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MKL1/miR34a/FOXP3 axis regulates cell proliferation in gastric cancer
Jia-Peng Li1, Xing-Hua Liao1, Yuan Xiang1
1Institute of Biology and Medicine, College of Life and Health Sciences, Wuhan University of Science and Technology, Hubei, China.
Journal of Cellular Biochemistry
|November 15, 2018
Summary
Megakaryoblastic leukemia 1 (MKL1) promotes gastric cancer cell proliferation by upregulating CDK6. MKL1 also inhibits Forkhead box protein 3 (FOXP3) via miR34a, further enhancing cancer cell growth.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- Megakaryoblastic leukemia 1 (MKL1) is implicated in various cancers.
- MicroRNA 34a (miR34a) is linked to cancer cell proliferation.
- Forkhead box protein 3 (FOXP3) has context-dependent roles in cancer.
- Cyclin-dependent kinase 6 (CDK6) regulates cell cycle progression and is often upregulated in cancers.
Purpose of the Study:
- To investigate the MKL1/miR34a/FOXP3 signaling axis in MGC803 gastric cancer cells.
- To elucidate the regulatory mechanisms of MKL1 on cell proliferation and gene expression in gastric cancer.
Main Methods:
- Overexpression of MKL1 in MGC803 cells.
- Knockdown of FOXP3 in MGC803 cells.
- Analysis of MKL1 binding to the CDK6 promoter.
- Investigation of miR34a's role in MKL1-mediated FOXP3 regulation.
Main Results:
- MKL1 overexpression significantly promoted MGC803 cell proliferation.
- MKL1 directly binds to the CDK6 promoter, increasing CDK6 expression.
- FOXP3 knockdown also enhanced MGC803 cell proliferation.
- MKL1 was found to inhibit FOXP3 expression through miR34a mediation.
Conclusions:
- The MKL1/miR34a/FOXP3 axis plays a crucial role in regulating gastric cancer cell proliferation.
- MKL1 promotes gastric cancer progression by upregulating CDK6 and downregulating FOXP3 via miR34a.
- This axis represents a potential therapeutic target for gastric cancer treatment.
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