Evidence map›Paper›PMID 36999424›Full record

ArticleCurrent molecular medicine2024

MT1G Regulates c-MYC/P53 Signal to Inhibit Proliferation, Invasion and Migration and Promote Apoptosis in Colon Cancer Cells.

Jie Li, Qiaozhen Hu, Zhongyan Li, Kaiyu Feng, Kangbao Li

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Article in Current molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Jie LiDepartment of Geriatrics, National Clinical Key Specialty, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, 510180, Guangdong, China.
Qiaozhen HuDepartment of Geriatrics, National Clinical Key Specialty, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, 510180, Guangdong, China.
Zhongyan LiDepartment of Geriatrics, National Clinical Key Specialty, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, 510180, Guangdong, China.
Kaiyu FengDepartment of Geriatrics, National Clinical Key Specialty, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, 510180, Guangdong, China.
Kangbao LiDepartment of Geriatrics, National Clinical Key Specialty, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, 510180, Guangdong, China.
Guangzhou First People's Hospital · CNGuangzhou Medical University · CN

Funding

Science and Technology Project of Guangdong Provincial Science and Technology Department 01548280218329060, 0445091120222076
6 · The paper itself

Abstract

introductionColon cancer is a common and malignant cancer featuring high morbidity and poor prognosis.

aimsThis study was performed to explore the regulatory role of MT1G in colon cancer as well as its unconcealed molecular mechanism.

methodsThe 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.

resultsIt 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.

conclusionTo 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.

Indexed as

Colonic NeoplasmsTumor Suppressor Protein p53ApoptosisCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMetallothioneinMetallothioneinMT1G protein, humanTumor Suppressor Protein p53c-MYCColon cancerHCT116.LoVo cellsMT1GP53

Identifiers

PMID36999424
OpenAlexW4361268113

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.