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TGF-beta1 (transforming growth factor-beta1)-mediated adhesion of gastric carcinoma cells involves a decrease in Ras/ERKs (extracellular-signal-regulated kinases) cascade activity dependent on c-Src activity.
Biochem J. 2004 Apr 01; 379(Pt 1):141-50.BJ

Abstract

Signalling by integrin-mediated cell anchorage to extracellular matrix proteins is co-operative with other receptor-mediated signalling pathways to regulate cell adhesion, spreading, proliferation, survival, migration, differentiation and gene expression. It was observed that an anchorage-independent gastric carcinoma cell line (SNU16) became adherent on TGF-beta1 (transforming growth factor beta1) treatment. To understand how a signal cross-talk between integrin and TGF-beta1 pathways forms the basis for TGF-beta1 effects, cell adhesion and signalling activities were studied using an adherent subline (SNU16Ad, an adherent variant cell line derived from SNU16) derived from the SNU16 cells. SNU16 and SNU16Ad cells, but not integrin alpha5-expressing SNU16 cells, showed an increase in adhesion on extracellular matrix proteins after TGF-beta1 treatment. This increase was shown to be mediated by an integrin alpha3 subunit, which was up-regulated in adherent SNU16Ad cells and in TGF-beta1-treated SNU16 cells, compared with the parental SNU16 cells. After TGF-beta1 treatment of SNU16Ad cells on fibronectin, Tyr-416 phosphorylation of c-Src was increased, but Ras-GTP loading and ERK1/ERK2 (extracellular-signal-regulated kinases 1 and 2) activity were decreased, which showed a dependence on c-Src family kinase activity. Studies on adhesion and signalling activities using pharmacological inhibitors or by transient-transfection approaches showed that inhibition of ERK1/ERK2 activity increased TGF-beta1-mediated cell adhesion slightly, but not the basal cell adhesion significantly, and that c-Src family kinase activity and decrease in Ras/ERKs cascade activity were required for the TGF-beta1 effects. Altogether, the present study indicates that TGF-beta1 treatment causes anchorage-independent gastric carcinoma cells to adhere by an increase in integrin alpha3 level and a c-Src family kinase activity-dependent decrease in Ras/ERKs cascade activity.

Authors+Show Affiliations

Cancer Research Institute, Department of Tumor Biology, College of Medicine, Seoul National University, 28, Yongon-Dong, Chongno-Gu, Seoul 110-799, South Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

14720123

Citation

Kim, Hwang-Phill, et al. "TGF-beta1 (transforming Growth Factor-beta1)-mediated Adhesion of Gastric Carcinoma Cells Involves a Decrease in Ras/ERKs (extracellular-signal-regulated Kinases) Cascade Activity Dependent On c-Src Activity." The Biochemical Journal, vol. 379, no. Pt 1, 2004, pp. 141-50.
Kim HP, Lee MS, Yu J, et al. TGF-beta1 (transforming growth factor-beta1)-mediated adhesion of gastric carcinoma cells involves a decrease in Ras/ERKs (extracellular-signal-regulated kinases) cascade activity dependent on c-Src activity. Biochem J. 2004;379(Pt 1):141-50.
Kim, H. P., Lee, M. S., Yu, J., Park, J. A., Jong, H. S., Kim, T. Y., Lee, J. W., & Bang, Y. J. (2004). TGF-beta1 (transforming growth factor-beta1)-mediated adhesion of gastric carcinoma cells involves a decrease in Ras/ERKs (extracellular-signal-regulated kinases) cascade activity dependent on c-Src activity. The Biochemical Journal, 379(Pt 1), 141-50.
Kim HP, et al. TGF-beta1 (transforming Growth Factor-beta1)-mediated Adhesion of Gastric Carcinoma Cells Involves a Decrease in Ras/ERKs (extracellular-signal-regulated Kinases) Cascade Activity Dependent On c-Src Activity. Biochem J. 2004 Apr 1;379(Pt 1):141-50. PubMed PMID: 14720123.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - TGF-beta1 (transforming growth factor-beta1)-mediated adhesion of gastric carcinoma cells involves a decrease in Ras/ERKs (extracellular-signal-regulated kinases) cascade activity dependent on c-Src activity. AU - Kim,Hwang-Phill, AU - Lee,Mi-Sook, AU - Yu,Jiyon, AU - Park,Jin-Ah, AU - Jong,Hyun-Soon, AU - Kim,Tae-You, AU - Lee,Jung Weon, AU - Bang,Yung-Jue, PY - 2004/01/14/accepted PY - 2003/12/11/revised PY - 2003/09/16/received PY - 2004/1/15/pubmed PY - 2004/7/17/medline PY - 2004/1/15/entrez SP - 141 EP - 50 JF - The Biochemical journal JO - Biochem J VL - 379 IS - Pt 1 N2 - Signalling by integrin-mediated cell anchorage to extracellular matrix proteins is co-operative with other receptor-mediated signalling pathways to regulate cell adhesion, spreading, proliferation, survival, migration, differentiation and gene expression. It was observed that an anchorage-independent gastric carcinoma cell line (SNU16) became adherent on TGF-beta1 (transforming growth factor beta1) treatment. To understand how a signal cross-talk between integrin and TGF-beta1 pathways forms the basis for TGF-beta1 effects, cell adhesion and signalling activities were studied using an adherent subline (SNU16Ad, an adherent variant cell line derived from SNU16) derived from the SNU16 cells. SNU16 and SNU16Ad cells, but not integrin alpha5-expressing SNU16 cells, showed an increase in adhesion on extracellular matrix proteins after TGF-beta1 treatment. This increase was shown to be mediated by an integrin alpha3 subunit, which was up-regulated in adherent SNU16Ad cells and in TGF-beta1-treated SNU16 cells, compared with the parental SNU16 cells. After TGF-beta1 treatment of SNU16Ad cells on fibronectin, Tyr-416 phosphorylation of c-Src was increased, but Ras-GTP loading and ERK1/ERK2 (extracellular-signal-regulated kinases 1 and 2) activity were decreased, which showed a dependence on c-Src family kinase activity. Studies on adhesion and signalling activities using pharmacological inhibitors or by transient-transfection approaches showed that inhibition of ERK1/ERK2 activity increased TGF-beta1-mediated cell adhesion slightly, but not the basal cell adhesion significantly, and that c-Src family kinase activity and decrease in Ras/ERKs cascade activity were required for the TGF-beta1 effects. Altogether, the present study indicates that TGF-beta1 treatment causes anchorage-independent gastric carcinoma cells to adhere by an increase in integrin alpha3 level and a c-Src family kinase activity-dependent decrease in Ras/ERKs cascade activity. SN - 1470-8728 UR - https://www.unboundmedicine.com/medline/citation/14720123/TGF_beta1__transforming_growth_factor_beta1__mediated_adhesion_of_gastric_carcinoma_cells_involves_a_decrease_in_Ras/ERKs__extracellular_signal_regulated_kinases__cascade_activity_dependent_on_c_Src_activity_ DB - PRIME DP - Unbound Medicine ER -