Evidence map›Paper›PMID 39093497›Full record

ArticleCell biology and toxicology2024

FOXC1 transcriptionally suppresses ABHD5 to inhibit the progression of renal cell carcinoma through AMPK/mTOR pathway.

Jianfa Li, Shuangchen Chen, Jing Xiao, Jiayuan Ji, Chenchen Huang, Ge Shu

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Article in Cell biology and toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

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4 · The record

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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.

Jianfa Li *Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Shuangchen Chen *Department of Urology, Peking University First Hospital, Beijing, China.
Jing Xiao *Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Jiayuan JiDepartment of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Chenchen HuangDepartment of Urology, Peking University First Hospital, Beijing, China. huangchenchen77@163.com.
Ge ShuShenzhen Key Laboratory of Male Reproductive Medicine and Genetics, Institute of Urology, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China. shuge2020@outlook.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreased activity of the transcription factor FOXC1 leads to elevated transcription of target genes, ultimately facilitating the progression of various cancer types. However, there are currently no literature reports on the role of FOXC1 in renal cell carcinoma.

methodsBy using RT-qPCR, immunohistochemistry and Western blotting, FOXC1 mRNA and protein expression was evaluated. Gain of function experiments were utilized to assess the proliferation and metastasis ability of cells. A nude mouse model was created for transplanting tumors and establishing a lung metastasis model to observe cell proliferation and spread in a living organism. Various techniques including biological analysis, CHIP assay, luciferase assay, RT-qRCR and Western blotting experiments were utilized to investigate how FOXC1 contributes to the transcription of ABHD5 on a molecular level. FOXC1 was assessed by Western blot for its impact on AMPK/mTOR signaling pathway.

resultsFOXC1 is down-regulated in RCC, causing unfavorable prognosis of patients with RCC. Further experiments showed that forced FOXC1 expression significantly restrains RCC cell growth and cell metastasis. Mechanically, FOXC1 promotes the transcription of ABHD5 to activate AMPK signal pathway to inhibit mTOR signal pathway. Finally, knockdown of ABHD5 recovered the inhibitory role of FOXC1 overexpression induced cell growth and metastasis suppression.

conclusionIn general, our study demonstrates that FOXC1 exerts its tumor suppressor role by promoting ABHD5 transcription to regulating AMPK/mTOR signal pathway. FOXC1 could serve as both a diagnostic indicator and potential treatment focus for RCC.

Indexed as

1-Acylglycerol-3-Phosphate O-AcyltransferaseAMP-Activated Protein KinasesCarcinoma, Renal CellCell ProliferationForkhead Transcription FactorsKidney NeoplasmsMice, NudeSignal TransductionTOR Serine-Threonine KinasesAnimalsCell Line, TumorDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMale1-Acylglycerol-3-Phosphate O-AcyltransferaseABHD5 protein, humanAMP-Activated Protein KinasesForkhead Transcription FactorsFOXC1 protein, humanMTOR protein, humanTOR Serine-Threonine KinasesABHD5AMPKFOXC1mTORRenal cell carcinoma

Identifiers

PMID39093497
PMCPMC11297099

What Socratic holds

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LicenceCC BY
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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 Socratic graph.