Hypoxic Signaling Is Modulated by Calcium Channel, CaV1.3, in Androgen-Resistant Prostate Cancer.

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 (O₂) (1%) condit

SUBMITTER: O'Reilly D 

PROVIDER: S-EPMC11441368 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature