Autophagy protects LNCaP cells under androgen deprivation conditions

Li, Mengqiang; Jiang, Xuejun; Liu, Di; Na, Yan-qun; Gao, George F.; Xi, Zhijun

doi:10.4161/auto.5209

Cited by 90 publications

(88 citation statements)

References 33 publications

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“…52 Similarly, LNCaP cells can resort to the autophagic pathway to survive under androgen deprivation conditions, which can be a novel mechanism involved in the transition of prostate cancer cells from an androgen-dependent to an androgen-independent phenotype. 53 On the other hand, cysmethynil inhibited the mTOR signaling, preferentially enhanced the autophagic cell death (not apoptosis) in PC3 prostate cancer cells, and inhibited tumor growth in a xenograft mouse model of prostate cancer cells. 54 Ionizing radiation induces autophagic cell death in LNCaP prostate cancer cells.…”

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

124

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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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

124

101

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“…[6][7][8] We have previously reported that autophagy plays a protective role in the prostate cancer cell line, LNCaP, under androgen deprivation conditions. 9 Here, we propose that autophagy might also play an important role in the apoptosis procedure of benign epithelial cells under androgen inhibition conditions. The present study evaluated the autophagy status in PWR-1E cells, a cell line derived from benign prostate epithelial cells, under androgen inhibition conditions in vitro and in hyperplasia prostate tissues from patients treated by 5-ARI.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of androgen induces autophagy in benign prostate epithelial cells

Wang

et al. 2013

Int J of Urology

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Abbreviations & Acronyms 3-MA = 3-methyladenine 5-ARI = 5-α reductase inhibitor AD = androgen deprivation medium BPH = benign prostatic hyperplasia CM = complete medium DAPI = 4, 6-diamidino-2-phenylindole Objective: 5-α Reductase inhibitor can reduce the volume of benign prostatic hyperplasia by lowering benign prostatic hyperplasia level and consequently inducing epithelial cells apoptosis. The present study investigated whether autophagy and apoptosis of benign prostatic hyperplasia epithelial cells are influenced by low benign prostatic hyperplasia levels. Methods: PWR-1E prostate epithelial cells transfected with GFP-LC3 plasmid were subjected to androgen deprivation conditions. Then the autophagic puncta were evaluated by fluorescence microscopy, and the cellular apoptosis rate was detected by 4, 6-diamidino-2-phenylindole staining after blocking of autophagic process by 3-methyladenine. Furthermore, autophagy status was also determined in hyperplasia prostate tissues from 5-α reductase inhibitor-treated patients by immunohistochemistry. Results: In the androgen deprivation medium, autophagic punta increased markedly in PWR-1E cells, and blockage of autophagy by 3-methyladenine significantly promoted PWR-1E cells' apoptosis rate. In vivo, the expression of LC3 protein (an important autophagic marker) in hyperplasia prostate tissue significantly increased after 5-α reductase inhibitor treatment. Meanwhile, the prostate-specific antigen, as an inner control, decreased. Conclusion: 5-α Reductase inhibitor treatment increases autophagy and possibly decreases the apoptosis of prostate epithelial cells.

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“…Autophagy is a general term for the degradation of cytoplasmic components, such as the turnover of long-lived proteins and organelles in lysosomes (11). Although autophagy was initially identified as a process induced by amino acid starvation promoting cell adaptation (12), the role of autophagy in cancer is not clearly defined. Under stressful conditions, the contribution of autophagy as a survival mechanism in cancer has been well recognized.…”

Section: Introductionmentioning

confidence: 99%

Autophagy inhibition enhances etoposide-induced cell death in human hepatoma G2 cells

Yao

2011

Int J Mol Med

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Abstract. Induction of autophagy usually acts as a survival mechanism of cancer cells in response to chemotherapy. However, the function and molecular mechanism of autophagy in human hepatoma cells under drug treatment is still not clear. To address this issue, we established an experimental model in which HepG2 cells were treated with etoposide, a widely used anticancer agent. We demonstrate the etoposide-induced accumulation of GFP-LC3 dots by fluorescent microscopy, the up-regulation of Lc3-II protein expression by Western blotting and the increased number of autophagic vacuoles by electron microscopy, confirming the activation of autophagy by etoposide in HepG2 cells. Inhibition of autophagy by either 3-methyladenine (3MA) or beclin-1 small interfering RNA enhanced etoposide-induced cell death. Furthermore, activation of p53 and AMPK was detected in etoposide-treated cells and inhibition of AMPK triggered apoptosis through suppression of autophagy. On the other hand, inactivation of p53 promoted cell survival through augmentation of autophagy. Collectively, these findings indicate that etoposide-induced autophagy promotes hepatoma cell adaptation and survival, and that autophagy inhibition improves the chemotherapeutic effect of etoposide. Moreover, AMPK activation is clearly associated with etoposide-induced autophagy. We conclude that manipulation of AMPK may be a promising approach of adjuvant chemotherapy for hepatocellular carcinoma.

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Autophagy protects LNCaP cells under androgen deprivation conditions

Cited by 90 publications

References 33 publications

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

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

Inhibition of androgen induces autophagy in benign prostate epithelial cells

Autophagy inhibition enhances etoposide-induced cell death in human hepatoma G2 cells

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