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

Debbie O'Reilly; Tim Downing; Sana Kouba; Marie Potier-Cartereau; Declan J McKenna; Christophe Vandier; Paul Buchanan

doi:10.1016/j.dib.2022.108143

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

Data Brief. 2022 Apr 17:42:108143. doi: 10.1016/j.dib.2022.108143. eCollection 2022 Jun.

Authors

Debbie O'Reilly^{1

2

3}, Tim Downing⁴, Sana Kouba⁵, Marie Potier-Cartereau⁵, Declan J McKenna⁶, Christophe Vandier⁵, Paul Buchanan^{1

2

3}

Affiliations

¹ DCU Cancer Research Group, DCU, Ireland.
² National Institute Cellular Biotechnology, DCU, Ireland.
³ School of Nursing, Psychotherapy and Community Health, DCU, Ireland.
⁴ School of Biotechnology, DCU, Ireland.
⁵ Department of Animal Physiology, UMR INSERM U 1069, Nutrition, Growth and Cancer (N2C), University of Tours, France.
⁶ Genomic Medicine Research Group, School of Biomedical Sciences, Ulster University, N.Ireland.

Abstract

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 androgen 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 in markers linked to androgen resistance, androgen receptor (AR) and neuron specific enolase (NSE), observing an increase under androgen deprivation. In addition, the gene expression of a range of calcium channels was measured, with only the L-type Voltage gated calcium channel, CACNA1D, demonstrating an increase during androgen deprivation. With CACNA1D knockdown the channel was found not to influence the gene expression of calcium channels, ORAI1 and STIM1. The calcium channel blocker (CCB), nifedipine, was employed to determine the impact of CaV1.3 on the observed store release and calcium entry measured via Fura-2AM ratiometric dye in our outlined PCa model. In both the presence and absence of androgen deprivation, 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, CACNA1D siRNA knockdown was able to reduce SOCE in PC3 cells. The effect of nifedipine on CaV1.3 in PCa biology was measured through cell proliferation assay, with no observed change in the presence of CCB. While siCACNA1D 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.

Keywords: ADT, Androgen Deprivation Therapy; AR, Androgen Receptor; Androgen deprivation; CACNA1D, L-type Calcium Channel Gene; CCB, Calcium Channel Blocker; CRPC, Castrate Resistant Prostate Cancer; CaV1.3; CaV1.3, L-type Calcium Channel Protein; Calcium channel blocker; ERG, ETS-Related Gene; HPRT1, Hypoxanthine Phosphoribosyltransferase 1; NSE, Neuron Specific Enolase; ORAI STIM; ORAI, ORAI Calcium Release-Activated Calcium Modulator 1; PCa, Prostate Cancer; Prostate cancer; SERCA, Sarco(endo)plasmic Reticulum Calcium-ATPase; SOCE, Store Operated Calcium Entry; STIM1, Stromal Interaction Molecule 1; Store operated calcium channels; Store operated calcium entry; Tg, Thapsigargin; Voltage gated calcium channels.