Muscarinic cholinergic receptors promote growth of human prostate cancer cells

Rayford, Walter; Noble, Mark J.; Austenfeld, Mark S.; Weigel, John W.; Mebust, Winston K.; Shah, Girish V.

doi:10.1002/(sici)1097-0045(19970215)30:3<160::aid-pros3>3.0.co;2-q

Cited by 84 publications

(63 citation statements)

References 20 publications

(47 reference statements)

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“…Some investigators have suggested a growth regulatory role for neurotransmitters. Rayford et al (1997) compared the response to carbachol, an analog of acetylcholine, of primary cultures derived from cancer and non-malignant prostatic tissues and observed a dramatically higher response by the cancer cells. The proliferative effect of carbachol suggests that muscarinic receptors may play a role in prostate cancer growth.…”

Section: Proliferation Of Cancer Cellsmentioning

confidence: 99%

“…That this may be feasible was demonstrated by the upregulation and activation of p53 in normal prostatic epithelial cells by leptomycin B, an antifungal agent that inhibits protein export from the nucleus to the cytoplasm and thus prevents the proteasomal degradation of p53 (Lecane et al 2003). While leptomycin B is too toxic for clinical use, new proteasomal inhibitors Peehl et al (1989), Chopra et al (1996) Resistance to growth inhibitory factors Gommersall et al (2004) Response to acetyl choline analog Rayford et al (1997) Behavior in collagen gels…”

Section: Chemopreventionmentioning

confidence: 99%

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Primary cell cultures as models of prostate cancer development

Peehl¹

2005

Endocr Relat Cancer

152

142

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This review focuses on primary cultures of human prostatic epithelial cells and their applications as models of normal and malignant biological behavior. Current abilities to culture cells from normal tissues, from premalignant dysplastic lesions (prostatic intraepithelial neoplasia), from primary adenocarcinomas, and from metastases are described. Evidence for representation of the interrelated cells of the normal prostatic epithelium -stem cells, basal epithelial cells, secretory epithelial cells, transit amplifying cells and neuroendocrine cells -in primary cultures is presented. Comparisons between normal and cancer-derived primary cultures are made regarding biological activities relevant to carcinogenesis, such as proliferation, apoptosis, differentiation, senescence, adhesion, migration, invasion, steroid hormone metabolism, other metabolic pathways and angiogenesis. Analyses of tumor suppressor activity, differential gene expression and cytogenetics in primary cultures have revealed changes relevant to prostate cancer progression. Preclinical studies with primary cultures have provided information useful for designing new strategies for chemoprevention, chemotherapy, cytotoxin therapy, radiation therapy, gene therapy and imaging. While the behavior of normal primary cultures is often used as a basis for comparison with established, immortal prostate cancer cell lines, the most informative studies are performed with donor-matched pairs of normal and malignant primary cultures, grown under identical conditions. Challenges that remain to be addressed if the full potential of primary cultures as a model system is to be realized include isolation, culture and characterization of stem cells, improved methodology to induce or maintain a fully differentiated, androgen-responsive phenotype, and identification of cell surface antigens or other markers with which to purify pure populations of live cancer or premalignant cells apart from non-malignant epithelial cells prior to culture.

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Section: Proliferation Of Cancer Cellsmentioning

confidence: 99%

Section: Chemopreventionmentioning

confidence: 99%

Primary cell cultures as models of prostate cancer development

Peehl¹

2005

Endocr Relat Cancer

152

142

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“…Muscarinic receptors are also expressed in primary and metastatic colon, ovary, prostate, and lung carcinomas, breast cancer and melanoma. [18][19][20][21][22][23] Interestingly, cell proliferation and migration appear modulated in these tumors mainly by the M3 receptor subtype. 19,[24][25][26] However, we have recently demonstrated that the M2 receptor subtype is able to inhibit cell growth and survival in human glioblastoma cells, highlighting a role for this receptor in the inhibition of cancer cell proliferation.…”

Section: Introductionmentioning

confidence: 99%

M2muscarinic receptors inhibit cell proliferation and migration in urothelial bladder cancer cells

Pacini

Falco

Bari

et al. 2014

Cancer Biology & Therapy

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The role of muscarinic receptors in several diseases including cancer has recently emerged. To evaluate the hypothesis that muscarinic acetylcholine receptors may play a role in bladder cancer as well as in other tumor types, we investigated their expression in bladder tumor specimens. All examined samples expressed the M1, M2 and M3 receptor subtypes. We also found that the level of M2 transcripts, but not those of M1 or M3, significantly increased with the tumor histologic grade. In view of these results, we proceeded to investigate whether the M2 agonist Arecaidine had any effect on in vitro cell growth and migration of T24 cells, a bladder tumor cell line expressing the muscarinic receptors, including the M2 subtype. We observed that Arecaidine significantly reduced T24 and 5637 cell proliferation and migration in a concentration dependent manner. The silencing of M2 receptor by siRNA in T24 and 5637 cell lines showed the inability of Arecaidine (100 mM) to inhibit cell proliferation after 48 hours, whereas the use of M1 and M3 antagonists in T24 appeared not to counteract the Arecaidine effect, suggesting that the inhibition of cell proliferation was directly dependent on M2 receptor activation. These data suggest that M2 muscarinic receptors may play a relevant role in bladder cancer and represent a new attractive therapeutic target.

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“…Recently chronic stress and other behavioral conditions have been reported to cause promotion and progression of cancers; catecholamines in ovarian cancers [21,22], muscarinic cholinergic receptors in prostate [23], colon [24], mammary carcinoma cells [25,26], and the receptors and ligands in small cell lung carcinoma [27,28] were shown to promote their growth and angiogenesis.…”

Section: Introductionmentioning

confidence: 99%