Data pertaining to aberrant intracellular calcium handling during androgen deprivation therapy in prostate cancer

The data generated here in relates to the research article “CaV1.3 enhanced store operated calcium promotes resistance to androgen deprivation in prostate cancer”. A model of prostate cancer (PCa) progression to castration resistance was employed, with untreated androgen sensitive LNCaP cell line alongside two androgens deprived (bicalutamide) sublines, either 10 days (LNCaP-ADT) or 2 years (LNCaP-ABL) treatment, in addition to androgen insensitive PC3. With this PCa model, qPCR was used to examined fold change markers linked to androgen resistance, androgen receptor (AR) and neuron specific enolase (NSE), observing an increase under ADT. In addition, the gene expression of a range of calcium channels was measured, with the L-type Voltage gated calcium channel, CaV1.3, demonstrating the largest increase during ADT compared to DMSO control. No effect of CaV1.3 on the gene expression of calcium channels Orai and STIM1 was found using CaV1.3 siRNA knockdown, which was validated at a gene and protein level. Protein fractionation and subsequent CaV1.3 western blot noted the presence of CaV1.3 c-terminus in the nucleus which was lost in LNCaP-ABL. The calcium channel blocker (CCB), nifedipine, was employed to determine the impact of CaV1.3 on store release and calcium entry measured with Fura-2AM ratiometric dye. In both the presence and absence ADT, nifedipine was found to have no impact on store release induced by thapsigargin (Tg) in 0mM Ca2+ nor store operated calcium entry (SOCE) following the addition of 2mM Ca2. However, CaV1.3 siRNA knockdown was able to reduce SOCE in PC3 cells. The effect of nifedipine on CaV1.3 in PCa biology was measured through cell survival colony formation assay, with no observed change in the presence of CCB. While siCaV1.3 reduced PC3 cell proliferation. This data can be reused to inform new studies investigating altered calcium handling in androgen resistant prostate cancer. It provides insight into the mechanism of CaV1.3 and its functional properties in altered calcium in cancer, which can be of use to researchers investigating this channel in disease. Furthermore, it could be helpful in interpreting studies investigating CCB’s as a therapeutic and in the development of future drugs targeting CaV1.3.