Download Gene Section PRKCI (protein kinase C, iota) Atlas of Genetics and Cytogenetics

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Gene Section
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PRKCI (protein kinase C, iota)
Verline Justilien, Alan P Fields
Department of Cancer Biology, Mayo Clinic College of Medicine, Jacksonville, Florida, 32224 USA (VJ,
APF)
Published in Atlas Database: June 2012
Online updated version : http://AtlasGeneticsOncology.org/Genes/PRKCIID41857ch3q26.html
DOI: 10.4267/2042/48364
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 2.0 France Licence.
© 2012 Atlas of Genetics and Cytogenetics in Oncology and Haematology
Identity
Protein
Other names: DXS1179E: nPKC-iota: PKCI
HGNC (Hugo): PRKCI
Location: 3q26.2
Local order
The PRKCI gene is located between the polyhomeotic
homolog 3 gene in centromeric position and the SKIlike oncogene in telomeric position (according to
GeneLoc).
Description
PKCι consist of 596 amino acids and has a molecular
mass of 68262 Da.
PKCι is a member of the PKCs, a diverse family of
lipid dependent serine/threonine kinases.
PKCι activity can be regulated by lipid second
messengers (ceramide, phosphatidylinositol 3,4,5-P3,
and phosphatidic acid), phosphoinositide-dependent
kinase (PDK1), tyrosine phosphorylation and specific
protein-protein interactions.
The PB1 domain within the N-terminal regulatory
domain mediates protein-protein interactions between
PKCι and other PB1 domain containing proteins such
as ZIP/p62 (Hirano et al., 2004; Puls et al., 1997), Par-6
(partitioning-defective 6) (Joberty et al., 2000; Lin et
al., 2000; Noda et al., 2001; Qiu et al., 2000) and
MEK5
(MAPK
(mitogen-activated
protein
kinase)/ERK (extracellular-signal-regulated kinase)
kinase 5) (Diaz-Meco and Moscat, 2001; Hirano et al.,
2004). In the inactive state, the PKCι PS is positioned
in the substrate binding cavity in the kinase domain and
is displaced upon PKCι activation.
DNA/RNA
Description
The PRKCI gene is composed of 18 exons and spans
83618 bases on the plus strand.
Transcription
The PRKCI transcript (NM_002740) contains 4884
bases and the open reading frame spans from 239 to
2029.
Pseudogene
There is a single exon pseudogene mapped on
chromosome X.
Location sequence of PRKCI on Chromosome 3. PRKCI gene is indicated by red arrow.
Atlas Genet Cytogenet Oncol Haematol. 2012; 16(12)
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PRKCI (protein kinase C, iota)
Justilien V, Fields AP
Exon-intron structure of the PRKCI gene. Blue vertical bars correspond to exons, green bar represents 5'UTR and orange 3'UTR.
Schematic diagram showing the domain structure of PKCι. PB-1 Phox-Bem1; PS: auto-inhibitory pseudosubstrate sequence.
Phosphatidylserine binds the C1 domain to anchor
PKCι to the membrane. The PKCι catalytic domain is
subdivided into the C3 and C4 domains that mediate
ATP-binding and substrate binding.
(Yang et al., 2008) and ovarian (Eder et al., 2005;
Zhang et al., 2006) cancers. A P118L mutation was
found in a metastatic melanoma sample (Greenman et
al., 2007).
Expression
Implicated in
PKCι is widely expressed with varying levels in
different tissues (Selbie et al., 1993).
Various cancers
Localisation
Note
PKCι overexpression has been observed in numerous
human cancers including cancers of the lung (Regala et
al., 2005b), pancreas (Scotti et al., 2010), stomach
(Takagawa et al., 2010), colon (Murray et al., 2004),
esophagus (Yang et al., 2008), liver (Du et al., 2009),
bile duct (Li et al., 2008), breast (Kojima et al., 2008),
ovary (Weichert et al., 2003; Eder et al., 2005; Zhang et
al., 2006), prostate (Ishiguro et al., 2009), and brain
(Patel et al., 2008). PKCι is itself an oncogene, which
appears to be activated through tumor-specific
overexpression. In addition, however, PKCι is activated
downstream of other oncogenes including oncogenic
Ras, Bcr-Abl and Src.
PKCι is mainly expressed in the cytoplasm. PKCι is
translocated to the cell membrane in response to second
messengers and colocalizes with p62/ZIP in lysosometargeted endosomes (Sanchez et al., 1998). Src
phosphorylation leads to translocation of PKCι into the
nucleus (White et al., 2002) where it forms a complex
with Cdk7 (Win and Acevedo-Duncan, 2008).
