Evidence mapPaperPMID 35897659Full record

ArticleInternational journal of molecular sciences2022

Metformin Enhances the Anti-Cancer Efficacy of Sorafenib via Suppressing MAPK/ERK/Stat3 Axis in Hepatocellular Carcinoma.

Sumit Siddharth, Panjamurthy Kuppusamy, Qitong Wu, Arumugam Nagalingam, Neeraj K Saxena, Dipali Sharma

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% of its field
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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Advances in the Use of Metformin for Liver Disease.Current medicinal chemistry · 2025
    Review
  10. Review
  11. Building of CuOPharmaceutics · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Metabolic Reprogramming in Thyroid Cancer.Endocrinology and metabolism (Seoul, Korea) · 2024
    Review
  17. Article
  18. Review
  19. Article
  20. Review
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 at 3 institutions in 1 country.

Sumit SiddharthDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Panjamurthy KuppusamyDepartment of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA.ORCID 0000-0003-3293-7220
Qitong WuDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Arumugam NagalingamDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.ORCID 0000-0002-4856-2630
Neeraj K SaxenaNational Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA.
Dipali SharmaDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Johns Hopkins University · USNational Institutes of Health · USUniversity of Maryland, Baltimore · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) incidence, as well as related mortality, has been steadily increasing in the USA and across the globe, partly due to the lack of effective therapeutic options for advanced HCC. Though sorafenib is considered standard-of-care for advanced HCC, it only improves median survival by a few months when compared to placebo. Sorafenib is also associated with several unpleasant side effects that often lead to early abatement of therapy. Here, we investigate whether a combination regimen including low-dose sorafenib and a non-toxic dose of anti-diabetic drug metformin can achieve effective inhibition of HCC. Indeed, combining metformin with low-dose sorafenib inhibited growth, proliferation, migration, and invasion potential of HCC cells. We observed a 5.3- and 1.9-fold increase in sub-G1 population in the combination treatment compared to sorafenib alone. We found that the combination of metformin enhanced the efficacy of sorafenib and inhibited the MAPK/ERK/Stat3 axis. Our in vivo studies corroborated the in vitro findings, and mice harboring HepG2-derived tumors showed effective tumor reduction upon treatment with low-dose sorafenib and metformin combination. This work sheds light on a therapeutic strategy aiming to augment sorafenib efficacy or dose-de-escalation that may prove beneficial in circumventing sorafenib resistance as well as minimizing related side effects.

Indexed as

Antineoplastic AgentsCarcinoma, HepatocellularLiver NeoplasmsMetforminAnimalsApoptosisCell Line, TumorCell ProliferationMiceNiacinamidePhenylurea CompoundsSorafenibXenograft Model Antitumor AssaysAntineoplastic AgentsMetforminNiacinamidePhenylurea CompoundsSorafenibcombination treatmentERKhepatocellular carcinomaMAPKmetforminsorafenibStat3

Identifiers

PMID35897659
PMCPMC9329836
OpenAlexW4286587514

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.