BCL-2 in prostate cancer: A minireview

  title={BCL-2 in prostate cancer: A minireview},
  author={Sergio D. Catz and J Johnson},
Prostate cancer progression and the development of androgen-independent prostate cancer have been largely related to a number of genetic abnormality that affect not only the androgen receptor but also crucial molecules involved in the regulation of survival or apoptotic pathways. One of these molecules, the pro-survival protein BCL-2, has been associated with the development of androgen-independent prostate cancer due to its high levels of expression in androgen-independent tumors in advanced… 

Implications of Bcl-2 and its interplay with other molecules and signaling pathways in prostate cancer progression

To identify more effective prostate cancer therapy, further mechanistic studies are required with BCL-2 inhibitors in AIPC and ADPC, considering a multi-target therapy against BCL -2 and its related signaling.

Up-regulation of Bcl-2 is required for the progression of prostate cancer cells from an androgen-dependent to an androgen-independent growth stage

It is reported that Bcl-2 is required for the progression of LNCaP prostate cancer cells from an androgens-dependent to an androgen-independent growth stage and shRNA-mediated gene silencing of Bcl1 promotes UV-induced apoptosis and suppresses the growth of prostate tumors in vivo.

SRC-3 is required for prostate cancer cell proliferation and survival.

It is demonstrated that reduction of SRC-3 expression by small interfering RNA decreases proliferation, delays the G1-S transition, and increases cell apoptosis of different prostate cancer cell lines, and findings indicate that S RC-3 is an important regulator of prostate cancer proliferation and survival.

Death receptor‐induced cell death in prostate cancer

This review has focused on what is known about apoptosis in prostate cancer and, more specifically, the receptor/ligand‐mediated pathways of apoptosis as potential therapeutic targets.

Signaling Pathways That Control Apoptosis in Prostate Cancer

Better knowledge of the apoptosis regulation in prostate epithelial cells is needed to understand mechanisms of androgen-independence and implement life-extending therapies for CRPC.

Prostate Cancer: A Continuous Evolutionary Search for Molecular Therapy Targets

  • Biology, Medicine
  • 2019
According to, androgens are involved in the normal prostate development, growth, and the maintenance of physiologic functions and progression of PCa, and alterations in AR leads to changes in androgen-responsive genes, hence AR signaling remains the most sort after an attractive target for intervention in PCa.

Molecular mechanisms of apoptosis in prostate cancer.

The most important signaling pathways implicated in prostate cancer apoptosis and cell growth and how they may be deregulated during prostate cancer progression are reviewed.

Inflammation and Prostatic Carcinogenesis - a morphological study of the human prostate

This study provides the first evidence of a direct link between COX-2 and angiogenesis in PCa tissues and demonstrates that chronic inflammation appeared to play a role in inducing C/EBPβ expression in atrophic prostate epithelial cells.

Quercetin-induced growth inhibition and cell death in prostatic carcinoma cells (PC-3) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression

It was concluded that quercetin inhibits prostate cancer cell proliferation by altering the expression of cell cycle regulators and apoptotic proteins.



Expression of the protooncogene bcl-2 in the prostate and its association with emergence of androgen-independent prostate cancer.

It is indicated that bcl-2 expression is augmented following androgen ablation and is correlated with the progression of prostate cancer from androgen dependence to androgen independence.

Expression of bcl-2 and the progression of human and rodent prostatic cancers.

The data demonstrate that the development of androgen independence and/or metastatic ability can be associated with the expression of bcl-2 protein but that b cl-2-independent mechanisms also exist for such progression.

Antagonism between PTEN/MMAC1/TEP-1 and Androgen Receptor in Growth and Apoptosis of Prostatic Cancer Cells*

The data suggest that the loss of PTEN function may induce tumorigenesis through unopposed activity of the AR as well as contribute to the resistance of prostate cancers to androgen ablation therapy.

PTEN Induces Chemosensitivity in PTEN-mutated Prostate Cancer Cells by Suppression of Bcl-2 Expression*

It is demonstrated that expression of Bcl-2 in prostate tumors correlates with loss of the PTEN protein, thus contributing to survival and chemoresistance of PCa cells and suggesting that thePTEN gene and its regulated pathway are potential therapeutic targets in prostate cancer.

Immunohistochemical analysis of bcl-2, bax, bcl-X, and mcl-1 expression in prostate cancers.

It is suggested that expression of several anti-apoptotic members of the bcl-2 gene family, including b cl-2, bcl -X, and mcl-1 increases during progression of prostate cancers, a finding that may be relevant to the hormone-insensitive, metastatic phenotype of most advanced adenocarcinomas of the prostate.

The association of p21((WAF-1/CIP1)) with progression to androgen-independent prostate cancer.

  • K. FizaziL. A. Martinez N. Navone
  • Biology, Medicine
    Clinical cancer research : an official journal of the American Association for Cancer Research
  • 2002
Tumor relapse, defining AIPC, was associated with increased expression of p21 to levels comparable with those found before castration, and p21 expression at relapse was also correlated with a high Ki-67 index.

Apoptosis: therapeutic significance in the treatment of androgen-dependent and androgen-independent prostate cancer

The results suggest that treatment of prostate cancer patients with suramin prior to irradiation is likely to inhibit radiation palliation, and that radiation therapy followed by suramin treatment may yield enhanced effectiveness.

Androgens down-regulate bcl-2 protooncogene expression in ZR-75-1 human breast cancer cells.

It is indicated that androgens can down-regulate bcl-2 protooncogene levels via an androgen receptor-mediated mechanism, thus providing a novel mechanism for their known inhibitory effect on breast cancer cell growth.

Role of PI3K signaling in survival and progression of LNCaP prostate cancer cells to the androgen refractory state.

Data show that androgen ablation alone can increase PI3K-Akt activation, which supports survival after acute androgens ablation and proliferation during chronic androgen deprivation, and successful progression to the androgen-independent state in the LNCaP cell line model requires intact PI3k signaling.

Role of the Bcl-2 gene family in prostate cancer progression and its implications for therapeutic intervention.

In vitro and in vivo studies have established that Bcl-2 expression confers an antiapoptotic activity against androgen withdrawal and cytotoxic chemotherapy, which offers a tempting potential target for therapeutic manipulations of PC.