Antisense Bcl-2 sensitizes prostate cancer cells to radiation

Mu, Zhaomei; Hachem, P.; Pollack, Alan

doi:10.1002/pros.20303

Cited by 47 publications

(37 citation statements)

References 33 publications

(49 reference statements)

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“…Androgen deprivation treatment causes an increase in Bcl-2 expression (1 -4), and the overexpression of Bcl-2 is associated with the development of androgen independence (1,5,6). Our in vitro studies also show Bcl-2 suppression by antisense Bcl-2 sensitizes prostate cancer cells to radiation (7).…”

supporting

confidence: 56%

Bcl-2 and Bax Expression Predict Prostate Cancer Outcome in Men Treated with Androgen Deprivation and Radiotherapy on Radiation Therapy Oncology Group Protocol 92-02

Khor

Moughan

Al‐Saleem

et al. 2007

Clinical Cancer Research

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Purpose: Bcl-2 is antiapoptotic, and its overexpression has been associated with resistance to androgen deprivation and poor outcome in some patients treated with radiotherapy. Bax is proapoptotic, regulating Bcl-2 through heterodimer formation. In a prior study, Bcl-2 and Bax were not related to outcome in locally advanced patients treated with radiotherapy or short-term androgen deprivation + radiotherapy (STAD+RT) on another RadiationTherapy Oncology Group trial (86-10). A follow-up investigation was carried out here in more contemporary high-risk men treated on Radiation Therapy Oncology Group 92-02 with STAD+RT or long-term AD+RT (LTAD+RT). Experimental Design: Adequate tissue was available to be analyzed immunohistochemically in 502 patients for Bcl-2 and 343 patients for Bax. Univariate and multivariate analyses by Cox proportional hazards models were applied to end points of failure. Results: Bcl-2 was positive in 45.6% cases, and Bax expression altered in 53.9% cases. Abnormal Bcl-2 was not related to any of the failure end points tested. Altered Bax expression was significantly associated with any failure (P = 0.023) and marginally with biochemical failure (P = 0.085). The combination of negative Bcl-2/normal Bax expression seemed more robust, being significantly related to reduced biochemical failure (P = 0.036) and any failure (P = 0.046). The predictive value of negative Bcl-2/normal Bax was most pronounced in those who received STAD+RT, as opposed to LTAD+RT. Conclusions: Normal Bax expression was associated with significantly more favorable outcome. The combination of negative Bcl-2 and normal Bax was more consistently significant, particularly when STAD+RT was the treatment administered. These data suggest that LTAD+RT should be used when either Bcl-2 or Bax is abnormally expressed.

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supporting

confidence: 56%

Bcl-2 and Bax Expression Predict Prostate Cancer Outcome in Men Treated with Androgen Deprivation and Radiotherapy on Radiation Therapy Oncology Group Protocol 92-02

Khor

Moughan

Al‐Saleem

et al. 2007

Clinical Cancer Research

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“…BPH-1 and PC3 cells were grown as described (67,68). Monocytes were obtained from the University of California, Los Angeles (UCLA) Virology Core in Iscove's modified Dulbecco's medium (Invitrogen) + 5% (vol/vol) human antibody serum + 15% (vol/vol) FBS and used the same day for experiments.…”

Section: Methodsmentioning

confidence: 99%

Trichomonas vaginalis homolog of macrophage migration inhibitory factor induces prostate cell growth, invasiveness, and inflammatory responses

Twu¹,

Dessì

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

149

138

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Significance Prostate cancer is the most common nonskin cancer in America and the fifth most common cancer worldwide. Inflammation is implicated in the initiation and progression of prostate cancer; however, sources of inflammation remain unidentified. Trichomonas vaginalis is a prevalent parasite that infects prostate epithelium and is associated with an increase in aggressive prostate cancer. Here, we demonstrate that a secreted T. vaginalis protein homologous to human macrophage migration inhibitory factor elicits antibodies in infected individuals, increases prostate cell proliferation and invasiveness, and induces cellular pathways linked to inflammation. This study demonstrates that a specific parasite-derived protein can mimic its human homolog to increase inflammation and cell proliferation, which, in turn, may result in the promotion and progression of prostate cancer.

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“…55 This observation is of particular importance taking into account the promising clinical studies on oblimersen sodium (antisense bcl-2) and the strong experimental evidence of its potent radiosenistizing properties in prostate cancer. 58,59 Human glioblastoma multiforme cells. Recently, it was shown that autophagy is responsible for the death of glioma cells in response to various anticancer agents, including temozolomide, rapamycin, tamoxifen and arsenic trioxide.…”

Section: Autophagy and Cancer Cellsmentioning

confidence: 99%

Radiation-induced autophagy in normal and cancer cells: Towards novel cytoprotection and radio-sensitization policies?

Zois¹,

Koukourakis²

2009

Autophagy

123

101

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Autophagy or Type II programmed cell death (PCD) is a major intracellular pathway for the degradation and recycling of proteins, ribosomes and entire organelles. The role of this pathway in the antitumor effect of radiotherapy and in radiation toxicity is obscure. A complicated machinery of genes and proteins is involved in the regulation of autophagy as a response to a variety of stress factors including hypoxia, nutrient deprivation, cytotoxic agents and radiotherapy. Continuously accumulating data suggest that autophagic response of cancer cells to radiotherapy is a major pathway which, in contrast to apoptosis that leads to death, may lead to either death or cellular survival. A variety of agents have been recognized that induce or block autophagy, directly interfering with the cytotoxic effect of radiotherapy. Simultaneous targeting of autophagy and apoptosis during radiotherapy seems to further augment the antitumor effect. Radiobiology research should focus on the differential effect of fractionation on the induction of autophagy in different tumors and on the manipulation of this with autophagy triggering agents. Whether manipulation of this pathway in normal tissues may be used to confer cytoprotection also deserves thorough investigation. Moreover, the role of pretreatment autophagic indices in tumor cells in predicting radiotherapy and chemotherapy outcome should be examined in translational studies.

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Antisense Bcl-2 sensitizes prostate cancer cells to radiation

Cited by 47 publications

References 33 publications

Bcl-2 and Bax Expression Predict Prostate Cancer Outcome in Men Treated with Androgen Deprivation and Radiotherapy on Radiation Therapy Oncology Group Protocol 92-02

Bcl-2 and Bax Expression Predict Prostate Cancer Outcome in Men Treated with Androgen Deprivation and Radiotherapy on Radiation Therapy Oncology Group Protocol 92-02

Trichomonas vaginalis homolog of macrophage migration inhibitory factor induces prostate cell growth, invasiveness, and inflammatory responses

Radiation-induced autophagy in normal and cancer cells: Towards novel cytoprotection and radio-sensitization policies?

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