ArticleDiscover oncology2024
lncRNA FLJ20021 regulates CDK1-mediated PANoptosis in a ZBP1-dependent manner to increase the sensitivity of laryngeal cancer-resistant cells to cisplatin.
Article in Discover oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Construction of PANoptosis-related lncRNA prognostic model and immunotherapy sensitivity analysis in lung adenocarcinoma.Journal of cardiothoracic surgery · 2026Article
- Integrative bioinformatics and machine learning approaches identify novel diagnostic signatures for oxaliplatin-resistant colorectal cancer.International journal of colorectal disease · 2026Article
- Non-Coding RNAs as key regulators of interferon signaling in cancer immunotherapy: mechanistic insights and clinical prospects.Clinical and experimental medicine · 2026Review
- The molecular mechanisms, roles, and potential applications of PANoptosis in cancer treatment.Frontiers in immunology · 2025Review
- Unveiling pathogenesis of pelvic organ prolapse through transcriptomic and bioinformatic analyses in uterosacral ligament tissues of postmenopausal women.Frontiers in genetics · 2025Article
- Dynamics of the immune microenvironment and immune cell PANoptosis in colorectal cancer: recent advances and insights.Frontiers in immunology · 2024Review
- Pterostilbene suppresses head and neck cancer cell proliferation via induction of apoptosis.Turkish journal of biology = Turk biyoloji dergisi · 2024Article
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Authors and funding
7 authors.
Funding
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Abstract
In this study, we investigated the role of the newly discovered lncRNA FLJ20021 in laryngeal cancer (LC) and its resistance to cisplatin treatment. We initially observed elevated lncRNA FLJ20021 levels in cisplatin-resistant LC cells (Hep-2/R). To explore its function, we transfected lncRNA FLJ20021 and cyclin-dependent kinase 1 (CDK1) into Hep-2/R cells, assessing their impact on cisplatin sensitivity and PANoptosis. Silencing lncRNA FLJ20021 effectively reduced cisplatin resistance and induced PANoptosis in Hep-2/R cells. Mechanistically, lncRNA FLJ20021 primarily localized in the nucleus and interacted with CDK1 mRNA, thereby enhancing its transcriptional stability. CDK1, in turn, promoted panapoptosis in a ZBP1-dependent manner, which helped overcome cisplatin resistance in Hep-2/R cells. This study suggests that targeting lncRNA FLJ20021 can be a promising approach to combat cisplatin resistance in laryngeal cancer by regulating CDK1 and promoting PANoptosis via the ZBP1 pathway. These findings open up possibilities for lncRNA-based therapies in the context of laryngeal cancer.
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