Protein Kinase C (PKC) βII Induces Cell Invasion through a Ras/Mek-, PKCι/Rac 1-dependent Signaling Pathway

Zhang, Jie; Anastasiadis, Panos Z.; Liu, Yan; Thompson, E. Aubrey; Fields, Alan P.

doi:10.1074/jbc.m400774200

Cited by 126 publications

(116 citation statements)

References 42 publications

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“…Stimulation of PKC in vitro was reported to reduce SASH1 expression in primary B-lymphocytes (Lindvall et al, 2005). Interestingly, PKC may play a role in colorectal cancer formation (Zhang et al, 2004), and the homologue SLY1 is regulated by PKC (Beer et al, 2005). However, we did not detect any regulation of SASH1 expression by PMA/ionomycin stimulation in vitro in various cell lines (HeLa, HEK293, HT29, Ramos).…”

Section: Discussioncontrasting

confidence: 70%

Prognostic significance of downregulated expression of the candidate tumour suppressor gene SASH1 in colon cancer

et al. 2006

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The gene SASH1 (SAM-and SH3-domain containing 1) has originally been identified as a candidate tumour suppressor gene in breast cancer. SASH1 is a member of the SH3-domain containing expressed in lymphocytes (SLY1) gene family that encodes signal adapter proteins composed of several protein -protein interaction domains. The other members of this family are expressed mainly in haematopoietic cells, whereas SASH1 shows ubiquitous expression. We have used quantitative real-time PCR to investigate the expression of SASH1 in tissue samples from 113 patients with colon carcinoma, and compared the expression with 15 normal colon tissue samples. Moreover, nine benign adenomas and 10 liver metastases were analysed. Expression levels of SASH1 were strongly and significantly reduced in colon cancer of UICC stage II, III, and IV, as well as in liver metastases. Moreover, SASH1 was also found to be downregulated on protein levels by immunoblot analysis. However, SASH1 expression was not significantly deregulated in precancerous adenomas and in earlier stage lesions (UICC I). Overall, 48 out of 113 primary colon tumours showed SASH1 expression that was at least 10-fold lower than the levels found in normal colon tissue. Downregulation of SASH1 expression was correlated with the formation of metachronous distant metastasis, and multivariate analysis identified SASH1 downregulation as an independent negative prognostic parameter for patient survival. This study demonstrates for the first time that expression of a member of the SLY1-gene family has prognostic significance in human cancer.

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Section: Discussioncontrasting

confidence: 70%

Prognostic significance of downregulated expression of the candidate tumour suppressor gene SASH1 in colon cancer

et al. 2006

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“…We have shown that PKCi is an oncogene that is activated by amplification in squamous cell carcinoma of the lung (Regala et al, 2005a). We have also shown that PKC plays a critical role in transformed growth (Zhang et al, 2004;Regala et al, 2005b), but does not appear to function as a survival gene. In contrast, our present results show that Evi1 is a survival gene in human colon cancers that have undergone amplification of the 3q26 locus.…”

Section: Discussionmentioning

confidence: 94%

Evi1 is a survival factor which conveys resistance to both TGFβ- and taxol-mediated cell death via PI3K/AKT

Liu

Chen

et al. 2006

Oncogene

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“…Lymph nodes were harvested and CD4 T cells were isolated by negative selection (CD4 isolation kit, Miltenyii Biotec). Samples containing 2-7 ϫ 10 6 cells were lysed and basal active Rap1 was precipitated with a GST-RalGDS-RBD fusion protein (49), basal active Rac1 was precipitated with a GST-Pak1 fusion protein (50), and basal active Ras was precipitated with a GST-Raf-RBD fusion protein (51). The resulting precipitates were analyzed by Western blotting with an anti-Rap1 antibody (Santa Cruz Biotechnology, Santa Cruz, CA), an anti-Rac antibody (Upstate Biotechnology, Lake Placid, NY), and an anti-Ras antibody (Transduction Laboratories, Lexington, KY) to assess the content of the active GTPase in the samples.…”

Section: Methodsmentioning

confidence: 99%

MHC class II deprivation impairs CD4 T cell motility and responsiveness to antigen-bearing dendritic cells in vivo

Fischer

Jacovetty

Medeiros

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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The role continuous contact with self-peptide/MHC molecules (self ligands) in the periphery plays in the function of mature T cells remains unclear. Here, we elucidate a role for MHC class II molecules in T cell trafficking and antigen responsiveness in vivo. We find that naïve CD4 T cells deprived of MHC class II molecules demonstrate a progressive and profound defect in motility (measured by real-time two-photon imaging) and that these cells have a decreased ability to interact with limiting numbers of cognate antigen-bearing dendritic cells, but they do not demonstrate a defect in their responsiveness to direct stimulation with anti-CD3 monoclonal antibody. Using GST fusion proteins, we show that MHC class II availability promotes basal activation of Rap1 and Rac1 but does not alter the basal activity of Ras. We propose that tonic T cell receptor signaling from self-ligand stimulation is required to maintain a basal state of activation of small guanosine triphosphatases critical for normal T cell motility and that T cell motility is critical for the antigen receptivity of naïve CD4 T cells. These studies suggest a role for continuous self-ligand stimulation in the periphery for the maintenance and function of mature naïve CD4 T cells.GTPases ͉ MHC class II deficiency ͉ self ligand

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Protein Kinase C (PKC) βII Induces Cell Invasion through a Ras/Mek-, PKCι/Rac 1-dependent Signaling Pathway

Cited by 126 publications

References 42 publications

Prognostic significance of downregulated expression of the candidate tumour suppressor gene SASH1 in colon cancer

Prognostic significance of downregulated expression of the candidate tumour suppressor gene SASH1 in colon cancer

Evi1 is a survival factor which conveys resistance to both TGFβ- and taxol-mediated cell death via PI3K/AKT

MHC class II deprivation impairs CD4 T cell motility and responsiveness to antigen-bearing dendritic cells in vivo

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