Evidence map›Paper›PMID 42251238›Full record

ArticleDaru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences2026

ALKBH5 promotes the progression of cisplatin-resistant oral squamous cell carcinoma by regulating FOXA1 expression via m

Ying Wang, Hui-Xin Yang, Yu-Jia Gu, Mei Tian, Qi-Feng Geng

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Article in Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Ying WangThe Fifth Outpatient Department, Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Hui-Xin YangThe Fifth Outpatient Department, Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Yu-Jia GuThe Fifth Outpatient Department, Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Mei TianThe Fifth Outpatient Department, Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Qi-Feng GengThe Fifth Outpatient Department, Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China. qifeng_Geng@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOral squamous cell carcinoma (OSCC) accounts for the vast majority of oral cancer cases. Accumulating evidence has implicated both AlkB homolog 5 (ALKBH5) and forkhead box protein A1 (FOXA1) in the emergence of cisplatin resistance in OSCC. This study aimed to define their functional roles and elucidate the underlying molecular mechanisms.

methodsThe expression of ALKBH5, FOXA1, and YTHDF2 was assessed by qPCR and Western blot. Cisplatin-resistant cell lines (H357 CisR and SCC4 CisR) were established via stepwise dose escalation. To investigate key functional phenotypes, a series of assays were employed: CCK-8 for viability, colony formation for proliferation, and Transwell for migration and invasion. Bioinformatics (SRAMP, RM2Target) predicted m⁶A sites on FOXA1 and its binding with ALKBH5, which were validated by MeRIP-qPCR and RIP. FOXA1 mRNA stability was measured by actinomycin D assay.

resultsALKBH5 and FOXA1 were upregulated in cisplatin-resistant OSCC, with FOXA1 essential for maintaining oncogenic phenotypes. Bioinformatic and biochemical analyses confirmed FOXA1 as a direct target of ALKBH5. ALKBH5 demethylates FOXA1 mRNA, stabilizing its transcript and enhancing its expression by inhibiting YTHDF2-mediated degradation. Functionally, ALKBH5 overexpression reversed the tumor-suppressive effects of FOXA1 knockdown.

conclusionOur study demonstrates that ALKBH5 promotes cisplatin resistance in OSCC through m

Indexed as

AlkB Homolog 5, RNA DemethylaseCarcinoma, Squamous CellCisplatinDrug Resistance, NeoplasmHepatocyte Nuclear Factor 3-alphaMouth NeoplasmsAdenosineAntineoplastic AgentsCell Line, TumorCell MovementCell ProliferationEpitranscriptomeGene Expression Regulation, NeoplasticHumansRNA-Binding ProteinsRNA MethylationAdenosineALKBH5 protein, humanAlkB Homolog 5, RNA DemethylaseAntineoplastic AgentsCisplatinFOXA1 protein, humanHepatocyte Nuclear Factor 3-alphaN-methyladenosineRNA-Binding ProteinsYTHDF2 protein, humanALKBH5Cisplatin-resistant oral squamous cell carcinomaFOXA1m6A RNA methylationYTHDF2

Identifiers

PMID42251238
PMCPMC13242349

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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.