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MKL1/miR34a/FOXP3 axis regulates cell proliferation in gastric cancer
Author(s) -
Li JiaPeng,
Liao XingHua,
Xiang Yuan,
Yao Ao,
Fan LiJuan,
Li Hui,
Zhang ZiJian,
Huang Feng,
Dai ZhouTong,
Zhang TongCun
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28056
Subject(s) - cell growth , gene knockdown , cancer research , cyclin dependent kinase 6 , cancer , foxp3 , cell cycle , cancer cell , downregulation and upregulation , cell , apoptosis , microbiology and biotechnology , chemistry , biology , immunology , medicine , cyclin dependent kinase 2 , gene , biochemistry , immune system
Megakaryoblastic leukemia 1 (MKL1) was closely related to the pathogenesis of various human malignant cancers. MiR34a was reported to be closely related to cancer cell proliferation. Forkhead box protein 3 (FOXP3) was a transcription factor that played a different role in different cancer types. CDK6 was involved in cell cycle progression and was upregulated in several types of cancers. The present study investigated the effects of MKL1/miR34a/FOXP3 axis on cell proliferation in MGC803 gastric cancer cells. Our results demonstrated that overexpression of MKL1 promoted proliferation of MGC80‐3 cells, MKL1 directly binding to the promoter of CDK6 to increase its expression. Knockdown of FOXP3 promoted proliferation of MGC80‐3 cells and MKL1 inhibited the expression of FOXP3 via miR‐34a. The finding can contribute to elucidating the regulatory mechanism involved in the cell cycle progression of gastric cancer cells and may aid in screening potential gene targets for the biological therapy of gastric cancer.