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Novel Role for γ-Catenin in the Regulation of Cancer Cell Migration via the Induction of Hepatocyte Growth Factor Activator Inhibitor Type 1 (HAI-1).

Sechler M, Borowicz S, Van Scoyk M, Avasarala S, Zerayesus S, Edwards MG, Kumar Karuppusamy Rathinam M, Zhao X, Wu PY, Tang K, Bikkavilli RK, Winn RA - J. Biol. Chem. (2015)

Bottom Line: Moreover, the affects of γ-catenin on cell migration were observed to be p53-dependent.Mechanistically, the anti-migratory effects seen via γ-catenin were driven by the expression of hepatocyte growth factor activator inhibitor Type I (HAI-1 or SPINT-1), an upstream inhibitor of the c-MET signaling pathway.Taken together, we identify γ-catenin as a novel regulator of HAI-1, which is a critical regulator of HGF/c-MET signaling.

View Article: PubMed Central - PubMed

Affiliation: From the Cancer Biology Program and.

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Related in: MedlinePlus

γ-catenin affects on cell proliferation and migration were p53-dependent.A, H157 cells were co-transfected with γ-catenin plasmids and p53 siRNAs and the proliferation rates of the cells were determined by MTS cell proliferation assays as described under “Experimental Procedures.” Data represent mean ± S.E. from three independent highly reproducible experiments. #, p < 0.05; versus control. *, p < 0.05; versus γ-catenin control. B, H157 cells were co-transfected with γ-catenin and p53 shRNA expression construct and allowed to grow to confluence. A 3-mm scrape wound was created in confluent cultures, and cell migration was recorded at 0 and 24 h as described under “Experimental Procedures.” The upper panel represents the quantification of migration as described under “Experimental Procedures,” while representative images were presented in the lower panel.
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Figure 2: γ-catenin affects on cell proliferation and migration were p53-dependent.A, H157 cells were co-transfected with γ-catenin plasmids and p53 siRNAs and the proliferation rates of the cells were determined by MTS cell proliferation assays as described under “Experimental Procedures.” Data represent mean ± S.E. from three independent highly reproducible experiments. #, p < 0.05; versus control. *, p < 0.05; versus γ-catenin control. B, H157 cells were co-transfected with γ-catenin and p53 shRNA expression construct and allowed to grow to confluence. A 3-mm scrape wound was created in confluent cultures, and cell migration was recorded at 0 and 24 h as described under “Experimental Procedures.” The upper panel represents the quantification of migration as described under “Experimental Procedures,” while representative images were presented in the lower panel.

Mentions: To further explore the p53-dependent effects of γ-catenin on cell proliferation and cell migration, we utilized short hairpin RNA (shRNA) or short interference RNAs (siRNAs) against p53. Interestingly, expression of γ-catenin failed to induce anti-proliferative (Fig. 2A), and anti-migratory (Fig. 2B) effects in p53 siRNA or p53 shRNA treated H157 cells, suggesting that the effects of γ-catenin were indeed p53-dependent.


Novel Role for γ-Catenin in the Regulation of Cancer Cell Migration via the Induction of Hepatocyte Growth Factor Activator Inhibitor Type 1 (HAI-1).

Sechler M, Borowicz S, Van Scoyk M, Avasarala S, Zerayesus S, Edwards MG, Kumar Karuppusamy Rathinam M, Zhao X, Wu PY, Tang K, Bikkavilli RK, Winn RA - J. Biol. Chem. (2015)

γ-catenin affects on cell proliferation and migration were p53-dependent.A, H157 cells were co-transfected with γ-catenin plasmids and p53 siRNAs and the proliferation rates of the cells were determined by MTS cell proliferation assays as described under “Experimental Procedures.” Data represent mean ± S.E. from three independent highly reproducible experiments. #, p < 0.05; versus control. *, p < 0.05; versus γ-catenin control. B, H157 cells were co-transfected with γ-catenin and p53 shRNA expression construct and allowed to grow to confluence. A 3-mm scrape wound was created in confluent cultures, and cell migration was recorded at 0 and 24 h as described under “Experimental Procedures.” The upper panel represents the quantification of migration as described under “Experimental Procedures,” while representative images were presented in the lower panel.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4505473&req=5

Figure 2: γ-catenin affects on cell proliferation and migration were p53-dependent.A, H157 cells were co-transfected with γ-catenin plasmids and p53 siRNAs and the proliferation rates of the cells were determined by MTS cell proliferation assays as described under “Experimental Procedures.” Data represent mean ± S.E. from three independent highly reproducible experiments. #, p < 0.05; versus control. *, p < 0.05; versus γ-catenin control. B, H157 cells were co-transfected with γ-catenin and p53 shRNA expression construct and allowed to grow to confluence. A 3-mm scrape wound was created in confluent cultures, and cell migration was recorded at 0 and 24 h as described under “Experimental Procedures.” The upper panel represents the quantification of migration as described under “Experimental Procedures,” while representative images were presented in the lower panel.
Mentions: To further explore the p53-dependent effects of γ-catenin on cell proliferation and cell migration, we utilized short hairpin RNA (shRNA) or short interference RNAs (siRNAs) against p53. Interestingly, expression of γ-catenin failed to induce anti-proliferative (Fig. 2A), and anti-migratory (Fig. 2B) effects in p53 siRNA or p53 shRNA treated H157 cells, suggesting that the effects of γ-catenin were indeed p53-dependent.

Bottom Line: Moreover, the affects of γ-catenin on cell migration were observed to be p53-dependent.Mechanistically, the anti-migratory effects seen via γ-catenin were driven by the expression of hepatocyte growth factor activator inhibitor Type I (HAI-1 or SPINT-1), an upstream inhibitor of the c-MET signaling pathway.Taken together, we identify γ-catenin as a novel regulator of HAI-1, which is a critical regulator of HGF/c-MET signaling.

View Article: PubMed Central - PubMed

Affiliation: From the Cancer Biology Program and.

Show MeSH
Related in: MedlinePlus