ArticleWorld journal of stem cells2025
DNA methyltransferase 1/miR-342-3p/Forkhead box M1 signaling axis promotes self-renewal in cervical cancer stem-like cells
Article in World journal of stem cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Nobiletin attenuates self-renewal in cervical cancer cells and spheres through miR-342-3p upregulation and FOXM1 downregulation.Molecular and cellular biochemistry · 2026Article
- Identification and validation of stemness-associated hub genes in cervical cancer: a bioinformatics and experimental study.World journal of surgical oncology · 2026Article
- DNMT Enzymes and Their Impact on Cervical Cancer: A State-of-the-Art Review.International journal of molecular sciences · 2025Review
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12 authors.
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Abstract
backgroundCervical cancer (CC) stem cell-like cells (CCSLCs), defined by the capacity of differentiation and self-renewal and proliferation, play a significant role in the progression of CC. However, the molecular mechanisms regulating their self-renewal are poorly understood. Therefore, elucidation of the epigenetic mechanisms that drive cancer stem cell self-renewal will enhance our ability to improve the effectiveness of targeted therapies for cancer stem cells.
aimTo explore how DNA methyltransferase 1 (DNMT1)/miR-342-3p/Forkhead box M1 (FoxM1), which have been shown to have abnormal expression in CCSLCs, and their signaling pathways could stimulate self-renewal-related stemness in CCSLCs.
methodsSphere-forming cells derived from CC cell lines HeLa, SiHa and CaSki served as CCSLCs. Self-renewal-related stemness was identified by determining sphere and colony formation efficiency, CD133 and CD49f protein level, and SRY-box transcription factor 2 and octamer-binding transcription factor 4 mRNA level. The microRNA expression profiles between HeLa cells and HeLa-derived CCSLCs or mRNA expression profiles that HeLa-derived CCSLCs were transfected with or without miR-342-3p mimic were compared using quantitative PCR analysis. The expression levels of
resultsCCSLCs derived from the established HeLa cell lines displayed higher self-renewal-related stemness, including enhanced sphere and colony formation efficiency, increased CD133 and CD49f protein level, and heightened transcriptional quantity of stemness-related factors SRY-box transcription factor 2 and octamer-binding transcription factor 4
conclusionOur findings suggested that a novel DNMT1/miR-342-3p/FoxM1 signal axis promotes CCSLC self-renewal and presented a potential target for the treatment of CC through suppression of CCSLC self-renewal. However, this pathway has been previously implicated in CC, as evidenced by prior studies showing miR-342-3p-mediated downregulation of FoxM1 in cervical cancer cells. Additionally, research on liver cancer further supports the involvement of miR-342-3p in suppressing FoxM1 expression. While our study contributed to this body of knowledge, we did not present a completely novel axis but reinforced the therapeutic potential of targeting the DNMT1/miR-342-3p/FoxM1 axis to suppress CCSLC self-renewal in CC treatment.
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