Evidence map›Paper›PMID 41155168›Full record

ArticleInternational journal of molecular sciences2025

Inhibiting Fatty Acid Oxidation Suppresses Acquired Resistance to Standard Chemotherapy in Melanoma.

Wonyoung Choi, Woojin Ham, Jeong Hwan Park, Sung Hoon Sim, Jung Won Chun, Mingyu Kang, Chaeyoung Kim, Woosol Hong, Eun-Byeol Koh, Joon Hee Kang and 2 more

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

12 authors.

Wonyoung ChoiDepartment of Cancer Biomedical Science, National Cancer Center Graduate School of Cancer Science and Policy, Goyang 10408, Republic of Korea.ORCID 0000-0002-8292-3903
Woojin HamDivision of Cancer Biology, Research Institute of National Cancer Center, Goyang 10408, Republic of Korea.
Jeong Hwan ParkDivision of Cancer Biology, Research Institute of National Cancer Center, Goyang 10408, Republic of Korea.
Sung Hoon SimDivision of Rare and Refractory Cancer, Research Institute, National Cancer Center, Goyang 10408, Republic of Korea.ORCID 0000-0002-1503-1075
Jung Won ChunDepartment of Cancer Biomedical Science, National Cancer Center Graduate School of Cancer Science and Policy, Goyang 10408, Republic of Korea.ORCID 0000-0003-1964-7501
Mingyu KangDivision of Cancer Biology, Research Institute of National Cancer Center, Goyang 10408, Republic of Korea.
Chaeyoung KimDivision of Cancer Biology, Research Institute of National Cancer Center, Goyang 10408, Republic of Korea.
Woosol HongDivision of Cancer Biology, Research Institute of National Cancer Center, Goyang 10408, Republic of Korea.
Eun-Byeol KohDivision of Cancer Biology, Research Institute of National Cancer Center, Goyang 10408, Republic of Korea.
Joon Hee KangDepartment of Cancer Biomedical Science, National Cancer Center Graduate School of Cancer Science and Policy, Goyang 10408, Republic of Korea.
Sang Myung WooDepartment of Cancer Biomedical Science, National Cancer Center Graduate School of Cancer Science and Policy, Goyang 10408, Republic of Korea.ORCID 0000-0003-3786-4403
Soo-Youl KimDivision of Cancer Biology, Research Institute of National Cancer Center, Goyang 10408, Republic of Korea.ORCID 0000-0002-4021-2206

Funding

National Cancer Center, Korea NCC 2410891-1National Cancer Center, Korea NCC 2410892-1National Cancer Center, Korea NCC 24H1210-1National Research Foundation of Korea NRF-2017R1A2B2003428
6 · The paper itself

Abstract

Immunotherapy and RAF-targeted therapy have become standard treatments for melanoma, significantly improving outcomes compared to earlier therapies. When resistance to initial treatment develops, the older chemotherapy drug Dacarbazine is used. However, resistance to both therapies has emerged, promoting ongoing research to further enhance survival rates. Among various theories, autophagy is believed to play a critical role in acquired drug resistance, as increased autophagy has been observed in resistance to multiple anticancer agents. In this study, Dabrafenib was administered to melanoma cells with an RAF mutation, while Dacarbazine was given to cells with an Raf wild type. Both cell lines showed increased autophagy and FAO following treatment with the anticancer drugs. When FAO was blocked during drug treatment, melanoma cells became more susceptible to cell death. In xenograft models, B16F10 melanoma (Raf wild type) demonstrated regrowth due to acquired resistance after two weeks of Dacarbazine treatment. Conversely, a combination of Dacarbazine and the FAO inhibitors KN510 and KN713 (a combination of KN510 and KN713:KN510713) caused near-complete remission without regrowth. A375 melanoma (

Indexed as

Antineoplastic AgentsDrug Resistance, NeoplasmFatty AcidsMelanomaAnimalsAutophagyCell Line, TumorDacarbazineHumansImidazolesMiceMutationOxidation-ReductionOximesProto-Oncogene Proteins B-rafXenograft Model Antitumor AssaysAntineoplastic AgentsdabrafenibDacarbazineFatty AcidsImidazolesOximesProto-Oncogene Proteins B-rafDabrafenibDacarbazinefatty acid oxidationKN510713melanoma

Identifiers

PMID41155168
PMCPMC12563080

What OpenQuestion holds

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Registered trials

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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.