Induction of Survivin Expression by Taxol (Paclitaxel) Is an Early Event, Which Is Independent of Taxol-mediated G2/M Arrest

Ling, Xiang; Bernacki, Ralph J.; Brattain, Michael G.; Li, Fengzhi

doi:10.1074/jbc.m310947200

Cited by 154 publications

(145 citation statements)

References 38 publications

(38 reference statements)

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“…Similar findings were described upon inhibition of Taxol-activated MEK/Erk signaling using MEK inhibitors that reduced Taxolmediated survivin induction synergistically. 22 The reason for this phenomenon is not clear, but it seems as if these cells, due to loss of protective kinase activity, downregulate survivin as part of a stress response preceding apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…17,18 It has been demonstrated that downregulation of survivin expression using conventional antisense or siRNA facilitated cancer cell apoptosis and sensitized cells to anti-cancer agents. [19][20][21][22] Despite increasing evidence in support of survivin as a promising target for molecular intervention, the mechanism of survivin overexpression in SCLC and its implication in drug resistance remain to be investigated. Evidence for the upregulation of survivin via the PI3K/Akt pathway was first demonstrated in response to pro-survival factors in myeloid leukemia cells, 23 endothelial cells 24 and prostate cancer cells.…”

mentioning

confidence: 99%

“…25 Recent data suggest that Akt is also activated in response to stress induced by UV irradiation and chemotherapy. 22,26,27 Whether activation of Akt constitutes a physiological stress response that enables cancer cells to evade apoptosis by upregulation of survivin remains to be demonstrated.…”

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confidence: 99%

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Cisplatin activates Akt in small cell lung cancer cells and attenuates apoptosis by survivin upregulation

Belyanskaya¹,

Hopkins-Donaldson²,

Kurtz³

et al. 2005

Intl Journal of Cancer

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The inhibitor of apoptosis protein (IAP) survivin is overexpressed in many tumors but is absent in most normal adult tissues. We report high levels of survivin expression in small cell lung cancer (SCLC), and describe the role of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway in survivin upregulation. Moreover, the cytoprotective function of survivin in response to the anti-cancer agent cisplatin (CDDP) was investigated. Negative modulation of PI3K/ Akt using pharmacological inhibitors or dominant negative Akt (DN-Akt) decreased Akt kinase activity and resulted in decreased survivin expression and phosphorylation on Thr34, whereas transfection of constitutively active Akt (CA-Akt) increased survivin expression and phosphorylation. Interestingly, we found that treatment of SCLC cells with CDDP further increased survivin expression in a cell cycle independent manner by activation of Akt. CA-Akt or lentiviral survivin also inhibited apoptosis induced by CDDP, whereas DN-Akt or survivin-specific RNA interference sensitized cells to CDDP. We identified survivin as an anti-apoptotic protein in SCLC cells that is regulated by Akt, and demonstrate that treatment with the DNA damaging agent CDDP activates the PI3K/Akt/survivin pathway that in part protects cells from drug-induced apoptosis. ' 2005 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Cisplatin activates Akt in small cell lung cancer cells and attenuates apoptosis by survivin upregulation

Belyanskaya¹,

Hopkins-Donaldson²,

Kurtz³

et al. 2005

Intl Journal of Cancer

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“…Survivin is regulated in a cell cycle-dependent manner; its expression is markedly increased in the G2/M phase and is associated with mitotic spindle microtubules, centromeres, and intracellular mid-bodies (Li et al 1998). Survivin inhibits cell death induced by a variety of apoptotic stimuli, including Fas/Fas ligand (FasL), caspases, and anticancer drugs (Ling et al 2004). Overexpression of survivin confers cytoprotection against a variety of apoptotic stimuli, whereas a decrease in survivin expression or function causes spontaneous apoptosis of cancer cells or sensitizes the cells to apoptotic stimuli (Altieri 2003a,b).…”

Section: Introductionmentioning

confidence: 99%

FSH inhibits ovarian cancer cell apoptosis by up-regulating survivin and down-regulating PDCD6 and DR5

