Induction of apoptosis by furanodiene in HL60 leukemia cells through activation of TNFR1 signaling pathway

Ma, Enlong; Wang, Xiaolong; Li, Yanchun; Sun, Xiaofeng; Tai, Wenjiao; Li, T e; Guo, Tao

doi:10.1016/j.canlet.2008.06.008

Cited by 53 publications

(40 citation statements)

References 25 publications

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“…A previous study reported that furanodiene showed no effect on Bcl-2, Bax and Bcl-xL protein expressions in HL-60 leukemia cells [16]. In the present study, furanodiene treatment downregulated Bcl-xL and upregulated Bad.…”

Section: Discussionsupporting

confidence: 58%

Furanodiene, a Natural Product, Inhibits Breast Cancer Growth Bothin vitroandin vivo

Zhong¹,

Dang²,

Yuan³

et al. 2012

Cell Physiol Biochem

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Purpose: Previous studies have reported that the Curcuma wenyujin Y.H. Chen et C. Ling extract, which has a high furanodiene content, showed anti-cancer effects in breast cancer cells in vitro. The present study was designed to evaluate the in vitro and in vivo anti-cancer activity of furanodiene. Methods: The in vitro effects of furanodiene were examined on two human breast cancer cell lines, MCF-7 and MDA-MB-231 cells. Assays of proliferation, LDH release, mitochondrial membrane potential (△Ψm), cell cycle distribution, apoptosis and relevant signaling pathways were performed. The in vivo effect was determined with MCF7 tumor xenograft model in nude mice. Results: Furanodiene significantly inhibited the proliferation and increased the LDH release in both cell lines in a dose-dependent manner. △Ψm depolarization, chromatin condensation, and DNA fragmentation were also observed after furanodiene treatment. Furanodiene dose-dependently induced cell cycle arrest at the G0/G1 phase. The protein expressions of p-cyclin D1, total cyclin D1, p-CDK2, total CDK2, p-Rb, total Rb, Bcl-xL, and Akt were significantly inhibited by furanodiene, whereas the protein expressions of Bad and Bax, and the proteolytic cleavage of caspase-9, caspase-7, and poly-ADP-ribose polymerase (PARP) were dramatically increased. Furthermore, the z-VAD-fmk markedly reversed the furanodiene-induced cell cytotoxicity, the proteolytic cleavage of caspase-9, and DNA fragmentation but did not affect the proteolytic cleavage of PARP, whereas the Akt inhibitor VIII increased the furanodiene-induced cytotoxicity and PARP cleavage. In addition, furanodiene dose-dependently suppressed the tumor growth in vivo, achieving 32% and 54% inhibition rates after intraperitoneal injection of 15 mg/kg and 30 mg/kg, respectively. Conclusions: Taken together, we concluded that furanodiene suppresses breast cancer cell growth both in vitro and in vivo and could be a new lead compound for breast cancer chemotherapy.

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Section: Discussionsupporting

confidence: 58%

Furanodiene, a Natural Product, Inhibits Breast Cancer Growth Bothin vitroandin vivo

Zhong¹,

Dang²,

Yuan³

et al. 2012

Cell Physiol Biochem

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“…27,28 Numerous studies have shown that curdione, curzerene, b-elemene, and furanodiene exhibit significant anticancer effects. 9,[29][30][31][32][33][34] Most notably, furanodiene was found to inhibit both in vitro and in vivo xenograft growth of cervical cancer cells. 29 However, it remains unclear how CWE modulates intracellular signal(s) to lead to the inhibition of cell proliferation and the subsequent induction of the apoptotic pathway, further studies into the anticancer mechanisms of CWE are necessary for better clinical application.…”

Section: Discussionmentioning

confidence: 99%

Curcuma wenyujin Extract Induces Apoptosis and Inhibits Proliferation of Human Cervical Cancer Cells In Vitro and In Vivo

