ArticleBiochemical genetics2025
LncRNA PGM5-AS1 Impairs the Resistance of Cervical Cancer to Cisplatin by Regulating the Hippo and PI3K-AKT Pathways.
Article in Biochemical genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed.
- Therapy resistance-related ncRNAs in cervical cancer: biomarkers and therapeutic targets.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Review
- The molecular puzzle of recurrent implantation failure: integrating genetic, epigenetic, and immune mechanisms for precision reproductive medicine.Journal of assisted reproduction and genetics · 2026Review
- Harnessing cuproptosis: a new avenue for targeted cancer therapies.Apoptosis : an international journal on programmed cell death · 2025Review
- Expression of Core Hippo Pathway Proteins in Cervical Cancer and Their Association with Clinicopathologic Parameters.Medicina (Kaunas, Lithuania) · 2025Article
- Nuclear receptor subfamily 1 group D member 2 induces chemoresistance in ovarian cancer by regulating ferroptosis and immune infiltration.Discover oncology · 2025Article
- Hippo signaling pathway in cervical cancer: insights into mechanisms and therapeutic potential.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Cisplatin, a platinum-based chemotherapeutic agent, can be used to treat cervical cancer (CC), but cisplatin resistance is increased during the cisplatin treatment. Long non-coding RNA PGM5-AS1 reportedly participates in CC tumorigenesis; however, its role in CC patients with cisplatin resistance has not been revealed. The present aimed to examine the role of PGM5-AS1 in modulating cisplatin resistance in CC. The PGM5-AS1 expression in CC tissues from 29 patients was quantified using quantitative reverse transcription-polymerase chain reaction. The cisplatin-resistant CC cells were constructed by using increasing cisplatin concentrations. The effects of cisplatin resistance interacting with PGM5-AS1 on CC cell malignancy were confirmed by performing Cell Counting Kit 8, colony formation, wound healing, and transwell assays. The key proteins of the Hippo and PI3K-AKT signaling pathways were evaluated by Western blotting. PGM5-AS1 with low expression in CC tissues was correlated to higher International Federation of Gynecology and Obstetrics stage, poor differentiation, lymph node metastasis, and cisplatin resistance. PGM5-AS1 overexpression suppressed the proliferation, migration, and invasion abilities of cisplatin-resistant CC cells. Additionally, PGM5-AS1 overexpression in cisplatin-resistant CC cells could induce the activation of the Hippo signaling pathway and the inactivation of the PI3K-AKT signaling pathway. PGM5-AS1 enhanced the CC cell's sensitivity to cisplatin by activating the Hippo signaling pathway and inactivating the PI3K-AKT signaling pathway. Our study data may provide a novel therapeutic biomarker to overcome cisplatin resistance in CC treatment.
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Registered trials
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