Expression level of wild-type survivin in gastric cancer is an independent predictor of survival

Meng, Hua; Lu, Cai-De; Sun, Yu-Lei; Dai, Dejian; Lee, Sang-Wong; Tanigawa, Nobuhiko

doi:10.3748/wjg.v10.i22.3245

Cited by 29 publications

(28 citation statements)

References 25 publications

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“…However, survivin-2B expression was significantly decreased in later tumour stage (III þ IV) in comparison with early stage (I þ II) (Krieg et al, 2002;Meng et al, 2004), and inversely correlated with tumour differentiation and invasion (Meng et al, 2004). Interestingly, although Krieg et al (2002) reported that the expression of survivin and survivin-DEx3 remained unchanged in different stages of cancer, Meng et al (2004) showed that the expression level of survivin-DEx3 is inversely correlated with apoptotic index. It was also reported that survivin-2B expression was dominant in benign brain tumours in comparison with the malignant ones (Yamada et al, 2003), and that survivin-DEx3 expression was prominent in comparison with survivin-2B expression in survivin-expressing acute lymphocytic leukaemia (ALL) and chronic lymphocytic leukaemia (CLL) patient bone marrow samples (Nakagawa et al, 2004).…”

Section: Survivin Variants In Tumorigenesismentioning

confidence: 87%

“…In renal cell carcinomas (RCC), while the expression levels of survivin and survivin-DEx3 did not show a decrease in late tumour stages in comparison with the early and intermediate tumour stages in 57 clinical RCC samples, survivin-2B expression was significantly decreased in late tumour stages (Mahotka et al, 2002a), indicating a possible unfavourable role of survivin-2B in cancer development. In gastric cancer, the expression of survivin-DEx3, survivin-2B, and survivin (dominant transcript) was found in cancer tissues, irrespective of their histological type, grade, or stage (Krieg et al, 2002) (Meng et al, 2004). However, survivin-2B expression was significantly decreased in later tumour stage (III þ IV) in comparison with early stage (I þ II) (Krieg et al, 2002;Meng et al, 2004), and inversely correlated with tumour differentiation and invasion (Meng et al, 2004).…”

Section: Survivin Variants In Tumorigenesismentioning

confidence: 96%

“…Similarly, among the 79 gastric tumour samples, the expression of survivin, survivin-2B, and survivin-DEx3 was 79 (100%), 62 (78.5%), and 51 (64.6%), respectively (Meng et al, 2004). Additionally, studies from Islam et al (2000) indicated that while the expression of survivin was downregulated during retinoic acidinduced apoptosis in CHP134 neuroblastoma cells, survivin-2B expression was unchanged or slightly increased during apoptosis.…”

Section: Survivin Variants In Tumorigenesismentioning

confidence: 99%

“…In gastric cancer, the expression of survivin-DEx3, survivin-2B, and survivin (dominant transcript) was found in cancer tissues, irrespective of their histological type, grade, or stage (Krieg et al, 2002) (Meng et al, 2004). However, survivin-2B expression was significantly decreased in later tumour stage (III þ IV) in comparison with early stage (I þ II) (Krieg et al, 2002;Meng et al, 2004), and inversely correlated with tumour differentiation and invasion (Meng et al, 2004). Interestingly, although Krieg et al (2002) reported that the expression of survivin and survivin-DEx3 remained unchanged in different stages of cancer, Meng et al (2004) showed that the expression level of survivin-DEx3 is inversely correlated with apoptotic index.…”

Section: Survivin Variants In Tumorigenesismentioning

confidence: 99%

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Role of survivin and its splice variants in tumorigenesis

2004

Br J Cancer

209

166

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Survivin, a unique member of the inhibitor of apoptosis (IAP) protein family, is highly expressed in cancer but is undetectable in nonproliferating normal adult tissues, suggesting a potential role in tumorigenesis. Differential splicing of survivin pre-mRNA results in three new survivin variants, survivin-DEx3, survivin-2B, and survivin-3B. Loss of survivin-2B expression was found in the later stage of cancer development, while survivin and survivin-DEx3 are not, suggesting a differential role of them in tumour development. In this minireview, the author intends to summarise and discuss the current data relevant to the role of survivin and its splicing variants in tumorigenesis, which may facilitate further investigation in this interesting area.

