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Glutathione levels and susceptibility to chemically induced injury in human prostate cancer cell lines (663.11)
Author(s) -
Lash Lawrence,
Putt David,
Jankovich Adam
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.663.11
Subject(s) - lncap , glutathione , oxidative stress , apoptosis , cell culture , cancer cell , chemistry , lactate dehydrogenase , cell growth , cytotoxicity , cancer research , microbiology and biotechnology , biology , medicine , biochemistry , in vitro , cancer , enzyme , genetics
More aggressive or invasive prostate cancer cells (PCCs) are often resistant to chemotherapy and have poor prognosis. Two immortalized human PCC lines, PC‐3 (more aggressive) and LNCaP (less aggressive) cells, were compared with regard to cellular redox state and susceptibility to either oxidants or glutathione (GSH) depletors. We tested the hypothesis that compared to less aggressive PCCs, more aggressive PCCs exhibit higher GSH concentrations and are relatively resistant to cytotoxicity from oxidants. PC‐3 cells exhibited 4.2‐fold higher GSH concentration than LNCaP cells but only exhibited lower lactate dehydrogenase (LDH) release after toxicant exposures at some time points. Only LNCaP cells underwent diamide‐induced apoptosis. Expression of several proteins involved in stress response and regulation of cell growth and proliferation were measured to determine their possible role in redox state and susceptibility to toxicants. PC‐3 cells exhibited higher levels of pro‐apoptotic and lower levels of anti‐apoptotic proteins than LNCaP cells. Consistent with a compensatory response to oxidative stress, LNCaP cells exhibited higher levels of certain antioxidant and stress response proteins than PC‐3 cells. Thus, significant differences in redox status and expression of proteins involved in apoptosis and stress response may contribute to PCC aggressiveness. Grant Funding Source : None.