Snail regulates cell survival and inhibits cellular senescence in human metastatic prostate cancer cell lines

Emadi‐Baygi, Modjtaba; Soheili, Zahra‐Soheila; Schmitz, Ingo; Sameie, Shahram; Schulz, Wolfgang A.

doi:10.1007/s10565-010-9163-5

Cited by 75 publications

(34 citation statements)

References 60 publications

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“…Moreover, the migratory potential of these cells was decreased by Snail siRNA treatment [25]. Clinically, Snail overexpression correlates significantly with lymph node [26] metastasis, histologic grade, and TNM stage [27]; however, factors resulting in the development of CSC-like properties have not been fully identified.…”

Section: Discussionmentioning

confidence: 99%

Snail regulates Nanog status during the epithelial-mesenchymal transition via the Smad1/Akt/GSK3β signaling pathway in non-small-cell lung cancer

Liu

Peng

et al. 2014

Oncotarget

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The epithelial–mesenchymal transition (EMT), a crucial step in cancer metastasis, is important in transformed cancer cells with stem cell-like properties. In this study, we established a Snail-overexpressing cell model for non-small-cell lung cancer (NSCLC) and investigated its underlying mechanism. We also identified the downstream molecular signaling pathway that contributes to the role of Snail in regulating Nanog expression. Our data shows that high levels of Snail expression correlate with metastasis and high levels of Nanog expression in NSCLC. NSCLC cells expressing Snail are characterized by active EMT characteristics and exhibit an increased ability to migrate, chemoresistance, sphere formation, and stem cell-like properties. We also investigated the signals required for Snail-mediated Nanog expression. Our data demonstrate that LY294002, SB431542, LDN193189, and Noggin pretreatment inhibit Snail-induced Nanog expression during EMT. This study shows a significant correlation between Snail expression and phosphorylation of Smad1, Akt, and GSK3β. In addition, pretreatment with SB431542, LDN193189, or Noggin prevented Snail-induced Smad1 and Akt hyperactivation and reactivated GSK3β. Moreover, LY294002 pretreatment prevented Akt hyperactivation and reactivated GSK3β without altering Smad1 activation. These findings provide a novel mechanistic insight into the important role of Snail in NSCLC during EMT and indicate potentially useful therapeutic targets for NSCLC.

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Section: Discussionmentioning

confidence: 99%

Snail regulates Nanog status during the epithelial-mesenchymal transition via the Smad1/Akt/GSK3β signaling pathway in non-small-cell lung cancer

Liu

Peng

et al. 2014

Oncotarget

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“…It has been reported that snail, a transcription factor and E-cadherin repressor, is a novel prognostic factor in many carcinomas (26-29). However, expression of snail in HC showed no significant relation to the expression of E-cadherin (Table 2).…”

Section: Discussionmentioning

confidence: 99%

Prognostic significance of snail expression in hilar cholangiocarcinoma

Kong

Liang

et al. 2012

Braz J Med Biol Res

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Many patients with hilar cholangiocarcinoma (HC) have a poor prognosis. Snail, a transcription factor and E-cadherin repressor, is a novel prognostic factor in many cancers. The aim of this study was to evaluate the relationship between snail and E-cadherin protein expression and the prognostic significance of snail expression in HC. We examined the protein expression of snail and E-cadherin in HC tissues from 47 patients (22 males and 25 females, mean age 61.2 years) using immunohistochemistry and RT-PCR. Proliferation rate was also evaluated in the same cases by the MIB1 index. High, low and negative snail protein expression was recorded in 18 (38%), 17 (36%), and 12 (26%) cases, respectively, and 40.4% (19/47) cases showed reduced E-cadherin protein expression in HC samples. No significant correlation was found between snail and E-cadherin protein expression levels (P = 0.056). No significant correlation was found between snail protein expression levels and gender, age, tumor grade, vascular or perineural invasion, nodal metastasis and invasion, or proliferative index. Cancer samples with positive snail protein expression were associated with poor survival compared with the negative expresser groups. Kaplan-Meier curves comparing different snail protein expression levels to survival showed highly significant separation (P < 0.0001, log-rank test). With multivariate analysis, only snail protein expression among all parameters was found to influence survival (P = 0.0003). We suggest that snail expression levels can predict poor survival regardless of pathological features and tumor proliferation. Immunohistochemical detection of snail protein expression levels in routine sections may provide the first biological prognostic marker.

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“…Forced expression of SNAIL in epithelial PC lines ARCaP E and LNCaP is sufficient to induce at least a partial EMT, as evidenced by altered biomarker expression and migration. In contrast, SNAIL inhibition in mesenchymal PC-3 cells induces epithelial biomarker expression [40]. Consequently, expression of SNAIL is thought to be both necessary and sufficient to induce EMT, but the relationship of SNAIL to human PC remains to be established.…”

Section: Preclinical Evidence Of Ep In Pcmentioning

confidence: 99%

The role of epithelial plasticity in prostate cancer dissemination and treatment resistance

Bitting

Schaeffer

Somarelli

et al. 2014

Cancer Metastasis Rev

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Nearly 30,000 men die annually in the USA of prostate cancer, nearly uniformly from metastatic dissemination. Despite recent advances in hormonal, immunologic, bone-targeted, and cytotoxic chemotherapies, treatment resistance and further dissemination are inevitable in men with metastatic disease. Emerging data suggests that the phenomenon of epithelial plasticity, encompassing both reversible mesenchymal transitions and acquisition of stemness traits, may underlie this lethal biology of dissemination and treatment resistance. Understanding the molecular underpinnings of this cellular plasticity from preclinical models of prostate cancer and from biomarker studies of human metastatic prostate cancer has provided clues to novel therapeutic approaches that may delay or prevent metastatic disease and lethality over time. This review will discuss the preclinical and clinical evidence for epithelial plasticity in this rapidly changing field and relate this to clinical phenotype and resistance in prostate cancer while suggesting novel therapeutic approaches.

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Snail regulates cell survival and inhibits cellular senescence in human metastatic prostate cancer cell lines

Abstract: CitationSnail regulates cell survival and inhibits cellular senescence in human metastatic prostate cancer cell lines. 2010, 26 (6):553-67 Cell Biol. Toxicol.

Cited by 75 publications

References 60 publications

Snail regulates Nanog status during the epithelial-mesenchymal transition via the Smad1/Akt/GSK3β signaling pathway in non-small-cell lung cancer

Snail regulates Nanog status during the epithelial-mesenchymal transition via the Smad1/Akt/GSK3β signaling pathway in non-small-cell lung cancer

Prognostic significance of snail expression in hilar cholangiocarcinoma

The role of epithelial plasticity in prostate cancer dissemination and treatment resistance

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