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We began analyzing https://link.springer.com/article/10.1007/s00280-008-0697-7, but it redirected us to https://link.springer.com/article/10.1007/s00280-008-0697-7. The analysis below is for the second page.

Title[redir]:
Inducing apoptosis and enhancing chemosensitivity to Gemcitabine via RNA interference targeting Mcl-1 gene in pancreatic carcinoma cell | Cancer Chemotherapy and Pharmacology
Description:
Purpose Resistance to chemotherapy is a major cause of treatment failure and poor prognosis in pancreatic carcinoma. Myeloid cell leukemia-1 (Mcl-1) is highly up-regulated in pancreatic carcinoma and is associated with the anti-apoptosis and the resistance to chemotherapy drugs. Suppression of Mcl-1 would be an approach to induce apoptosis and enhance the chemosensitivity. Methods In this study, three pancreatic cancer cell lines (PANC-1, BxPC-3 and SW1900) stably expressing shRNAs targeting Mcl-1 gene were established and gene expression inhibition was assessed by Real-Time QPCR and Western blotting. The effects of Mcl-1 downregulation mediated by RNAi were explored in vitro and in vivo. Results We showed that the specific downregulation of Mcl-1 strikingly inhibited cell growth, colony formation, cell cycle arrest and induced apoptosis in pancreatic cancer cells in vitro, and markedly decreased the tumorigenicity in a mouse xenograft model. Moreover, knockdown of Mcl-1 significantly increased the chemosensitivity to Gemcitabine in pancreatic carcinoma cells. Conclusions Our data suggests that the specific downregulation of Mcl-1 by RNAi is a promising approach to induce apoptosis and enhance the chemosensitivity for pancreatic carcinoma gene therapy.

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Keywords {🔍}

article, google, scholar, cas, pubmed, cancer, mcl, pancreatic, cell, apoptosis, gene, cells, carcinoma, human, gemcitabine, rna, bcl, chemotherapy, interference, expression, therapy, access, content, chemosensitivity, zhang, protein, res, privacy, cookies, analysis, research, targeting, lin, resistance, yang, data, publish, search, wang, huizhong, treatment, downregulation, open, sirnas, nat, oncol, biol, craig, programmed, death,

Topics {✒️}

qing zhang & hui-zhong zhang month download article/chapter u6 promoter-driven sirnas mitogen-activated protein kinases hui-zhong zhang j-physiol-renal-physiol 292 extracellular-signalregulated protein kinase gene expression inhibition small interfering rna gene therapy today rna interference article cancer chemotherapy pancreatic carcinoma cell full article pdf programmed cell death multifocal hepatocellular carcinoma simultaneously targeting mcl-1 related subjects target sirnas reveals pancreatic carcinoma cells human mcl-1 gene human pancreatic carcinoma privacy choices/manage cookies pancreatic cancer cells kozopas km antisense strategy shows myeloid cell leukemia-1 human pancreatic tumors pancreatic cancer biology cell cycle arrest article wei human myeloma cells epithelial ovarian cancer relevant therapeutic target gene expressed mouse xenograft model cisplatin-induced apoptosis european economic area real-time qpcr m6a/m5c/m1a mitochondria-mediated apoptosis il-6 autocrine loop diverse apoptotic stimuli von hott dd natural science foundation cultured mammalian cells bmc cancer 6 mcl-1 significantly increased conditions privacy policy gemcitabine-induced apoptosis

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      headline:Inducing apoptosis and enhancing chemosensitivity to Gemcitabine via RNA interference targeting Mcl-1 gene in pancreatic carcinoma cell
      description:Resistance to chemotherapy is a major cause of treatment failure and poor prognosis in pancreatic carcinoma. Myeloid cell leukemia-1 (Mcl-1) is highly up-regulated in pancreatic carcinoma and is associated with the anti-apoptosis and the resistance to chemotherapy drugs. Suppression of Mcl-1 would be an approach to induce apoptosis and enhance the chemosensitivity. In this study, three pancreatic cancer cell lines (PANC-1, BxPC-3 and SW1900) stably expressing shRNAs targeting Mcl-1 gene were established and gene expression inhibition was assessed by Real-Time QPCR and Western blotting. The effects of Mcl-1 downregulation mediated by RNAi were explored in vitro and in vivo. We showed that the specific downregulation of Mcl-1 strikingly inhibited cell growth, colony formation, cell cycle arrest and induced apoptosis in pancreatic cancer cells in vitro, and markedly decreased the tumorigenicity in a mouse xenograft model. Moreover, knockdown of Mcl-1 significantly increased the chemosensitivity to Gemcitabine in pancreatic carcinoma cells. Our data suggests that the specific downregulation of Mcl-1 by RNAi is a promising approach to induce apoptosis and enhance the chemosensitivity for pancreatic carcinoma gene therapy.
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External Links {🔗}(214)

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Libraries {📚}

  • Clipboard.js
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Mail Servers:

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