The overexpression and altered localization of the atypical protein kinase C λ/ι in breast cancer correlates with the pathologic type of these tumors

Kojima, Yasuyuki; Akimoto, Kazunori; Nagashima, Yoji; Ishiguro, Hitoshi; Shirai, Sumiko; Chishima, Takashi; Ichikawa, Yasushi; Ishikawa, Takashi; Sasaki, Takeshi; Kubota, Yoshinobu; Inayama, Yoshiaki; Aoki, Ichiro; Ohno, Shigeo; Shimada, Hiroshi

doi:10.1016/j.humpath.2007.11.001

Cited by 89 publications

(89 citation statements)

References 28 publications

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“…Overexpression of PKCi in breast cancer has been reported previously by Kojima et al (2008). Our findings are consistent with the results of this previous study, except that we observed PKCi overexpression in ductal carcinoma in situ.…”

Section: Discussionsupporting

confidence: 93%

Repression of cancer cell senescence by PKCι

et al. 2011

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Section: Discussionsupporting

confidence: 93%

Repression of cancer cell senescence by PKCι

et al. 2011

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“…In previous studies, we implicated the exocyst complex in MT1-MMP trafficking to invadopodia in MDA-MB-231 breast-tumor cells (15) and identified a coordinated function of the exocyst complex and aPKCζ/ι in migrating cells (19). MT1-MMP and aPKCι are overexpressed in various cancers, including breast cancers, and up-regulation is associated with poor prognosis (8,9,22,24). These data suggested the possible interplay between MT1-MMP and aPKCζ/ι in the invasive program of breast-tumor cells.…”

Section: Co-up-regulation Of Mt1-mmp and Apkcι Mrnas Is Associated Withmentioning

confidence: 93%

“…In addition, several lines of evidence implicate aPKCζ/ι in cancer: aPKCς is required for epidermal growth factor-induced chemotaxis of human breast-cancer cells (20), and aPKCζ/ι promotes matrix degradation by Src-transformed mouse NIH 3T3 fibroblasts (21). Moreover, aPKCι expression is up-regulated in various cancers, including breast cancer, and correlates with poor prognosis (22,23). The ability of aPKCζ/ι to control both cell polarity and the migration of cells makes it a prime candidate for a role in tumor progression and metastasis although the specific functions of aPKCζ/ι in metastatic cells are currently only poorly understood.…”

Section: Significancementioning

confidence: 99%

Control of MT1-MMP transport by atypical PKC during breast-cancer progression

Rossé

Lodillinsky

Fuhrmann

et al. 2014

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

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Dissemination of carcinoma cells requires the pericellular degradation of the extracellular matrix, which is mediated by membrane type 1-matrix metalloproteinase (MT1-MMP). In this article, we report a co-up-regulation and colocalization of MT1-MMP and atypical protein kinase C iota (aPKCι) in hormone receptor-negative breast tumors in association with a higher risk of metastasis. Silencing of aPKC in invasive breast-tumor cell lines impaired the delivery of MT1-MMP from late endocytic storage compartments to the surface and inhibited matrix degradation and invasion. We provide evidence that aPKCι, in association with MT1-MMP-containing endosomes, phosphorylates cortactin, which is present in F-actin-rich puncta on MT1-MMP-positive endosomes and regulates cortactin association with the membrane scission protein dynamin-2. Thus, cell line-based observations and clinical data reveal the concerted activity of aPKC, cortactin, and dynamin-2, which control the trafficking of MT1-MMP from late endosome to the plasma membrane and play an important role in the invasive potential of breast-cancer cells.membrane traffic | actin cytoskeleton | multi-vesicular body | MMP14

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“…Indeed, upregulation of aPKC is observed in non-small-cell lung cancers (Regala et al, 2005) and in ovarian cancers, where it correlates with the upregulation of CycE and poor prognosis (Eder et al, 2005). Furthermore, aPKCl/i is upregulated in invasive ductal carcinoma of the breast (Kojima et al, 2008). As to the Crumbs complex in mammalian cells, Crumbs3 is important in tight junction establishment, and overexpression leads to a delay in tight junction assembly and loss of cell polarity in MDCK epithelial cells (Roh et al, 2003).…”

Section: Scribble/dlg/lgl and Other Polarity Complexesmentioning

confidence: 99%

Control of tumourigenesis by the Scribble/Dlg/Lgl polarity module

et al. 2008

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The neoplastic tumour suppressors, Scribble, Dlg and Lgl, originally discovered in the vinegar fly Drosophila melanogaster, are currently being actively studied for their potential role in mammalian tumourigenesis. In Drosophila, these tumour suppressors function in a common genetic pathway to regulate apicobasal cell polarity and also play important roles in the control of cell proliferation, survival, differentiation and in cell migration/invasion. The precise mechanism by which Scribble, Dlg and Lgl function is not clear; however, they have been implicated in the regulation of signalling pathways, vesicle trafficking and in the Myosin II-actin cytoskeleton. We review the evidence for the involvement of Scribble, Dlg, and Lgl in cancer, and how the various functions ascribed to these tumour suppressors in Drosophila and mammalian systems may impact on the process of tumourigenesis.

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The overexpression and altered localization of the atypical protein kinase C λ/ι in breast cancer correlates with the pathologic type of these tumors

Cited by 89 publications

References 28 publications

Repression of cancer cell senescence by PKCι

Repression of cancer cell senescence by PKCι

Control of MT1-MMP transport by atypical PKC during breast-cancer progression

Control of tumourigenesis by the Scribble/Dlg/Lgl polarity module

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