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Göteborgs universitets publikationer

PKN I modulates TGF beta and EGF signaling in HEC-I-A endometrial cancer cell line

Författare och institution:
S. Attarha (-); Ravi Kanth Rao Saini (Sahlgrenska Cancer Center); S. Andersson (-); M. Mints (-); S. Souchelnytskyi (-)
Publicerad i:
Oncotargets and Therapy, 7 s. 1397-1408
Artikel, refereegranskad vetenskaplig
Sammanfattning (abstract):
Background: The response of cells to TGF beta and EGF is mediated by a network of various intracellular regulators. The signaling crosstalk between different regulators is of key importance for tumorigenesis. The crosstalk may explain the modulation of cellular responses to the same regulator by another signaling molecule. As PKN1-a serine/threonine kinase implicated in tumorigenesis was identified as potential crosstalk node for TGF beta and EGF signaling, the cellular functions that may be affected by PKN1 in a crosstalk of TGF beta and EGF were explored. Methods: To investigate the contribution of PKN1 to TGF beta and EGF signaling, transiently PKN1-transfected HEC-1-A endometrial cancer cells were generated and subjected to treatment with TGF beta, EGF, and their combination. Proliferation, apoptosis, invasion, wound healing, and migration assays were performed. The impact of PKN1 on the expression and phosphorylation of intracellular proteins was monitored by immunoblotting. Results: It was demonstrated that PKN1 modulated the responses of HEC-A-1 endometrial cancer cells to TGF beta and EGF PKN1 had an inhibitory effect on the stimulation of cell migration, and PKN1 kinase activity was required for the inhibitory effect of TGF beta and EGF on cell proliferation and invasiveness. It was observed that phosphorylation of Smad2, FAK, and Erk1/2 correlated with responses of the cells to TGF beta and EGE Conclusion: PKN1 modulates TGF beta- and EGF-dependent regulation of cell proliferation, migration, and invasiveness, and therefore is a component of the network signaling downstream of IGO and EGE
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
Klinisk medicin
PKN1 kinase, TGF beta, EGF, cell migration, proliferation, invasiveness, GROWTH-FACTOR-BETA, P21-ACTIVATED-KINASE-1, PROGRESSION, METASTASIS, EXPRESSION, APOPTOSIS, SOFTWARE, RECEPTOR, Biotechnology & Applied Microbiology, Oncology
Postens nummer:
Posten skapad:
2014-09-03 11:43

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