G<sub>1</sub>/S Cell Cycle Arrest Provides Anoikis Resistance through Erk-Mediated Bim Suppression

Collins, Nicole L.; Reginato, Maurico J.; Paulus, Jessica K.; Sgroi, Dennis; LaBaer, Joshua; Brugge, Joan S.

doi:10.1128/mcb.25.12.5282-5291.2005

Cited by 123 publications

(113 citation statements)

References 65 publications

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“…Cytoplasmic localization of p21 has been reported to correspond with a poor clinical outcome of patients with breast cancer 95,96 , which could therefore be explained by the observation that besides losing its CDK-inhibitory function, cytoplasmic p21 also gains anti-apoptotic functions 93,94 . Consistent with its role in resistance to apoptosis, ectopic expression of p21 prevents anoikis (detachment-induced apoptosis) 97 . Consequently, complete loss of p21 function is predicted to provide a selective disadvantage to cancer cells, as it could result in a lower apoptotic threshold.…”

Section: Is P21 Required For Oncogenic Transformation?mentioning

confidence: 79%

KLF4, p21 and context-dependent opposing forces in cancer

2005

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| Krüppel-like factors are transcriptional regulators that influence several cellular functions, including proliferation. Recent studies have shown that one family member, KLF4, can function both as a tumour suppressor and an oncogene. The ability of KLF4 to affect the levels of expression of the cell-cycle regulator p21 seems to be involved, in that this protein might function as a switch that determines the outcome of KLF4 signalling. Is this role of p21 restricted to KLF4, or does p21 represent a nodal point for signals from multiple other factors with opposing functions in cancer?

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Section: Is P21 Required For Oncogenic Transformation?mentioning

confidence: 79%

KLF4, p21 and context-dependent opposing forces in cancer

2005

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“…In fact, despite the cytoplasmic vesicle-like staining of p53 in Noc-treated cells, the cellular morphology was different from control cells (Figure 3b). To exclude this possibility, we pre-treated Aphidicolin (Aph; Collins et al, 2005) to block the cell cycle at the G1 phase and monitored the effect of Noc on the expression of p53. Similar to our earlier result, Noc blocked p53 reduction ( Figure 3c).…”

Section: Resultsmentioning

confidence: 99%

p53, secreted by K-Ras–Snail pathway, is endocytosed by K-Ras-mutated cells; implication of target-specific drug delivery and early diagnostic marker

Lee

Chung

et al. 2009

Oncogene

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“…This is the first report that SKP2 is involved in anoikis resistance. Given the report of Collins et al (27) that overexpression of p27 conferred anoikis resistance in MCF-10A cells and p27 is one of the most important substrates for SKP2, we also detected the effect of p27 on anoikis. The results showed that knockdown of p27 had no effect on anoikis in EC9706 cells, suggesting the effect of SKP2 on anoikis in ESCC was not mediated by p27.…”

Section: Discussionmentioning

confidence: 98%

“…Kim et al (28) proposed that galectin-3 inhibition of anoikis involves cell cycle arrest at an anoikis-insensitive point (late G 1 ) through modulation of gene expression and activities of cell cycle regulators. Collins et al (27) also reported that G 1 -S cell cycle arrest provides anoikis resistance through Erk-mediated Bim suppression. However, our results showed that SKP2 knockdown had no effect on cell cycle progress of EC9706 cells during induction of anoikis on polyHEMA plates.…”

Section: Discussionmentioning

confidence: 99%

Suppression of Anoikis by SKP2 Amplification and Overexpression Promotes Metastasis of Esophageal Squamous Cell Carcinoma

Wang

Ye³

et al. 2009

Molecular Cancer Research

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The gene of SKP2, located on chromosome 5p13, plays a critical role in cell cycle progression, especially at the G 1 -S transition, putatively through its control of several cell cycle regulator proteins including p27 kip1 , p21 cip1 , p57 kip2 , p130, cyclin E, and c-Myc. Previous studies in this laboratory revealed that gain of chromosome 5p was often seen in esophageal squamous cell carcinoma (ESCC). In the present study, we examined the amplification status and expression level of SKP2 in ESCC and investigated its clinicopathologic significance. Amplification and elevated expression of SKP2 correlated significantly with tumor stage and positive lymph node metastasis (P < 0.05). The SKP2 protein expression level as determined by immunohistochemical staining showed a significant inverse correlation with p27 protein. In vivo assay showed that inhibition of SKP2 expression also decreased tumor growth and lung metastasis of ESCC cells. At the molecular level, knockdown of SKP2 by RNA interference inhibited cell migration and invasion ability. Knockdown of SKP2 expression sensitized cancer cells to anoikis, and a wobble mutant of SKP2 that is resistant to SKP2 small interfering RNA can rescue this effect. Expression level of pAkt decreased after SKP2 knockdown. Treatment of cells with phosphoinositidyl 3-kinase inhibitor (LY294002) and constitutively activator (insulin-like growth factor I) had significant effects on the anoikis of SKP2 RNA interference cells. These results show for the first time that SKP2 is amplified and overexpressed in ESCC. Elevated expression of SKP2 protected cancer cells from anoikis, and this effect was mediated, at least in part, by the phosphoinositidyl 3-kinase-Akt pathway.

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G₁/S Cell Cycle Arrest Provides Anoikis Resistance through Erk-Mediated Bim Suppression

Cited by 123 publications

References 65 publications

KLF4, p21 and context-dependent opposing forces in cancer

KLF4, p21 and context-dependent opposing forces in cancer

p53, secreted by K-Ras–Snail pathway, is endocytosed by K-Ras-mutated cells; implication of target-specific drug delivery and early diagnostic marker

Suppression of Anoikis by SKP2 Amplification and Overexpression Promotes Metastasis of Esophageal Squamous Cell Carcinoma

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G1/S Cell Cycle Arrest Provides Anoikis Resistance through Erk-Mediated Bim Suppression

Cited by 123 publications

References 65 publications

KLF4, p21 and context-dependent opposing forces in cancer

KLF4, p21 and context-dependent opposing forces in cancer

p53, secreted by K-Ras–Snail pathway, is endocytosed by K-Ras-mutated cells; implication of target-specific drug delivery and early diagnostic marker

Suppression of Anoikis by SKP2 Amplification and Overexpression Promotes Metastasis of Esophageal Squamous Cell Carcinoma

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G₁/S Cell Cycle Arrest Provides Anoikis Resistance through Erk-Mediated Bim Suppression