کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5509363 1538510 2017 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
TGFβ1 induces endometrial cancer cell adhesion and migration by up-regulating integrin αvβ3 via SMAD-independent MEK-ERK1/2 signaling
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
TGFβ1 induces endometrial cancer cell adhesion and migration by up-regulating integrin αvβ3 via SMAD-independent MEK-ERK1/2 signaling
چکیده انگلیسی
Endometrial cancer is the most common, and second most lethal, gynecological malignancy, and its rates of incidence and death are growing. This is likely attributable to increased numbers of high-risk type II endometrial cancers which account for ~ 30% of cases but ~ 75% of deaths due to their aggressive and metastatic behaviour. Histopathological and in vitro functional studies suggest that aberrant TGFβ1 signaling may contribute to endometrial cancer development and the acquisition of invasive/metastatic characteristics. However, little is known about the cellular and molecular mechanisms of TGFβ1 in high-risk endometrial cancers. In the present study, we examined the roles and mechanisms of TGFβ1 on cell adhesion and motility in type II endometrial cancer cell lines, KLE and HEC-1B. We show that treatment with TGFβ1 increases cell adhesion to vitronectin and transwell cell migration. We also demonstrate that TGFβ1 treatment increases integrin β3 and αv mRNA and protein levels via SMAD-independent MEK-ERK1/2 signaling. Importantly, siRNA depletion or antibody-mediated blocking of integrin αvβ3 reversed the effects of TGFβ1 on cell adhesion and migration. Our results suggest that TGFβ1-MEK-ERK1/2-integrin αvβ3 signaling could contribute to the invasive behaviour of high-risk endometrial cancer by promoting cell adhesion and migration.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 34, June 2017, Pages 92-101
نویسندگان
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