The impact of cell adhesion changes on proliferation and survival during prostate cancer development and progression
- PMID: 16676354
- DOI: 10.1002/jcb.20934
The impact of cell adhesion changes on proliferation and survival during prostate cancer development and progression
Abstract
In the normal prostate epithelium, androgen receptor (AR) negative basal epithelial cells adhere to the substratum, while AR expressing secretory cells lose substratum adhesion. In contrast, prostate cancer cells both express AR and adhere to a tumor basement membrane. In this review, we describe the differential expression of integrins, growth factor receptors (GFRs), and AR in normal and cancerous epithelium. In addition, we discuss how signals from integrins, GFRs, and AR are integrated to regulate the proliferation and survival of normal and malignant prostate epithelial cells. While cell adhesion is likely of great importance when considering therapeutic approaches for treatment of metastatic prostate cancer, no data on integrin expression are available from tissues of prostate cancer metastasis. However, several drug targets that are upregulated after androgen ablative therapy regulate cell adhesion and thus novel targeted therapies indirectly interfere with cell adhesion mechanisms in prostate cancer cells.
Copyright 2006 Wiley-Liss, Inc.
Similar articles
-
Differentiation pathways and histogenetic aspects of normal and abnormal prostatic growth: a stem cell model.Prostate. 1996 Feb;28(2):98-106. doi: 10.1002/(SICI)1097-0045(199602)28:2<98::AID-PROS4>3.0.CO;2-J. Prostate. 1996. PMID: 8604398 Review.
-
Molecular regulation of androgen action in prostate cancer.J Cell Biochem. 2006 Oct 1;99(2):333-44. doi: 10.1002/jcb.20794. J Cell Biochem. 2006. PMID: 16518832 Review.
-
5alpha-androstane-3alpha,17beta-diol supports human prostate cancer cell survival and proliferation through androgen receptor-independent signaling pathways: implication of androgen-independent prostate cancer progression.J Cell Biochem. 2008 Aug 1;104(5):1612-24. doi: 10.1002/jcb.21731. J Cell Biochem. 2008. PMID: 18320593
-
Emergence of metastatic hormone-refractory disease in prostate cancer after anti-androgen therapy.J Cell Biochem. 2004 Mar 1;91(4):662-70. doi: 10.1002/jcb.20040. J Cell Biochem. 2004. PMID: 14991758 Review.
-
Androgens modulate expression of transcription intermediary factor 2, an androgen receptor coactivator whose expression level correlates with early biochemical recurrence in prostate cancer.Cancer Res. 2006 Nov 1;66(21):10594-602. doi: 10.1158/0008-5472.CAN-06-1023. Cancer Res. 2006. PMID: 17079484
Cited by
-
Evaluation of the expression of integrins and cell adhesion molecules through tissue microarray in lymph node metastases of prostate cancer.J Carcinog. 2009;8:3. doi: 10.4103/1477-3163.48453. J Carcinog. 2009. PMID: 19240373 Free PMC article.
-
Functional live-cell imaging demonstrates that beta1-integrin promotes type IV collagen degradation by breast and prostate cancer cells.Mol Imaging. 2008 Sep-Oct;7(5):199-213. Mol Imaging. 2008. PMID: 19123990 Free PMC article.
-
Targeting integrin α5β1 in urological tumors: opportunities and challenges.Front Oncol. 2023 Jul 6;13:1165073. doi: 10.3389/fonc.2023.1165073. eCollection 2023. Front Oncol. 2023. PMID: 37483505 Free PMC article. Review.
-
Potential Urinary Protein Biomarker Candidates for the Accurate Detection of Prostate Cancer among Benign Prostatic Hyperplasia Patients.J Cancer. 2014 Jan 5;5(2):103-14. doi: 10.7150/jca.6890. eCollection 2014. J Cancer. 2014. PMID: 24494028 Free PMC article.
-
Cysteine-linked dimerization of BST-2 confers anoikis resistance to breast cancer cells by negating proapoptotic activities to promote tumor cell survival and growth.Cell Death Dis. 2017 Mar 16;8(3):e2687. doi: 10.1038/cddis.2017.68. Cell Death Dis. 2017. PMID: 28300825 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical
Research Materials