ArticleMolecular biology reports2023
Knocking down SOX2 overcomes the resistance of prostate cancer to castration via notch signaling.
Article in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Tumour Jagged1 expression as a prognostic marker of bevacizumab response and modulation of 5-fluorouracil efficacy through γ-secretase inhibition in colorectal cancer.Gastroenterology report · 2026Article
- The molecular pathogenesis of SOX2 in prostate cancer.Discover oncology · 2025Review
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6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCastration-resistant prostate cancer (CRPC) is a terminal type of advanced cancer resistant to androgen deprivation therapy (ADT). Due to the poor therapeutic response of CRPC, novel treatment strategies are urgently required. This study aimed to clarify the regulatory roles of the SOX2/Notch axis in CRPC.
methodsFor the evaluation of the SOX2, Notch, and Hey1 expression in the prostate cancer (PCa) and CRPC tissues, we conducted immunohistochemistry (IHC) analyses. RT-PCR, Western blotting, and immunofluorescence were performed to evaluate SOX2 and Notch expression in enzalutamide-resistant LNCaP cells (Enza-R). CCK-8, Transwell, Wound healing, and Western blotting assays were used to assess the viability, invasion, migration, cell cycle, and drug-resistant in Enza-R cells.
resultsCompared to the PCa tissues, CRPC tissues exhibited significantly elevated SOX2, Notch1, and Hey1 expression. SOX2-positive patients were more likely to develop bone metastases than SOX2-negative ones. Significant activation of the signaling associated with SOX2 and Notch was detected in Enza-R cells. The suppression of SOX2 clearly inactivated the Notch signaling and inhibited malignant behaviors, including proliferation, invasion, migration, and drug resistance in Enza-R cells. Theγsecretase inhibitor, GSI-IX, abrogated the enzalutamide resistance by inhibiting Notch signaling in vitro in vitro. Also, GSI-IX alone had a significant anti-tumor effect in Enza-R cells.
conclusionWe demonstrated that SOX2/Notch signaling was responsible for Enzalutamide resistance in CRPC. Targeting SOX2/Notch signaling might represent a new choice for the treatment and therapy of CRPC.
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