Lim

et al. 2010

Integr Cancer Ther

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An essential oil extract, derived from the rhizome of Curcuma wenyujin (CWE), possesses antioxidative, antimicrobial, and anti-inflammatory properties. However, it remains unknown how exactly CWE inhibits tumor growth. In this study, using human cervical cancer HeLa cells, the authors postulated that CWE has the ability to inhibit tumor growth. The study shows that CWE dose-dependently suppressed colony formation and inhibited the proliferation of HeLa cells through blockade of cell cycle progression at G1 phase and apoptosis. CWE-induced G1 arrest was associated with retinoblastoma protein dephosphorylation and reduced amounts of cyclins D1 and D3, and cyclin-dependent kinase 4 and 6 proteins. CWE treatment resulted in apoptosis in HeLa cells as evidenced by morphological changes, caspase activation and PARP cleavage, which can be reversed by a pan-caspase inhibitor. It was observed that CWE treatment activated the mitochondrial apoptotic pathway indicated by a decrease in Mcl-1 and Bcl-xL levels, resulting in mitochondrial membrane potential loss and caspases 9 activation. CWE-treated cells displayed reduced PTEN, AKT, and STAT3 phosphorylation and downregulation of NFkB signaling, providing a mechanism for the G1 arrest and apoptosis observed. Furthermore, CWE inhibited tumor growth of HeLa in a xenograft mouse tumor model, suggesting that CWE inhibited tumorigenesis by inhibiting cell proliferation and inducing apoptosis. These findings are the first to reveal the molecular basis for the anticervical cancer action of CWE. The results suggest that CWE could be developed as a drug for the management of cervical cancer.

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“…It has been demonstrated that TNF alpha can induce apoptosis thru caspase 8 activation which leads to Bid activation and subsequent cytochrome c release from the mitochondria followed by caspase 9 activation then caspase 3 activation and parp cleavage [66,72] but also thru caspase 8 activation and direct caspase 3 activation with Parp cleavage [73][74] yet there is also evidence of TNF alpha induced apoptosis independent of caspase 3 activation thru Bak [75].…”

Section: Discussionmentioning

confidence: 99%

NSP 5a3a: A Potential Novel Cancer Target in Head and Neck Carcinoma

D’Agostino

Giordano

2010

Oncotarget

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AbstrAct:NSP 5a3a along with three other distinct though similar splice variants were initially identified corresponding to locus HCMOGT-1 on chromosome 17p11. Subsequent investigation, elucidated NSP 5a3a's potential involvement in cellular processes such as ribosome biogenesis and rRNA processing by validating NSP 5a3a's novel interaction with B23 and ribonuclear protein hnRNP-L possibly implicating NSP 5a3a's involvement in cellular activities such as RNA metabolism and processing [4]. In this preliminary investigation, we wanted to observe the effect that over-expressing NSP 5a3a may have on cell cycle and its potential application in cancer treatment in aggressive cancers such as head and neck carcinomas. Over-expressed NSP 5a3a in HN30 cells induced a significant degree of apoptosis, an average of a 10.85 fold increase compared to controls 3 days post-transfection. This effect was more significant then the apoptosis observed between Fadu cells over-expressing NSP 5a3a and its controls. Though, the apoptosis induced in the WI38 control cell line showed an average of a 13.2 fold increase between treated and controls comparable to the HN30 cell line 3 days post-transfection. Molecular analysis indentified a novel p73 dependent mechanism independent of p53 and caspase 3 activity through which NSP 5a3a is inducing apoptosis. We propose NSP 5a3a as a potential therapeutic target for site directed cancer treatment in perhaps certain head and neck carcinomas by induction of apoptosis.

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Induction of apoptosis by furanodiene in HL60 leukemia cells through activation of TNFR1 signaling pathway

Cited by 53 publications

References 25 publications

Furanodiene, a Natural Product, Inhibits Breast Cancer Growth Bothin vitroandin vivo

Furanodiene, a Natural Product, Inhibits Breast Cancer Growth Bothin vitroandin vivo

Curcuma wenyujin Extract Induces Apoptosis and Inhibits Proliferation of Human Cervical Cancer Cells In Vitro and In Vivo

NSP 5a3a: A Potential Novel Cancer Target in Head and Neck Carcinoma

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