MKL1/miR34a/FOXP3 axis regulates cell proliferation in gastric cancer
MKL1/miR34a/FOXP3 axis regulates cell proliferation in gastric cancer
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MKL1/miR34a/FOXP3轴调节胃癌细胞增殖
DOI：
10.1002/jcb.28056
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发表时间：
2018
期刊：
影响因子：
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通讯作者：
Tong‐Cun Zhang
中科院分区：
文献类型：
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作者：
Jia‐Peng Li;Xing‐Hua Liao;Yuan Xiang;Ao Yao;Li‐Juan Fan;Hui Li;Zi‐Jian Zhang;Feng Huang;Zhou‐Tong Dai;Tong‐Cun Zhang
巨核细胞白血病1（MKL 1）与人类多种恶性肿瘤的发生密切相关。MiR 34 a与癌细胞增殖密切相关。叉头盒蛋白3（FOXP 3）是一种转录因子，在不同的癌症类型中发挥不同的作用。CDK 6参与细胞周期进程，并在几种类型的癌症中上调。本研究探讨了MKL 1/miR 34 a/FOXP 3轴对胃癌MGC 803细胞增殖的影响。我们的结果表明，MKL 1的过表达促进了MGC 80 - 3细胞的增殖，MKL 1直接结合CDK 6的启动子以增加其表达。FOXP 3的敲低促进了MGC 80 - 3细胞的增殖，MKL 1通过miR-34 a抑制FOXP 3的表达。这一发现有助于阐明胃癌细胞周期进程的调控机制，并可能有助于筛选潜在的基因靶点，用于胃癌的生物治疗。
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.