Down-Regulation of Survivin by Nemadipine-A Sensitizes Cancer Cells to TRAIL-Induced Apoptosis

Kim, Joo-Oh; Shin, Ji Hyun; Kim, Eun Sung; Jo, Yoon Kyung; Kim, Jae-Sung; Park, Soo‐Young; Jin, Dayong; Hwang, Jung Jin; Lee, Seung Jin; Jeong, Seong‐Yun; Lee, Chaeyoung; Kim, InKi; Cho, Dong‐Hyung

doi:10.4062/biomolther.2012.088

Cited by 13 publications

(8 citation statements)

References 37 publications

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“…Consistently, it was also found that nemadipine-A potentiates TRAILinduced apoptosis by reducing survivin expression in lung cancer cells. Although, the precise mechanisms are not clear, it was recently reported that survivin expression could be up-regulated by cellular calcium level [53] . Moreover, derivatives of the natural alkaloid camptothecin have the ability to provoke proteasomal degradation of survivin in cells with defective p53 function and elevated XAFI (another tumor suppressor) expression [54] .…”

Section: Chemotherapy and Survivinmentioning

confidence: 99%

Association of survivin splice variants with prognosis and treatment of breast cancer

Pavlidou

Kroupis

Dimas

2014

WJCO

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The purpose of this study was the overview of current knowledge regarding the use of survivin and its isoforms in prognosis and treatment of breast cancer. An advanced search of Medline was performed using the following search strategy: "(survivin isoforms) OR (survivin transcript variants) AND (breast cancer) AND (neoplasm OR tumor OR cancer OR carcinoma)". Relevant studies were retrieved and processed thoroughly in order to analyze the related data. Besides wild-type survivin full-length transcript, another six splice variants have been identified. Overexpression of survivin and its isoforms leads to shorter overall and disease-free survival; the transcript variants are correlated with apoptosis and could assist prognosis prediction. It has been proved through numerous studies that inhibiting survivin isoforms might become a promising target of drug therapy of carcinomas. Use of small molecule YM155 could offer new therapy for triple negative breast cancer patients, while, chemotherapy with 5-fluorouracil + epirubicin + cyclophosphamide and Tax-Epi could be guided by survivin splice variants measurements. Survivin transcript variants could become prognostic biomarkers and could provide information about clinical management of patients suffering from breast cancer.© 2014 Baishideng Publishing Group Inc. All rights reserved.Key words: Survivin gene; Isoforms; Therapy; Prognosis; Breast cancer Core tip: Besides wild type survivin full length transcript, another six splice variants have been identified. Overexpression of survivin and its isoforms leads to shorter overall and disease-free survival; the transcript variants are positively correlated with apoptosis and could assist prognosis prediction. It has been proved through numerous studies that inhibiting survivin isoforms might become a promising target of drug therapy of carcinomas. Use of small molecule YM155 could offer new therapy for triple negative breast cancer patients while, chemotherapy with 5-fluorouracil + epirubicin + cyclophosphamide and Tax-Epi could be guided by survivin splice variants measurements. Survivin transcript variants could become prognostic biomarkers and could provide information about clinical management of patients suffering from breast cancer.Pavlidou A, Kroupis C, Dimas K. Association of survivin splice variants with prognosis and treatment of breast cancer. World J

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Section: Chemotherapy and Survivinmentioning

confidence: 99%

Association of survivin splice variants with prognosis and treatment of breast cancer

Pavlidou

Kroupis

Dimas

2014

WJCO

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“…Thus, survivin protein represents an attractive target in cancer therapy. Indeed, downregulation of survivin by chemotherapeutic agents or RNA interference resulted in caspase activation and increased apoptotic cell death in cancer cells (27, 28). In addition to its role in promoting cell survival through inhibition of apoptosis, it has been postulated that survivin also plays a role as mitotic inducer.…”

