PKC mediates fluctuant ERK-paxillin signaling for hepatocyte growth factor-induced migration of hepatoma cell HepG2

Hu, Chi-Tan; Cheng, Chuan-Chu; Pan, Siou-Mei; Wu, Jia-Ru; Wu, Wen-Sheng

doi:10.1016/j.cellsig.2013.03.011

Cited by 22 publications

(45 citation statements)

References 46 publications

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“…Downregulation of PKC by adding TPA into Hep3B cells also decreases the production of erythropoietin [263], which is a glycoprotein hormone that is stimulated under the hypoxic environment [275]. On the other hand, expression of PKC and suppresses HGFinduced phosphorylation of ERK and paxillin, resulting in the reduction of HepG2 cell migration, whereas PKC and are required for phosphorylation of paxillin [276]. However, high levels of PKC mRNA in HCC tissues are correlated with poor survival in patients [277].…”

Section: Liver Cancer [Hepatocellular Carcinoma (Hcc)]mentioning

confidence: 99%

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Protein Kinase C (PKC) Isozymes and Cancer

Kang

2014

New Journal of Science

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Protein kinase C (PKC) is a family of phospholipid-dependent serine/threonine kinases, which can be further classified into three PKC isozymes subfamilies: conventional or classic, novel or nonclassic, and atypical. PKC isozymes are known to be involved in cell proliferation, survival, invasion, migration, apoptosis, angiogenesis, and drug resistance. Because of their key roles in cell signaling, PKC isozymes also have the potential to be promising therapeutic targets for several diseases, such as cardiovascular diseases, immune and inflammatory diseases, neurological diseases, metabolic disorders, and multiple types of cancer. This review primarily focuses on the activation, mechanism, and function of PKC isozymes during cancer development and progression.

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Section: Liver Cancer [Hepatocellular Carcinoma (Hcc)]mentioning

confidence: 99%

“…In addition, PKC may be involved in growth and migration of HCC cells [276,285], while the PKC -specific inhibitor LY317615 or siRNA significantly reduces migration and invasion of HCC cells [286].…”

Section: Liver Cancer [Hepatocellular Carcinoma (Hcc)]mentioning

confidence: 99%

Protein Kinase C (PKC) Isozymes and Cancer

Kang

2014

New Journal of Science

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“…Our recent study [32] demonstrated that PKC mediated HGF-induced fluctuant FA signaling within 24 h, which is associated with alternate actin reorganization [16]. Such signal fluctuation is reminiscent of c-Met endocytosis.…”

Section: Introductionmentioning

confidence: 97%

“…Moreover, HGF may recruit Golgi-localized, gamma-ear-containing, Arf-binding proteins 3 (GGA3) to promote c-Met recycling and sustain ERK activation [12]. Several lines of evidences supported that PKC may regulate endosomal processing of RTK [33,38], including c-Met [32,39,40]. Taken together, it is highly probable that PKC mediates HGF-induced fluctuant signaling by controlling the critical steps in c-Met endocytosis.…”

Section: Introductionmentioning

confidence: 99%

PKCε-mediated c-Met endosomal processing directs fluctuant c-Met-JNK-paxillin signaling for tumor progression of HepG2

Cheng

et al. 2015

Cellular Signalling

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“…The PKC was known to play an important role in progression of HCC [25] and Hansen et al [15] demonstrated that cavin-2 was essential for the expression levels of cavin-1 protein which had a function in the development of tumors. Thus, we hypothesized that there was a correlation between cavin-2 and tumors.…”

Section: Introductionmentioning

confidence: 99%

Prognostic and Diagnostic Significance of SDPR-Cavin-2 in Hepatocellular Carcinoma

Wei

Luo

Zhu

et al. 2016

Cell Physiol Biochem

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Background: Hepatocellular carcinoma (HCC) is a malignant tumor worldwide. Due to the lack of early prediction marker, numerous patients were diagnosed in their late stage. The family of cavins plays important roles in caveolae formation and cellular processes. Cavin-2, one of the members of cavins, has been reported as a suppresser in cancers. In this study, we have investigated its expression pattern and clinical significance in HCC. Methods: RT‑qPCR was performed to detect the expression of cavin-2. Results: Cavin-2 was down-regulated in HCC and associated with tumor differentiation (r=-0.275, P=0.013) and tumor-node-metastasis (TNM) stage (r=-0.216, P=0.035). The Overall survival analysis showed that patients with lower cavin-2 expression had a relatively poor prognosis. Meanwhile, the multivariate analysis revealed that cavin-2 was an independent prognostic factor. The receiver operating characteristic curve analyses indicated that plasma cavin-2 presented a high accuracy (AUC=0.727, 0.865, 0.901) for diagnosing HCC cases from controls, hepatitis B and cirrhosis patients, respectively. Meanwhile, plasma cavin-2 showed a high sensitivity (88.4%, 89.9%) for detecting HCC with the serum α‑fetoprotein (AFP) levels below 200 ng/ml from those hepatitis B and cirrhosis cases. Conclusion: Our data suggested that cavin-2 might be considered as a potential prognostic and diagnostic indicator in HCC.

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PKC mediates fluctuant ERK-paxillin signaling for hepatocyte growth factor-induced migration of hepatoma cell HepG2

Cited by 22 publications

References 46 publications

Protein Kinase C (PKC) Isozymes and Cancer

Protein Kinase C (PKC) Isozymes and Cancer

PKCε-mediated c-Met endosomal processing directs fluctuant c-Met-JNK-paxillin signaling for tumor progression of HepG2

Prognostic and Diagnostic Significance of SDPR-Cavin-2 in Hepatocellular Carcinoma

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