Crk-like adapter protein is required for TGF-β-induced AKT and ERK-signaling pathway in epithelial ovarian carcinomas

Cheng, Shaomei; Guo, Jingyan; Yang, Qing; Lin, Han

doi:10.1007/s13277-014-2724-0

Cited by 11 publications

(15 citation statements)

References 28 publications

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“…Because AKT phosphorylation is a hallmark of phosphatidylinositol 3-kinase (PI3K) activity, this finding indicates that Crk proteins are needed for LFA-1 dependent PI3K activation. In support of this idea, Crk proteins have been implicated in PI3K signaling in fibroblasts and transformed cells (45–50).…”

Section: Resultsmentioning

confidence: 88%

Crk adaptor proteins mediate actin-dependent T cell migration and mechanosensing induced by the integrin LFA-1

et al. 2018

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T cell entry into inflamed tissue involves firm adhesion, spreading, and migration of the T cells across endothelial barriers. These events depend on “outside-in” signals through which engaged integrins direct cytoskeletal reorganization. We investigated the molecular events that mediate this process and found that T cells from mice lacking expression of the adaptor protein Crk exhibited defects in phenotypes induced by the integrin lymphocyte function–associated antigen 1 (LFA-1); namely, actin polymerization, leading edge formation, and two-dimensional cell migration. Crk protein was an essential mediator of LFA-1 signaling–induced phosphorylation of the E3 ubiquitin ligase c-Cbl and its subsequent interaction with the phosphatidylinositol 3-kinase (PI3K) subunit p85, thus promoting PI3K activity and cytoskeletal remodeling. In addition, we found that Crk proteins was required for T cells to respond to changes in substrate stiffness, as measured by alterations in cell spreading and differential phosphorylation of the force-sensitive protein CasL. These findings identify Crk proteins as key intermediates coupling LFA-1 signals to actin remodeling and provide mechanistic insights into how T cells sense and respond to substrate stiffness.

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Section: Resultsmentioning

confidence: 88%

Crk adaptor proteins mediate actin-dependent T cell migration and mechanosensing induced by the integrin LFA-1

et al. 2018

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“…MAPK/ERK signaling is an important pathway that affects cell proliferation, and can be activated by growth factors such as TGF-β1 [26], [27], [28]. Because our data showed that GTP induced the expression of TGF-β1, we therefore examined the effect of GTP on ERK signaling pathway by Western blotting and immunofluorescence staining.…”

Section: Resultsmentioning

confidence: 99%

Panax ginseng total protein promotes proliferation and secretion of collagen in NIH/3T3 cells by activating extracellular signal-related kinase pathway

Chen

Wang

et al. 2017

Journal of Ginseng Research

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BackgroundRecently, protein from ginseng was studied and used for the treatment of several kinds of diseases. However, the effect of ginseng total protein (GTP) on proliferation and wound healing in fibroblast cells remains unclear.MethodsIn this study, cell viability was analyzed using the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay. Cell cycle distribution was analyzed by flow cytometer. The levels of transforming growth factor β1, vascular endothelial growth factor, and collagens were analyzed by enzyme-linked immunosorbent assay and immunofluorescence staining. The expressions of cyclin A, phosphorylation of extracellular signal-related kinase (p-ERK1/2), and ERK1/2 were analyzed by Western blotting.ResultsOur results showed that GTP promoted cell proliferation and increased the percentage of cells in S phase through the upregulation of cyclin A in NIH/3T3 cells. We also found that GTP induced the secretion of type I collagen, and promoted the expression of other factors that regulate the synthesis of collagen such as transforming growth factor β1 and vascular endothelial growth factor. In addition, the phosphorylation of ERK1/2 at Thr202/Tyr204 was also increased by GTP.ConclusionOur studies suggest that GTP promoted proliferation and secretion of collagen in NIH/3T3 cells by activating the ERK signal pathway, which shed light on a potential function of GTP in promoting wound healing.

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“…The stagnation of treatment is attributed to a lack of understanding of the PAH pathophysiological mechanisms and the absence of any efficacious drug against pulmonary vascular remodeling [4]. Recent studies have shown that the muscularization of nonmuscular pulmonary arterioles is a key characteristic of pulmonary vascular remodeling in PAH pathogenesis [5–9]. The new smooth muscle cells in muscularized nonmuscular pulmonary arterioles may originate from transdifferentiation and proliferation of pulmonary arterial endothelial cells (PAECs).…”

Section: Introductionmentioning

confidence: 99%

Quercetin Inhibits Pulmonary Arterial Endothelial Cell Transdifferentiation Possibly by Akt and Erk1/2 Pathways

Huang

Zhu

Huang

et al. 2017

BioMed Research International

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This study aimed to investigate the effects and mechanisms of quercetin on pulmonary arterial endothelial cell (PAEC) transdifferentiation into smooth muscle-like cells. TGF-β1-induced PAEC transdifferentiation models were applied to evaluate the pharmacological actions of quercetin. PAEC proliferation was detected with CCK8 method and BurdU immunocytochemistry. Meanwhile, the identification and transdifferentiation of PAECs were determined by FVIII immunofluorescence staining and α-SMA protein expression. The related mechanism was elucidated based on the levels of Akt and Erk1/2 signal pathways. As a result, quercetin effectively inhibited the TGF-β1-induced proliferation and transdifferentiation of the PAECs and activation of Akt/Erk1/2 cascade in the cells. In conclusion, quercetin is demonstrated to be effective for pulmonary arterial hypertension (PAH) probably by inhibiting endothelial transdifferentiation possibly via modulating Akt and Erk1/2 expressions.

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Crk-like adapter protein is required for TGF-β-induced AKT and ERK-signaling pathway in epithelial ovarian carcinomas

Cited by 11 publications

References 28 publications

Crk adaptor proteins mediate actin-dependent T cell migration and mechanosensing induced by the integrin LFA-1

Crk adaptor proteins mediate actin-dependent T cell migration and mechanosensing induced by the integrin LFA-1

Panax ginseng total protein promotes proliferation and secretion of collagen in NIH/3T3 cells by activating extracellular signal-related kinase pathway

Quercetin Inhibits Pulmonary Arterial Endothelial Cell Transdifferentiation Possibly by Akt and Erk1/2 Pathways

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