The role of survivin and Bcl-2 in zinc-induced apoptosis in prostate cancer cells

Ku, Ja Hyeon; Seo, Soo Yeon; Kwak, Cheol; Kim, Hyeon Hoe

doi:10.1016/j.urolonc.2010.06.001

Cited by 35 publications

(31 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…4). These data indicated that the effect of Livin differs from that of other IAP members on zinc-induced apoptosis in prostate cancer cells [8,9].…”

Section: Expression Of Livin In Prostate Cancer Cells Treated With Zimentioning

confidence: 99%

See 1 more Smart Citation

Zinc sensitizes prostate cancer cells to sorafenib and regulates the expression of Livin

Chen¹,

Che²,

Wang³

et al. 2013

ABBS

View full text Add to dashboard Cite

In prostate carcinogenesis, normal zinc-accumulating epithelial cells are transformed into malignant cells that do not accumulate zinc. Increased levels of zinc have been shown to induce apoptosis through a caspase-dependent mechanism with down-regulated anti-apoptotic proteins in prostate cancer cells. Our previous study showed that, as a member of the inhibitor of apoptosis proteins (IAPs) family, Livin could play an important role in the initiation of human prostate cancer and promote cell proliferation by altering the G1 -S cell cycle transition. In the present study, we measured the apoptosis sensitivity of prostate cancer cells to zinc and sorafenib and found that zinc sensitized prostate cancer cells to sorafenib-induced apoptosis. Surprisingly, we also found that, unlike its counterparts Survivin and cIAP2, Livin was not decreased all the time; instead, it was compensatively increased in zinc-mediated apoptosis at 48 h in prostate cancer cells. Our results offer potential treatment combinations that may augment the effect of sorafenib, and also reveal, for the first time, that increased Livin expression may play a role in the early cell death response of prostate cancer cells to zinc.

show abstract

“…4). These data indicated that the effect of Livin differs from that of other IAP members on zinc-induced apoptosis in prostate cancer cells [8,9].…”

Section: Expression Of Livin In Prostate Cancer Cells Treated With Zimentioning

confidence: 99%

“…It has been reported that zinc may induce apoptosis through a caspase-dependent mechanism with down-regulated IAPs (such as Survivin or cIAP2) in androgen-independent prostate cancer cells [8,9]. However, as the family member of IAPs, Livin has not been reported in this process.…”

Section: Introductionmentioning

confidence: 99%

Zinc sensitizes prostate cancer cells to sorafenib and regulates the expression of Livin

Chen¹,

Che²,

Wang³

et al. 2013

ABBS

View full text Add to dashboard Cite

show abstract

“…The cell suspension (500 µl) was then incubated with 5 µl of Αnnexin V-FITC and 10 µl of propidium iodide (PI) for 10 min at room temperature in the dark. The population of Αnnexin V-positive cells was evaluated by flow cytometry (BD FACScan, Becton-Dickinson Immunocytometry Systems, San Jose, CA, USA) (31,32). to each tube.…”

Section: Methodsmentioning

confidence: 99%

The dietary flavonol fisetin enhances the apoptosis-inducing potential of TRAIL in prostate cancer cells

Szliszka

Helewski²,

Mizgała³

et al. 2011

Int J Oncol

View full text Add to dashboard Cite

Abstract. Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) is an endogenous agent that induces apoptosis selectively in cancer cells. Soluble or expressed in immune cells, TRAIL plays an important role in the defense against tumour cells. The resistance of cancer cells to TRAIL immune surveillance is implicated in tumour development. Naturally occurring flavonoids can sensitize TRAIL-resistant cancer cells and augment their apoptotic activity. Fisetin, a dietary flavonol has cancer preventive properties. This study was designed to investigate the effect of fisetin on the TRAILinduced apoptosis potential in prostate cancer cells. Prostate cancer cell lines represent an ideal model for research in chemoprevention. Cytotoxicity was measured by MTT and LDH assays. Apoptosis was detected using Αnnexin V-FITC by flow cytometry and fluorescence microscopy. Mitochondrial membrane potential (ΔΨm) was evaluated using DePsipher staining by fluorescence microscopy. Death receptor (TRAIL-R1 and TRAIL-R2) expression was analysed by flow cytometry. Inhibition of NF-κB (p65) activation was confirmed with an ELISA-based TransAM NF-κB kit. Caspase-8 and caspase-3 activities were determined by colorimetric protease assays. Our study demonstrates that fisetin sensitizes the TRAIL-resistant androgen-dependent LNCaP and the androgen-independent DU145 and PC3 prostate cancer cells to TRAIL-induced death. Fisetin augmented TRAIL-mediated cytotoxicity and apoptosis in prostate cancer LNCaP cells by engaging the extrinsic (receptor-mediated) and intrinsic (mitochondrial) apoptotic pathways. Fisetin increased the expression of TRAIL-R1 and decreased the activity of NF-κB. Co-treatment of cancer cells with TRAIL and fisetin caused significant activation of caspase-8 and caspase-3 and disruption of ΔΨm. Our data indicate the usefulness of fisetin in prostate cancer chemoprevention through enhancement of TRAIL-mediated apoptosis.

show abstract

“…In most androgen-independent prostate cancers, Bcl-2 is overexpressed [2]. In preclinical prostate cancer models, inhibition of Bcl-2 expression probably increases apoptosis in the prostate cancer cells [31]. The Bax protein is pro-apoptotic; Bcl-2 has been shown to form a heterodimer complex with the pro-apoptotic member Bax, thereby neutralizing its pro-apoptotic effects.…”

Section: Figurementioning

confidence: 99%

Treatment of PC-3 cells with ultrasound combined with microbubbles induces distinct alterations in the expression of Bcl-2 and Bax

et al. 2013

View full text Add to dashboard Cite

The role of survivin and Bcl-2 in zinc-induced apoptosis in prostate cancer cells

Cited by 35 publications

References 18 publications

Zinc sensitizes prostate cancer cells to sorafenib and regulates the expression of Livin

Zinc sensitizes prostate cancer cells to sorafenib and regulates the expression of Livin

The dietary flavonol fisetin enhances the apoptosis-inducing potential of TRAIL in prostate cancer cells

Treatment of PC-3 cells with ultrasound combined with microbubbles induces distinct alterations in the expression of Bcl-2 and Bax

Contact Info

Product

Resources

About