Evidence map›Paper›PMID 39540351›Full record

ArticleMolecular medicine reports2025

KRAS inhibitors may prevent colorectal cancer metachronous metastasis by suppressing TGF‑β mediated epithelial‑mesenchymal transition.

Yaoyu Guo, Chuling Hu, Kuntai Cai, Guojie Long, Du Cai, Zhaoliang Yu, Xinxin Huang, Zerong Cai, Peishan Hu, Yufeng Chen and 2 more

Abstract read
In one paragraph

Article in Molecular medicine reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. [Advances in Immunotherapy of KRAS-mutated Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025
    Review
  8. Article
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.

Yaoyu Guo *Guangdong Institute of Gastroenterology, Department of General Surgery, Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510655, P.R. China.
Chuling Hu *Guangdong Institute of Gastroenterology, Department of General Surgery, Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510655, P.R. China.
Kuntai Cai *Guangdong Institute of Gastroenterology, Department of General Surgery, Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510655, P.R. China.
Guojie LongDepartment of General Surgery (Department of Pancreatic Hepatobiliary Surgery), The Sixth Affiliated Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510655, P.R. China.
Du CaiGuangdong Institute of Gastroenterology, Department of General Surgery, Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510655, P.R. China.
Zhaoliang YuGuangdong Institute of Gastroenterology, Department of General Surgery, Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510655, P.R. China.
Xinxin HuangGuangdong Institute of Gastroenterology, Department of General Surgery, Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510655, P.R. China.
Zerong CaiGuangdong Institute of Gastroenterology, Department of General Surgery, Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510655, P.R. China.
Peishan HuGuangdong Institute of Gastroenterology, Department of General Surgery, Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510655, P.R. China.
Yufeng ChenGuangdong Institute of Gastroenterology, Department of General Surgery, Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510655, P.R. China.
Feng GaoGuangdong Institute of Gastroenterology, Department of General Surgery, Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510655, P.R. China.
Xiaojian WuGuangdong Institute of Gastroenterology, Department of General Surgery, Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510655, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In colorectal cancer (CRC), KRAS mutations enhance metachronous metastasis, a condition without prognostic biomarkers or preventive measures. The present study demonstrated that KRAS mutation may be a risk factor for CRC metachronous metastasis through meta‑analysis of public databases. A risk scoring model was constructed using machine learning for predicting metachronous metastasis in KRAS‑mutant CRC. Wound healing and Transwell assay indicated that KRAS inhibitors strongly suppress migration and invasion capabilities of high‑risk CRC cells and these findings were validated through ex vivo organoid and a mouse model of splenic‑liver metastasis. Mechanistically, RNA sequencing, reverse transcription‑quantitative PCR and western blot analyses revealed that KRAS inhibitors suppressed epithelial‑mesenchymal transition (EMT) and transforming growth factor β (TGF‑β) signaling. Notably, addition of TGF‑β1 protein partially reversed the inhibitory effects of KRAS inhibitors on CRC. These results suggested that KRAS inhibitors may prevent CRC metachronous metastasis by downregulating TGF‑β‑mediated EMT, suggesting they can be used prophylactically in high‑risk KRAS‑mutant CRC.

Indexed as

Colorectal NeoplasmsEpithelial-Mesenchymal TransitionProto-Oncogene Proteins p21(ras)Transforming Growth Factor betaAnimalsCell Line, TumorCell MovementFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMutationNeoplasm MetastasisSignal TransductionKRAS protein, humanProto-Oncogene Proteins p21(ras)Transforming Growth Factor betacolorectal cancerKRAS inhibitormachine learningmeta‑analysismetastasis

Identifiers

PMID39540351
PMCPMC11576929

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.