ArticleBioelectricity2022
Hypoxic Signaling Is Modulated by Calcium Channel, CaV1.3, in Androgen-Resistant Prostate Cancer.
Article in Bioelectricity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Impact of CaInternational journal of molecular sciences · 2026Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Androgen deprivation therapy (ADT) remains a key treatment for advance prostate cancer (PCa), but resistance leads to terminal castrate-resistant prostate cancer (CRPC). Its development is linked to the emergence of a hypoxic tumor microenvironment and associated hypoxia inducible factor (HIF) signaling, which is known to be modulated by intracellular calcium. ADT is also known to upregulate store-operated calcium entry (SOCE) through voltage-gated calcium channel, CaV1.3. Consequently, the role of CaV1.3 in supporting hypoxic signaling and CRPC biology was explored. Materials: Androgen-sensitive PCa LNCaP cells were cultured with and without ADT bicalutamide, alongside ADT-resistant CRPC cells (LNCaP-ABL), either in normal or low oxygen (O Results: CaV1.3 expression was increased during ADT but not hypoxia, correlating with an associated increase in SOCE. HIF-1α expression was upregulated by ADT under normal O Conclusion: This study highlights that CaV1.3 can modulated HIF signaling and impact on PCa tumor biology under hypoxia, but further investigation is required to ascertain if this mediated through SOCE or a noncanonical mechanism.
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