2. Academic Validation
  3. The mechanism of protriptyline-induced Ca2+ movement and non-Ca2+-triggered cell death in PC3 human prostate cancer cells

The mechanism of protriptyline-induced Ca2+ movement and non-Ca2+-triggered cell death in PC3 human prostate cancer cells

  • J Recept Signal Transduct Res. 2015;35(5):429-34. doi: 10.3109/10799893.2014.1000464.
Hong-Tai Chang 1,  Chiang-Ting Chou 2 3,  Chia-Cheng Yu 1,  Jeng-Yu Tsai 1,  Te-Kung Sun 4,  Wei-Zhe Liang 5,  Ko-Long Lin 6,  Hui-Wen Tseng 7,  Chun-Chi Kuo 8,  Fu-An Chen 9,  Daih-Huang Kuo 9,  Chih-Chuan Pan 10,  Chin-Man Ho 5,  Pochuen Shieh 9,  Chung-Ren Jan 5
Affiliations

Affiliations

  • 1 a Department of Surgery , Kaohsiung Veterans General Hospital , Kaohsiung , Taiwan .
  • 2 b Department of Nursing, Division of Basic Medical Sciences , Chang Gung Institute of Technology , Chia-Yi , Taiwan .
  • 3 c Chronic Diseases and Health Promotion Research Center, Chang Gung Institute of Technology , Chia-Yi , Taiwan .
  • 4 d Division of Pediatrics , St. Joseph Hospital , Kaohsiung , Taiwan .
  • 5 e Department of Medical Education and Research .
  • 6 f Department of Rehabilitation , and.
  • 7 g Department of Dermatology , Kaohsiung Veterans General Hospital , Kaohsiung , Taiwan .
  • 8 h Department of Nursing , Tzu Hui Institute of Technology , Pingtung , Taiwan .
  • 9 i Department of Pharmacy , Tajen University , Pingtung , Taiwan , and.
  • 10 j Department of Psychiatry , Kaohsiung Veterans General Hospital , Kaohsiung , Taiwan.
PMID: 26096164 DOI: 10.3109/10799893.2014.1000464
Abstract

Protriptyline, a tricyclic anti-depressant, is used primarily to treat the combination of symptoms of anxiety and depression. However, the effect of protriptyline on prostate caner is unknown. This study examined whether the anti-depressant protriptyline altered CA(2+) movement and cell viability in PC3 human prostate Cancer cells. The CA(2+)-sensitive Fluorescent Dye fura-2 was used to measure [CA(2+)](i). Protriptyline evoked [CA(2+)](i) rises concentration-dependently. The response was reduced by removing extracellular CA(2+). Protriptyline-evoked CA(2+) entry was inhibited by store-operated channel inhibitors (nifedipine, econazole and SKF96365), protein kinase C activator (phorbol 12-myristate 13 acetate, PMA) and protein kinase C inhibitor (GF109203X). Treatment with the endoplasmic reticulum CA(2+) pump inhibitor 2,5-di-tert-butylhydr-oquinone (BHQ) in CA(2+)-free medium inhibited 60% of protriptyline-evoked [CA(2+)](i) rises. Conversely, treatment with protriptyline abolished BHQ-evoked [CA(2+)](i) rises. Inhibition of Phospholipase C with U73122 suppressed 50% of protriptyline-evoked [CA(2+)](i) rises. At concentrations of 50-70 µM, protriptyline decreased cell viability in a concentration-dependent manner; which were not reversed by chelating cytosolic CA(2+) with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester (BAPTA/AM). Collectively, in PC3 cells, protriptyline evoked [CA(2+)](i) rises by inducing Phospholipase C-associated CA(2+) release from the endoplasmic reticulum and other stores, and CA(2+) influx via protein kinase C-sensitive store-operated CA(2+) channels. Protriptyline caused cell death that was independent of [CA(2+)](i) rises.

Keywords

Ca2+; endoplasmic reticulum; phospholipase C; prostate cancer cells; protriptyline; store-operated Ca2+ channels.

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