Expression of survivin mRNA and livin mRNA in non-small-cell lung cancer

Tanabe, Hiromi; Yagihashi, Atsuhito; Tsuji, Naoki; Shijubo, Yasuharu; Abe, Shosaku; Watanabe, Naoki

doi:10.1016/j.lungcan.2004.05.002

Cited by 76 publications

(66 citation statements)

References 17 publications

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“…Livin has been identified as a member of the IAP family [2][3][4]. Its expression spectrum includes melanoma, leukemias, bladder cancer, breast cancer, cervical cancer, nasopharyngeal cancer and lung cancer [5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

“…Due to its distinctive enrichment in tumors but none or low expression in normal tissue, Livin has been proposed as a potential therapeutic target [19]. Several reports helped to expand its expression profile to variant tumors such as melanoma, leukemias, bladder, breast, cervical, nasopharyngeal and lung cancer [5][6][7][8]. However, there are only limited reports regarding its expression in CRC except some preliminary studies [17][18][19][20][21].…”

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confidence: 99%

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Upregulation of the antiapoptotic factor Livin contributes to cisplatin resistance in colon cancer cells

Ding

Liu

Olsson³

et al. 2012

Tumor Biol.

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The anti-apoptotic factor Livin has been considered critical for tumor progression and poor prognosis for variant types of tumors. But there are only limited reports regarding its expression and biological functions in colon cancer. Here we examined Livin expression in four colon cancer cell lines (HCT116, RKO, KM12C and SW620) in the presence or absence of cisplatin which was used as a model reagent. We found the different response to cisplatin was related to endogenous Livin expression level. From among a panel of apoptosis-related factors (p53, Bcl-2, Bcl-XL, BAX, and survivin), the expression of Livin was up-regulated after cisplatin treatment in a dose-dependent manner. Both the immunocytochemistry and nuclear cytoplasmic fractionation indicated Livin remained in the cytoplasm after treatment with cisplatin. In an attempt to explore the mechanism, we found the elevated expression of Livin was not due to the decreased degradation by proteosome but was enhanced at the mRNA level. Besides, cisplatin treatment activated the mammalian target of rapamycin (mTOR) pathway as shown by increased phosphorylation of Akt1, mTOR, S6K, and 4E-BP1, together with the elevated Livin. The PI3K inhibitor LY294002 inhibited both the phosphorylation of mTOR and up-regulation of Livin. The stable over-expression of Livin inhibited the activation of caspase-3 and led to resistance to cisplatin, while the knock-down of Livin by siRNA rendered colon cancer cells more sensitive to cisplatin. Our study along with others highlighted the potential of Livin for cancer therapy in colon cancer.

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%

Upregulation of the antiapoptotic factor Livin contributes to cisplatin resistance in colon cancer cells

Ding

Liu

Olsson³

et al. 2012

Tumor Biol.

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“…More recently, however, livin expression was also detected in various additional cancers, including leukaemias (Qiuping et al, 2004;Choi et al, 2007), bladder cancer (Gazzaniga et al, 2003), lung cancer (Tanabe et al, 2004;Hariu et al, 2005;Crnković-Mertens et al, 2006b), neuroblastoma (Kim et al, 2005), nasopharyngeal carcinoma (Xiang et al, 2006), astrocytoma (Liu et al, 2006), malignant pleural mesothelioma (Gordon et al, 2007), pancreatic cancer (Lopes et al, 2007), and renal cell carcinoma (RCC) (Crnković-Mertens et al, 2007). Notably, studies of biopsies from bladder cancer (Gazzaniga et al, 2003), lung cancer (Hariu et al, 2005), nasopharyngeal carcinoma (Xiang et al, 2006), malignant pleural mesothelioma (Gordon et al, 2007), and pancreatic cancer (Lopes et al, 2007) reported that Livin is typically expressed in the tumour samples, but not in the corresponding normal tissues.…”

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confidence: 99%

Expression of inhibitor of apoptosis protein Livin in renal cell carcinoma and non-tumorous adult kidney

et al. 2007

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The antiapoptotic Livin/ML-IAP gene has recently gained much attention as a potential new target for cancer therapy. Reports indicating that livin is expressed almost exclusively in tumours, but not in the corresponding normal tissue, suggested that the targeted inhibition of livin may present a novel tumour-specific therapeutic strategy. Here, we compared the expression of livin in renal cell carcinoma and in non-tumorous adult kidney tissue by quantitative real-time reverse transcription-PCR, immunoblotting, and immunohistochemistry. We found that livin expression was significantly increased in tumours (P ¼ 0.0077), but was also clearly detectable in non-tumorous adult kidney. Transcripts encoding Livin isoforms a and b were found in both renal cell carcinoma and normal tissue, without obvious qualitative differences. Livin protein in renal cell carcinoma samples exhibited cytoplasmic and/or nuclear staining. In non-tumorous kidney tissue, Livin protein expression was only detectable in specific cell types and restricted to the cytoplasm. Thus, whereas the relative overexpression of livin in renal cell carcinoma indicates that it may still represent a therapeutic target to increase the apoptotic sensitivity of kidney cancer cells, this strategy is likely to be not tumour-specific.

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“…Thus, the development and application of survivin signaling pathway are beneficial for the early diagnosis of cancers and the determination of prognosis of cancer patients and also provide new targets for the biotherapy of cancers. Antisense oligonucleotide targeting survivin (ASODN) can induce the apoptosis of hepatic cancer cells and inhibit their growth (Grossman et al, 2006;Altieri and Marchisio, 2006;Tanabe et al, 2006). In the present study, survivin ASODN was transfected into human gastric cancer cells and the anti-tumor effects were then observed.…”

Section: Introductionmentioning

confidence: 81%

Effect of antisense oligodeoxynucleotide targeting survivin on growth of human gastric cancer cells

2013

Bangladesh J Pharmacol

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Expression of survivin mRNA and livin mRNA in non-small-cell lung cancer

Cited by 76 publications

References 17 publications

Upregulation of the antiapoptotic factor Livin contributes to cisplatin resistance in colon cancer cells

Upregulation of the antiapoptotic factor Livin contributes to cisplatin resistance in colon cancer cells

Expression of inhibitor of apoptosis protein Livin in renal cell carcinoma and non-tumorous adult kidney

Effect of antisense oligodeoxynucleotide targeting survivin on growth of human gastric cancer cells

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