Evidence map›Paper›PMID 37948019›Full record

ArticleMolecular and cellular biochemistry2024

MIA3 promotes the degradation of GSH (glutathione) by binding to CHAC1, thereby promoting the progression of hepatocellular carcinoma.

Zhou Wanbiao, Man Jing, Zuo Shi, Chen Tengxiang, Zhao Xueke, Li Haiyang

Abstract read
In one paragraph

Article in Molecular and cellular biochemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

  1. Article
  2. Review
  3. Relationship between theAnimal biotechnology · 2025
    Article
  4. Article
  5. Article
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  7. Article
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  9. Article
  10. ER exit in physiology and disease.Frontiers in molecular biosciences · 2024
    Review
  11. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Zhou Wanbiao *Department of Hepatobiliary Surgery, The Affiliated Hospital of Guizhou Medical University, 28 Guiyi Street, Guiyang, Guizhou, People's Republic of China.
Man Jing *Department of Hepatobiliary Surgery, The Affiliated Hospital of Guizhou Medical University, 28 Guiyi Street, Guiyang, Guizhou, People's Republic of China.
Zuo ShiDepartment of Hepatobiliary Surgery, The Affiliated Hospital of Guizhou Medical University, 28 Guiyi Street, Guiyang, Guizhou, People's Republic of China.
Chen TengxiangSchool of Clinical Medicine, Guizhou Medical University, Guiyang, Guizhou, People's Republic of China.
Zhao XuekeDepartment of Infectious Diseases, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, People's Republic of China. zhaoxueke1@163.com.
Li HaiyangDepartment of Hepatobiliary Surgery, The Affiliated Hospital of Guizhou Medical University, 28 Guiyi Street, Guiyang, Guizhou, People's Republic of China. haiyang_li@sina.com.

Funding

National Natural Science Foundation of China No.82060116 and No.82260129Science and Technology Program of Guizhou Province No. [2019]1267;[2020]4Y232 and No. [2021] 094.
6 · The paper itself

Abstract

MIA3 (melanoma inhibitory active protein 3)/TANGO1 (Golgi transporter component protein) plays an important role in the initiation, development, and metabolism of cancer. We aimed to explore the role and underlying molecular mechanisms of MIA3/TANGO1 in the growth and migration of hepatoma cells. According to the analysis of The Cancer Genome Atlas (TCGA) database, MIA3 is expressed at higher levels in hepatocellular carcinoma (HCC) tissues than in normal tissues. Real-time quantitative polymerase chain reaction (qRT-PCR), immunohistochemistry, and western blotting were used to detect mRNA and protein expression in HCC tissues and cells. The in vitro function of MIA3 in HCC cells was evaluated using Cell Counting Kit-8 (CCK-8), colony formation, cell migration and invasion, and flow cytometry assays. Hep-G2 cells with MIA3 overexpression were subjected to RNA-seq, and the downstream target gene CHAC1 (glutathione-specific γ-glutamyl cyclotransferase 1) was selected according to the results of the volcano map of gene enrichment. The relationship between MIA3 and CHAC1 was revealed by coimmunoprecipitation and confocal microscopy. MIA3 expression was upregulated in HCC organizations and HCC samples in the TCGA dataset. Knocking out MIA3 inhibited the proliferation, migration, and invasion of Hep-G2 cells and promoted the apoptosis of Hep-G2 cells. Overexpression of MIA3 in Huh7 cells promoted the proliferation, migration, and invasion and suppressed the apoptosis of Huh7 cells. Overexpression of MIA3 promoted the expression of CHAC1 and the degradation of glutathione (GSH), thereby promoting the growth and metastasis of HCC cells. Knocking out MIA3 inhibited the expression of CHAC1 and slowed the degradation of glutathione, thereby inhibiting the growth and metastasis of HCC cells. MIA3 further promotes the growth, metastasis, and invasion of hepatoma cells by binding to the CHAC1 protein and promoting GSH degradation.

Indexed as

Aryl Hydrocarbon Receptor Nuclear TranslocatorCarcinoma, Hepatocellulargamma-GlutamylcyclotransferaseGlutathioneLiver NeoplasmsCell MovementCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHep G2 CellsHumansNeoplasm ProteinsProteolysisARNT protein, humanAryl Hydrocarbon Receptor Nuclear TranslocatorCHAC1 protein, humangamma-GlutamylcyclotransferaseGlutathioneNeoplasm ProteinsCHAC1 (glutathione-specific γ-glutamyl cyclotransferase 1)GSH (glutathione)Hepatocellular carcinomaMIA3 (melanoma inhibiting active protein 3)PrognosisTANGO1 (Golgi transporter component protein)

Identifiers

PMID37948019
PMCPMC11455670

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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.