ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
Doublecortin-like kinase 1, regulated by STIP1 homology and U-box containing protein 1 or Sp1 transcription factor, affects the malignant behaviors and drug sensitivity in adriamycin-resistant breast cancer cells.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. 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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Abstract
backgroundThe emergence of drug resistance poses a formidable obstacle in the treatment of breast cancer (BC). Doublecortin-like kinase 1 (DCLK1) has been identified as a tumor promoter in BC. However, the impact of DCLK1 on adriamycin (ADM) resistance in BC remains largely unknown.
methodsThe factors linked to ADM resistance in BC, the interaction between DCLK1 and STIP1 homology and U-box containing protein 1 (STUB1), and the binding sequence between Sp1 transcription factor (SP1) and DCLK1 were predicted by bioinformatics. The impact on cell phenotypes was evaluated by measuring the IC
resultsDCLK1 was upregulated in ADM-resistant BC tissues and cell lines. DCLK1 depletion impaired cell proliferation, invasion, and migration and sensitized them to ADM in vitro, as well as enhanced the sensitivity of subcutaneous xenografts to ADM. Mechanistically, STUB1 degraded DCLK1 protein through ubiquitination, and SP1 transcriptionally increased DCLK1 expression. DCLK1 upregulation reversed the effects of STUB1 on ADM sensitivity and malignant behaviors of ADM-resistant BC cells, and DCLK1 expression restoration reversed the impact of SP1 silencing.
conclusionOur findings have identified DCLK1 as a crucial regulator in the malignant phenotypes and ADM sensitivity of ADM-resistant BC cells, providing a potential target for enhancing the anti-cancer efficacy of ADM in BC.
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