Huang

Jin

Liu

et al. 2010

Endocrine Related Cancer

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Ovarian epithelial cancer is the leading cause of death among gynecological malignancies. FSH may increase the risk of ovarian malignancy and play an important role in ovarian carcinogenesis. Our previous studies showed that FSH increases the expression of VEGF through survivin. In this study, the function and mechanism of FSH in ovarian cancer were further explored. We found that FSH promoted proliferation and prevented apoptosis of ovarian cancer cells by activating survivin through the SAPK/JNK and PI3K/AKT pathways. FSH also down-regulated the expression of programmed cell death gene 6 (PDCD6) and death receptor 5 (DR5), two molecules required for induction of apoptosis. RNA interference was applied to knock down survivin and PDCD6 expression, and we found that the blockage of survivin reversed the effects of FSH on apoptosis and proliferation, whereas knock down of PDCD6 enhanced these effects. The expression of DR5, cyclin D1, and cyclin E correlated with survivin expression, but PDCD6 did not. Using immunohistochemical staining, we further showed that ovarian serous cystadenocarcinoma samples had higher expression of survivin than did benign ovarian cystadenoma and borderline cystadenoma samples (P!0.01). Furthermore, survivin expression in the ovarian serous cystadenocarcinoma specimens was correlated with disease stage (P!0.05). Our results suggest that FSH promotes ovarian cancer development by regulating the expression of survivin, PDCD6, and DR5. Greater understanding of the molecular mechanisms of FSH in ovarian epithelial carcinogenesis and development will ultimately help in the development of a novel targeted therapy for ovarian cancer.

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“…To characterize the induction of survivin by taxol, a hallmark in chemoresistant cancers, 26,27 in SKOV3.ip1 cells, we first determined the effects of taxol on survivin expression in vitro. Results of these studies indicated that taxol treatment of SKOV3.ip1 cells results in upregulation of survivin ( Figure 5).…”

Section: Growth Inhibitory Effect Of Antiangiogenic Gene Therapy Is Imentioning

confidence: 99%

Intraperitoneal gene therapy by rAAV provides long-term survival against epithelial ovarian cancer independently of survivin pathway

2006

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Epithelial ovarian carcinoma is the leading cause of death from gynecological malignancies. Owing to the lack of an effective screening method, insidious onset, and non-specific symptoms, a majority of women present with advanced stage disease. Despite improvements from cytoreductive surgery and chemotherapy, recurrent disease remains a formidable challenge. In the present study, we demonstrate for the first time that stable intra-abdominal genetic transfer of endostatin and angiostatin (E+A) by recombinant adeno-associated virus (rAAV) provides sustained antitumor effects on the growth and dissemination of epithelial ovarian cancer in a mouse model. Further, when combined with paclitaxel (taxol), the effect of this therapy was dramatically increased and resulted in long-term tumor-free survival overcoming prior limitations of chemotherapy and gene therapy. The combined effects of angiosuppressive therapy and chemotherapy were found to be independently of survivin pathway. Evidence for the superior effects of the combination therapy was indicated by significantly lower ascites volume with less hemorrhage and tumor conglomerates, lower ascites vascular endothelial growth factor, higher tumor cell apoptosis and decreased blood vasculature, and long-term disease-free survival. Histopathology of visceral organs and liver enzyme assays indicated no toxicity or pathology.

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Induction of Survivin Expression by Taxol (Paclitaxel) Is an Early Event, Which Is Independent of Taxol-mediated G2/M Arrest

Cited by 154 publications

References 38 publications

Cisplatin activates Akt in small cell lung cancer cells and attenuates apoptosis by survivin upregulation

Cisplatin activates Akt in small cell lung cancer cells and attenuates apoptosis by survivin upregulation

FSH inhibits ovarian cancer cell apoptosis by up-regulating survivin and down-regulating PDCD6 and DR5

Intraperitoneal gene therapy by rAAV provides long-term survival against epithelial ovarian cancer independently of survivin pathway

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