Function
PKCι is a lipid-dependent, serine/threonine kinase.
PKCι participates a number of signaling pathways that
regulate cell survival (Sanz et al., 1999; Wooten et al.,
1999; Xie et al., 2000), differentiation (Wooten et al.,
2000), polarity (Joberty et al., 2000), and microtubule
dynamics in the early secretory pathway (Tisdale,
2002).
Non Small Cell Lung Cancer (NSCLC)
Prognosis
Elevated levels of PKCι expression correlate with poor
clinical outcome in NSCLC patients (Regala et al.,
2005b).
Cytogenetics
The PRKCI gene is amplified as part of the 3q26
amplicon in NSCLC.
Oncogenesis
PKCι is an oncogene in NSCLC. PRKCI is amplified
as part of the 3q26 amplicon in NSCLC and
amplication drives PKCι overexpression in NSCLC cell
lines and primary NSCLC tumours. PKCι is required
for transformed (anchorage-independent) growth and
invasion of human NSCLC cells (Frederick et al., 2008;
Regala et al., 2005a). Disruption of the Prkci gene
inhibits oncogenic Kras induced expansion and
transformation of tumor-initiating, lung stem-like cells.
Consequently, genetic loss of Prkci dramatically
Homology
PRKCI is highly evolutionarily conserved. PKCι and
PKCζ exhibit 72% overall amino acid sequence
homology and 86% identity within the kinase domain.
PKCι shows less homology with the other PKC
isoform, with less than 53% identity in the highly
conserved catalytic domain (Selbie et al., 1993).
Mutations
Germinal
No germline mutations in the PRKCI gene have been
reported.
Somatic
The PKCι gene is amplified as part of the 3q26
amplicon in lung (Regala et al., 2005b), esophageal
Atlas Genet Cytogenet Oncol Haematol. 2012; 16(12)
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PRKCI (protein kinase C, iota)
Justilien V, Fields AP
et al., 2010). Analysis of human PDAC cells after
orthotopic injection into the mouse pancreas revealed
that PKCι-deficient tumor cells yielded significantly
smaller tumors and significantly fewer metastases to
the kidney, liver, diaphragm and mesentery (Scotti et
al., 2010). The Rac1-MEK/ERK1/2 signaling axis is
required for PKCiota-mediated transformed growth and
cellular invasion of PDAC cells (Scotti et al., 2010).
inhibits Kras-initiated hyperplasia and subsequent lung
tumor formation in vivo. PKCι enhances resistance of
NSCLC to NNK-induced apoptosis by phosphorylating
the pro-apoptotic protein BAD (Jin et al., 2005). PKCι
forms an oncogeneic complex with Par6 that activates a
Rac1-Mek-Erk signaling axis that drives the
transformed growth and invasion of NSCLC cells in
vitro (Frederick et al., 2008; Regala et al., 2005a) and
tumorigenicity in vivo (Regala et al., 2005a). PKCι and
the oncogene ECT2 are genetically linked through
coordinate gene amplification as part of the 3q26
amplicon in NSCLC tumors (Justilien and Fields,
2009). PKCι phosphorylates Ect2 and forms an
oncogenic PKCι-Par6-Ect2 complex that drives
NSCLC cell transformation by activating Rac1
(Justilien and Fields, 2009; Justilien et al., 2011).
Expression of MMP10 is regulated through the PKCιPar6-Rac1 signaling axis and MMP10 represents a key
downstream effector in PKCι mediated transformation
in lung cancer cells that is required for transformed
growth and invasion (Frederick et al., 2008). PKCι also
regulates expression of COPB2, ELF3, RFC4, and
PLS1 in primary lung adenocarcinoma (Erdogan et al.,
2009). The PKCι inhibitor aurothiomalate (ATM)
disrupts the PB1-PB1 domain interaction between
PKCι and Par6 and inhibits PKCι-mediated Rac1
activation and blocks anchorage-independent growth of
NSCLC cells in vitro and tumorigenicity in vivo
(Erdogan et al., 2006; Stallings-Mann, 2006).
Ovarian cancer
Prognosis
PKCι expression is a strong predictor of survival when
combined in a multi-variate analysis with tumor cyclin
E expression (Eder et al., 2005).
Cytogenetics
The PRKCI gene is amplified as part of the 3q26
amplicon in ovarian cancer (Eder et al., 2005).