Section: Discussionmentioning

confidence: 99%

Origanum majorana Ethanolic Extract Promotes Colorectal Cancer Cell Death by Triggering Abortive Autophagy and Activation of the Extrinsic Apoptotic Pathway

et al. 2019

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Colorectal cancer is considered as the third leading cause of cancer death. In the present study, we investigated the potential anticancer effect and the molecular mechanism of Origanum majorana ethanolic extract (OME) against human colorectal cancer cells. We showed that OME exhibited strong anti-proliferative activity in a concentration- and time-dependent manner against two human colorectal cancer cell lines (HT-29 and Caco-2). OME inhibited cell viability, colony growth and induced mitotic arrest of HT-29 cells. Also, OME induced DNA damage, triggered abortive autophagy and activated a caspase 3 and 7-dependent extrinsic apoptotic pathway, most likely through activation of the TNFα pathway. Time-course analysis revealed that DNA damage occurred concomitantly with abortive autophagy after 4 h post-OME treatment while apoptosis was activated only 24 h later. Blockade of autophagy initiation, by 3-methyladenine, partially rescued OME-induced cell death. Cell viability arose from 37% in control group to 67% in group pre-treated with 3-MA before addition of OME. Inhibition of apoptosis, however, had a minimal effect on cell viability; it rose from 37% in control group to 43% in group pre-treated with Z-VAD-FMK. We also found that OME downregulated survivin in HT-29 cells. Our findings provide a strong evidence that O. majorana extract possesses strong anti-colon cancer potential, at least, through induction of autophagy and apoptosis. These finding provide the basis for therapeutic potential of O. majorana in the treatment of colon cancer.

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“…Survivin is expressed in various types of cancer, including YM155 sensitizes HeLa cells to TRAIL-mediated apoptosis via cFLIP and survivin downregulation breast cancer (16), cervical cancer (17), non-small cell lung cancer (18) and osteosarcoma (19). Its upregulation is associated with survival and resistance to TRAIL-based therapy (20,21).…”

Section: Introductionmentioning

confidence: 99%

YM155 sensitizes HeLa cells to TRAIL‑mediated apoptosis via cFLIP and survivin downregulation

Chandrasekaran

Poondla

et al. 2020

Oncol Lett

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Tumor necrosis factor-related apoptosis inducing ligand (TRAIL)-mediated apoptosis is a safe method for the treatment of various types of cancer. However, TRAIL therapy is less effective in certain types of cancer, including cervical cancer. To address this problem, a combinatorial approach was employed to sensitize cervical cancer at low dosages. YM155, a survivin inhibitor, was used at low dosages along with TRAIL to induce apoptosis in HeLa cells. The effects of the individual treatment with TRAIL and YM155 on apoptosis were assessed by propidium iodide assay. In addition, to validate the DNA damage exhibited by the combination treatment, the phosphorylation status of γH2A histone family member X was investigated by immunofluorescence and western blot analysis. TRAIL or YM155 alone had no significant effect on DNA damage and apoptosis. However, the TRAIL/YM155 combination triggered a synergistic pro-apoptotic stimulus in HeLa cells. The mRNA and protein levels of CASP8- and FADD-like apoptosis regulator (cFLIP), death receptor 5 (DR5) and survivin were monitored using RT-PCR and western blot analysis, respectively. This combinatorial approach downregulated both mRNA and protein expression levels of cFLIP and survivin. Further experimental results suggested that the combination treatment significantly reduced cell viability, invasion and migration of HeLa cells. Overall, the present findings indicated that the low dosage of YM155 sensitized HeLa cells to TRAIL-induced apoptosis via a mechanism involving downregulation of cFLIP and survivin. The results indicated the importance of combination drug treatment and reveal an effective therapeutic alternative for TRAIL therapy in human cervical cancer.

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Down-Regulation of Survivin by Nemadipine-A Sensitizes Cancer Cells to TRAIL-Induced Apoptosis

Cited by 13 publications

References 37 publications

Association of survivin splice variants with prognosis and treatment of breast cancer

Association of survivin splice variants with prognosis and treatment of breast cancer

Origanum majorana Ethanolic Extract Promotes Colorectal Cancer Cell Death by Triggering Abortive Autophagy and Activation of the Extrinsic Apoptotic Pathway

YM155 sensitizes HeLa cells to TRAIL‑mediated apoptosis via cFLIP and survivin downregulation

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