Evidence map›Paper›PMID 32104224›Full record

ArticleExperimental and therapeutic medicine2020

FGF9 promotes cisplatin resistance in colorectal cancer via regulation of Wnt/β-catenin signaling pathway.

Zhijin Zhang, Yuhao Zhang, Xinju Qin, Yuexia Wang, Jun Fu

Abstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. FGF9 Recruits β-Catenin to Increase Hepatic ECM Synthesis and Promote NASH-Driven HCC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  10. Molecular mechanisms associated with chemoresistance in esophageal cancer.Cellular and molecular life sciences : CMLS · 2022
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. 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

5 authors.

Zhijin ZhangDepartment of Gastroenterological Surgery, Shanghai Eighth People's Hospital, Shanghai 200235, P.R. China.
Yuhao ZhangDepartment of Gastroenterological Surgery, Shanghai Eighth People's Hospital, Shanghai 200235, P.R. China.
Xinju QinDepartment of Gastroenterological Surgery, Shanghai Eighth People's Hospital, Shanghai 200235, P.R. China.
Yuexia WangDepartment of Gastroenterological Surgery, Shanghai Eighth People's Hospital, Shanghai 200235, P.R. China.
Jun FuDepartment of Gastroenterological Surgery, Shanghai Eighth People's Hospital, Shanghai 200235, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Development of cisplatin resistance in colorectal cancer is largely caused by dysregulation of signaling pathways, including the Wnt/β-catenin signaling pathway, in cancer cells. Further investigation into the molecular mechanism of chemoresistance could improve outcomes for patients with colorectal cancer. The present study determined that fibroblast growth factor 9 (FGF9) was overexpressed in tumor tissues compared with normal tissues from patients with colorectal cancer. Using the colorectal cancer cell line LoVo, transfection of recombinant FGF9 decreased cisplatin-induced cell apoptosis whilst FGF9 silencing increased cisplatin-induced apoptosis. Western blot analysis and reverse transcription-quantitative polymerase chain reaction demonstrated that FGF9 decreased adenomatous polyposis coli (APC) mRNA and protein expression and contributed to activation of the Wnt/β-catenin signaling pathway. Notably, an increase in FGF9 and β-catenin protein expression and a decrease in APC protein expression was observed in the established LoVo cisplatin resistant cell line (LoVo/cisplatin). Silencing of FGF9 reversed cisplatin resistance of LoVo/cisplatin cells. In conclusion, the present findings suggested that FGF9 activated the Wnt signaling pathway and was a mediator of cisplatin resistance in colorectal cancer.

Indexed as

cisplatin resistancecolorectal cancerfibroblast growth factor 9Wnt/β-catenin signaling pathway

Identifiers

PMID32104224
PMCPMC7026987

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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.