast cancer cells
Author(s) -
Le Ma,
Lihua Zheng,
Dongmei Zhang,
Zhimin Fan
Publication year - 2022
Publication title -
tropical journal of pharmaceutical research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.209
H-Index - 36
eISSN - 1596-5996
pISSN - 1596-9827
DOI - 10.4314/tjpr.v20i3.7
Subject(s) - transfection , cell growth , biology , small interfering rna , microbiology and biotechnology , cell migration , rna interference , gene silencing , signal transduction , cell , plasmid , cancer research , cell culture , gene , rna , genetics
Purpose: To study the effect of CBX4/miR-137/Notch1 signaling axis on the migration and proliferative capacity of breast cancer. Methods: Breast cancer MCF7 cell lines were cultured in vitro and transfected with CBX4- overexpressed plasmid and interfering plasmid, which served as CBX4 over-expressing group and CBX4 interfering group, respectively. A control group (blank plasmid transfection) was set up. The MCF7 cells were transfected with miR-137 over-expressed plasmid, miR-137 interfering plasmid and Notch1 interfering plasmid, which served as miR-137 over-expressing, miR-137 interference and Notch1 interference groups, respectively. Cell proliferation and migration capacity were determined with methylthiazolyldiphenyl-tetrazolium (MTT) method and Transwell migration assay, respectively, while reverse transcription-polymerase chain reaction (RT-PCR) and immunoblotting were used to assay related gene expressions. Results: Cell migration in CBX4 over-expressing group was significantly raised (p < 0.05). The expression of miR-137 in CBX4 over-expressing group was markedly decreased (p < 0.05). Compared with the control group, mRNA and protein expressions of Notch1 (NICD), Hey2 and Jag1 in miR-137 over-expressing cells were increased in the miR-137 interfering group (p < 0.05). Conclusion: CBX4 level is increased in mammary cancer cells. Moreover, CBX4 enhances cell proliferation and migration through induction of Notch1 signaling route by inhibiting miR-137 expression. These findings provide a new strategy for clinical therapy of mammary cancer.

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