Publication: Neuropeptides bombesin and calcigonin induce resistance to etoposide
induced apoptosis in prostate cancer cell lines
Authors
Salido, M. ; Vilches, J. ; Lopez, A.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Background: Neuroendocrine differentiation
in prostatic carcinoma has been related to regulation of
proliferation and metastatic potential and correlated with
prognosis. More than 80% of prostate carcinomas
initially respond to androgen ablation, but most relapse,
due to the heterogeneous presence of androgendependent
and independent clones. The pathways of
cellular proliferation and apoptosis are inexorabily
linked to minimize the ocurrence of neoplasia, and
disfunction of apoptosis is proposed as a pathogenic
process in malignant tumors. Androgen-dependent
prostatic cancer cells undergo apoptosis after androgen
deprivation, but not androgen-independent ones due to a
defect in the initiation step. Anyway, they retain the
basic cellular machinery to undergo apoptosis. We
suggest a possible role of neuroendocrine differentiation
in the onset and regulation of apoptosis in prostatic
neoplasia. Methods: LNCaP, PC-3 and DU 145 prostatic
cancer cell lines were induced to undergo apoptosis after
treatment with etoposide alone or plus androgen
ablation. We tested the role of neuropeptides bombesin
and calcitonin at modulating etoposide induced
apoptosis. Results: Etoposide-induced apoptosis in all
cancer cell lines was achieved. In LNCaP androgen
ablation was also required. Apoptosis is prevented in all
three lines when bombesin was added. Calcitonin
addition prevents apoptosis in PC-3, LNCaP and in an etoposide dose-dependent way in DU 145. Conclusion:
Neuropeptides bombesin and calcitonin can modulate
the apoptotic response of prostate cancer cells by
inducing resistance to etoposide-induced apoptosis,
suggesting that neuropeptides can be used as a target of
therapeutical approach in prostatic carcinoma.
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