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Section: Survivin Variants In Tumorigenesismentioning

confidence: 87%

Section: Survivin Variants In Tumorigenesismentioning

confidence: 96%

Section: Survivin Variants In Tumorigenesismentioning

confidence: 99%

Section: Survivin Variants In Tumorigenesismentioning

confidence: 99%

See 2 more Smart Citations

Role of survivin and its splice variants in tumorigenesis

2004

Br J Cancer

209

166

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show abstract

“…Previous clinical studies have reported the survivin expression to be associated with tumour cell proliferation, apoptotic inhibition, and a poor prognosis in various human cancers, including NSCLCs (Martinez et al, 2004;Shinohara et al, 2005). However, only a few clinical reports studied these splice variants of survivin in human cancers (Mahotka et al, 2002a;Meng et al, 2004;Ling et al, 2005;Taubert et al, 2005). Therefore, to clarify the clinical significance of these splice variants of survivin in NSCLCs, we performed the present study on the gene expressions of wild-type survivin, survivin-2B, and survivin-deltaEx3 in relation to the subcellular localisation of survivin proteins, tumour cell proliferation, and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

The clinical significance of splice variants and subcellular localisation of survivin in non-small cell lung cancers

et al. 2008

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Survivin is a member of the inhibitor of apoptosis protein family. Survivin has splice variants with different biological functions associated with tumorigenesis. We investigated 134 non-small cell lung cancers (NSCLCs) to study the clinical significance of wildtype survivin, survivin-2B, and survivin-deltaEx3. Real-time PCR analyses were performed for their gene expressions. The subcellular localisation of survivin proteins was evaluated by immunohistochemistry. The Ki-67 proliferation index and the apoptotic index were also evaluated. The survivin-deltaEx3 gene expression was significantly higher in stage II -III than in stage I (P ¼ 0.0174), and significantly correlated with the nuclear pan-survivin expression (Po0.0001). The Ki-67 index was significantly higher in wild-type survivin-positive tumours (Po0.0001), survivin-deltaEx3-positive tumours (Po0.0001), and tumours with positive expression of the nuclear pansurvivin (P ¼ 0.0047). In contrast, the apoptotic index was significantly lower only in wild-type survivin-positive tumours (Po0.0001). Thus, the wild-type survivin gene expression was associated with apoptotic inhibition and tumour proliferation. Furthermore, the survivin-deltaEx3 gene expression was strongly associated with tumour proliferation, especially in advanced stage NSCLCs. In contrast, the survivin-2B gene expression did not correlate with tumour proliferation or tumour apoptosis.

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Small interfering RNA targeting survivin sensitizes lung cancer cell with mutant p53 to adriamycin

Yonesaka

Tamura

Kurata

et al. 2005

Intl Journal of Cancer

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Survivin is a member of the inhibitor of apoptosis protein (IAP) family that is specifically overexpressed in cancer tissues. p53 is one of the tumor suppressor genes; its induction in response to DNA damage causes apoptosis and correlates with drug sensitivity. To investigate the possible regulation of survivin by p53, we examined the level of survivin expression in lung cancer cell lines in response to adriamycin. Levels of survivin mRNA and protein in cell lines with wild-type p53 decreased dramatically after p53 induction, but no such reduction of survivin was observed in cell lines with mutated or null p53. Inhibition of wild-type p53 in A549 cells by small interfering (si) RNA significantly upregulated the expression of survivin. Survivin inhibition by siRNA in PC9 cells with mutated p53 significantly depressed cell proliferation. To investigate the sensitivity of cancer cells to adriamycin after inhibition of survivin, we depressed survivin expression using siRNA, and then added adriamycin at an IC 50 dose. After a further 48 hr incubation with adriamycin, proliferation was significantly depressed in the cells treated with siRNA targeting survivin, in comparison with siRNA targeting scramble. Furthermore, both TUNEL and pro-caspase3 expression assay showed a significant increase in apoptosis after combined treatment with adriamycin and siRNA targeting survivin. Our results demonstrate that survivin is downregulated by p53, and that siRNA targeting of survivin increases cell sensitivity to adriamycin and promotes apoptosis. siRNA targeting of survivin could be potentially useful for increasing sensitivity to anticancer drugs, especially in drug-resistant cells with mutated p53. ' 2005 Wiley-Liss, Inc.

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Expression level of wild-type survivin in gastric cancer is an independent predictor of survival

Abstract: Wild-type survivin mRNA expression levels are of important prognostic value and significant participation of survivin-2B and survivin-DeltaEx3 is suggested in gastric cancer development.

Cited by 29 publications

References 25 publications

Role of survivin and its splice variants in tumorigenesis

Role of survivin and its splice variants in tumorigenesis

The clinical significance of splice variants and subcellular localisation of survivin in non-small cell lung cancers

Small interfering RNA targeting survivin sensitizes lung cancer cell with mutant p53 to adriamycin

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