Title:MT1G Regulates c-MYC/P53 Signal to Inhibit Proliferation, Invasion
and Migration and Promote Apoptosis in Colon Cancer Cells
Volume: 24
Issue: 3
Author(s): Jie Li, Qiaozhen Hu, Zhongyan Li, Kaiyu Feng and Kangbao Li*
Affiliation:
- Department of Geriatrics, National Clinical Key Specialty, Guangzhou First People’s Hospital, School of
Medicine, South China University of Technology, Guangzhou, 510180, Guangdong, China
Keywords:
Colon cancer, MT1G, c-MYC, P53, LoVo cells, HCT116.
Abstract:
Introduction: Colon cancer is a common and malignant cancer featuring high
morbidity and poor prognosis.
Aims: This study was performed to explore the regulatory role of MT1G in colon cancer
as well as its unconcealed molecular mechanism.
Methods: The expressions of MT1G, c-MYC, and p53 were assessed with the
application of RT-qPCR and western blot. The impacts of MT1G overexpression on the
proliferative ability of HCT116 and LoVo cells were measured by CCK-8 and BrdU
incorporation assays. Additionally, transwell wound healing, and flow cytometry assays
were employed to evaluate the invasive and migrative capacities as well as the
apoptosis level of HCT116 and LoVo cells. Moreover, the activity of the P53 promoter
region was assessed with the help of a luciferase reporter assay.
Results: It was found that the expressions of MT1G at both mRNA and protein levels
were greatly decreased in human colon cancer cell lines, particularly in HCT116 and
LoVo cell lines. After transfection, it was discovered that the MT1G overexpression
suppressed the proliferation, migration and invasion but promoted the apoptosis of
HCT116 and LoVo cells, which were then partially reversed after overexpressing c-MYC.
Additionally, MT1G overexpression reduced c-MYC expression but enhanced the p53
expression, revealing that the MT1G overexpression could regulate c-MYC/P53 signal.
Elsewhere, it was also shown that c-MYC overexpression suppressed the regulatory
effects of MT1G on P53.
Conclusion: To conclude, MT1G was verified to regulate c-MYC/P53 signal to repress
the proliferation, migration and invasion but promote the apoptosis of colon cancer cells,
which might offer a novel targeted-therapy for the improvement of colon cancer.
