| Data have identified protein kinase C (PKC)l/i as a tumor suppressor in advanced prostate cancer (PCa), whose loss promotes a metabolic reprogramming that prostate cancer cells exploit to sustain their increased proliferation and epigenetic needs, thus favoring cancer cell plasticity and neuroendocrine prostate cancer (NEPC) differentiation. | prostate, |
| Data demonstrate that protein kinase C (PKC) iota is required for oncogenic Ras- and carcinogen-mediated colon carcinogenesis in vivo and define a procarcinogenic signaling axis consisting of Ras, PKCiota, and Rac1. | colorectal, |
| Atypical PKCiota contributes to poor prognosis through loss of apical-basal polarity and cyclin E overexpression in ovarian cancer. | ovarian, |
| PKCiota as a potential oncogene in ovarian cancer regulating epithelial cell polarity and proliferation | ovarian, |
| Ect2 and PKCiota are genetically and functionally linked in NSCLC, acting to coordinately drive tumor cell proliferation and invasion through formation of an oncogenic PKCiota-Par6alpha-Ect2 complex. | lung, |
| The PRKCI and SOX2 oncogenes are coamplified and cooperate to activate Hedgehog signaling in lung squamous cell carcinoma. | lung, |
| The PRKCI and SOX2 oncogenes are coamplified and cooperate to activate Hedgehog signaling in lung squamous cell carcinoma. | lung, |
| Protein kinase C iota: human oncogene, prognostic marker and therapeutic target. | None |
| evidence that PKC iota is a human oncogene is discussed; review of mechanisms controlling PKC iota expression in human cancers; description of the molecular details of PKC iota-mediated oncogenic signaling [review] | None |
| Oncogenic activity of Ect2 is regulated through protein kinase C iota-mediated phosphorylation. | None |
| a model in which PKCiota-mediated phosphorylation regulates Ect2 binding to the oncogenic PKCiota-Par6 complex thereby activating Rac1 activity and driving transformed growth and invasion. | None |
| The Proto-oncogene PKCiota regulates the alternative splicing of Bcl-x pre-mRNA. | None |
| he oncogenic activity of PRKCI relates in part to the up-regulation of TNFalpha to promote an immune-suppressive tumor microenvironment characterized by an abundance of myeloid-derived suppressor cells and inhibition of cytotoxic T-cell infiltration | None |