Evidence mapPaperPMID 39627451Full record

ArticleExperimental & molecular medicine2024

The anticancer effect of metformin targets VDAC1 via ER-mitochondria interactions-mediated autophagy in HCC.

Minjeong Ko, Jiho Kim, Raudah Lazim, Ju Yeon Lee, Jin Young Kim, Vijayakumar Gosu, Yoonji Lee, Sun Choi, Ho Jeong Kwon

Abstract read
In one paragraph

Article in Experimental & molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

17 citing papers in PubMed.

  1. Review
  2. iScience · 2026
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  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Cannabidiol-Ion Channel Interactions Represent a Promising Preventive and Therapeutic Strategy in Hepatocellular Carcinoma.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
  10. Article
  11. Article
  12. Review
  13. Article
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  15. 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

9 authors.

Minjeong Ko *Chemical Genomics Leader Research Laboratory, Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, Republic of Korea.
Jiho Kim *Chemical Genomics Leader Research Laboratory, Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, Republic of Korea.
Raudah Lazim *Global AI Drug Discovery Center, College of Pharmacy and Graduate School of Pharmaceutical Sciences, Ewha Womans University, Seoul, Republic of Korea.
Ju Yeon LeeResearch Center of Bioconvergence Analysis, Korea Basic Science Institute, Ochang, Republic of Korea.ORCID 0000-0003-0855-6516
Jin Young KimResearch Center of Bioconvergence Analysis, Korea Basic Science Institute, Ochang, Republic of Korea.ORCID 0000-0002-0656-1269
Vijayakumar GosuGlobal AI Drug Discovery Center, College of Pharmacy and Graduate School of Pharmaceutical Sciences, Ewha Womans University, Seoul, Republic of Korea.
Yoonji LeeGlobal AI Drug Discovery Center, College of Pharmacy and Graduate School of Pharmaceutical Sciences, Ewha Womans University, Seoul, Republic of Korea.ORCID 0000-0002-2494-5792
Sun ChoiGlobal AI Drug Discovery Center, College of Pharmacy and Graduate School of Pharmaceutical Sciences, Ewha Womans University, Seoul, Republic of Korea. sunchoi@ewha.ac.kr.
Ho Jeong KwonChemical Genomics Leader Research Laboratory, Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, Republic of Korea. kwonhj@yonsei.ac.kr.ORCID 0000-0002-6919-833X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metformin (MetF) is used worldwide as a first-line therapy for type 2 diabetes. Recently, interest in the pleiotropic effects of MetF, such as its anticancer and antiaging properties, has increased. However, the molecular target of MetF and the detailed mechanism underlying its ability to inhibit cell growth through autophagy induction remain incompletely understood. In this study, using an innovative label-free drug affinity responsive target stability (DARTS)-LC-MS/MS method, we discovered that mitochondrial voltage-dependent anion channel 1 (VDAC1) is a novel binding protein involved in the induction of autophagy-related cell death by high-dose MetF in hepatocellular carcinoma (HCC). Computational alanine scanning mutagenesis revealed that MetF and VDAC1 (D9, E203) interact electrostatically. MetF disrupts the IP

Indexed as

AutophagyCarcinoma, HepatocellularEndoplasmic ReticulumLiver NeoplasmsMetforminMitochondriaVoltage-Dependent Anion Channel 1AnimalsAntineoplastic AgentsCell Line, TumorHumansProtein BindingAntineoplastic AgentsMetforminVDAC1 protein, humanVoltage-Dependent Anion Channel 1

Identifiers

PMID39627451
PMCPMC11671597

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.