Oncogenesis
PKCι is frequently overexpressed in patients with
ovarian cancer (Eder et al., 2005; Weichert et al., 2003;
Zhang et al., 2006). PKCι expression in ovarian cancer
patients correlates with tumor stage suggesting the
involvement of PKCι in tumor progression and
aggressiveness (Eder et al., 2005; Weichert et al., 2003;
Zhang et al., 2006). Decreased PKCι expression
reduced anchorage-independent growth of ovarian
cancer cells, whereas overexpression of PKCι
promoted murine ovarian surface epithelium
transformation (Zhang et al., 2006).
Colon cancer
Chronic myelogenous leukemia
Oncogenesis
PKCι expression is elevated in human colon tumors,
AOM-induced colon tumors in mice (Murray et al.,
2004) and intestinal tumors in APCMin/+ mice (Murray
et al., 2009; Oster and Leitges, 2006). Expression of
caPKCι in the colonic epithelium of mice led to an
increase in the number of AOM-induced colon tumors,
and promoted tumor progression from benign adenoma
to malignant intramucosal carcinoma (Murray et al.,
2004) PKCι is required for oncogenic Ras-mediated
transformation of the intestinal epithelium in vitro and
in vivo. PKCι is also required for the formation of
intestinal tumors in APCMin/+ mice (Murray et al.,
2009).
Oncogenesis
PKCι is highly expressed in human K562 leukemia
cells and functions as a survival gene in chronic
myelogenous leukemia (CML). The chimeric tyrosine
kinase oncogene Bcr-Abl activates a Ras/Mek/Erk
signaling pathway that stimulates PKCι expression
through an Elk1 transcription factor site in the proximal
promoter of PKCι (Gustafson et al., 2004). Bcr-Abl
activation of PKCι is necessary and sufficient to
mediate apoptotic resistance to chemotherapy in K562
CML cells (Murray and Fields, 1997).
Gliomas
Oncogenesis
PKCι is overexpressed in glioblastoma multiforme.
PKCι is required for survival and chemoresistance of
glioblastoma cells. Genetic disruption of PKCι
expression results in sensitization of glioblastoma cells
to cisplatin (Baldwin et al., 2008). RNAi mediated
depletion of PKCι also blocks the proliferative and
invasive properties of glioma cell lines in vitro
(Baldwin et al., 2008; Patel et al., 2008). PKCι
promotes survival in glioblastoma cells through
attenuation of p38 mitogen-activated protein kinase
signaling that protects these cells against cytotoxicity to
chemotherapeutic agents (Baldwin et al., 2008).
Pancreatic cancer
Prognosis
PKCι overexpression predicts poor survival in
pancreatic cancer patients (Scotti et al., 2010).
Oncogenesis
PKCι is significantly overexpressed in human
pancreatic cancer. Knock down of PKCι expression
using lentiviral-mediated shRNA blocked transformed
(anchorage-independent) growth and invasion of
human Pancreatic Ductal Adenocarcinoma (PDAC)
cells (Scotti et al., 2010). Disruption of PKCι
expression also blocks tumorigenicity of PDAC cell
tumors injected orthotopically into the pancreas (Scotti
Atlas Genet Cytogenet Oncol Haematol. 2012; 16(12)
915
PRKCI (protein kinase C, iota)
Justilien V, Fields AP
Esophageal cancer
Noda Y, Takeya R, Ohno S, Naito S, Ito T, Sumimoto H.
Human homologues of the Caenorhabditis elegans cell polarity
protein PAR6 as an adaptor that links the small GTPases Rac
and Cdc42 to atypical protein kinase C. Genes Cells. 2001
Feb;6(2):107-19
Cytogenetics
PRKCI gene is amplified as part of the 3q26 amplicon
(Yang et al., 2008).
Oncogenesis
PRKCI is amplified in 53% of esophageal squamous
cell carcinomas (ESCC) and PKCι protein expression
correlated with PRKCI gene amplification in these
tumors (Yang et al., 2008). Examination of
clinicopathologic features of ESCC tumors revealed a
significant correlation between PRKCI expression and
larger tumor size, later stage and lymph node
metastasis suggesting that PRKCI overexpression is a
hallmark of tumor progression and metastasis in ESCC
(Yang et al., 2008).
Tisdale EJ. Glyceraldehyde-3-phosphate dehydrogenase is
phosphorylated by protein kinase Ciota /lambda and plays a
role in microtubule dynamics in the early secretory pathway. J
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White WO, Seibenhener ML, Wooten MW. Phosphorylation of
tyrosine 256 facilitates nuclear import of atypical protein kinase
C. J Cell Biochem. 2002;85(1):42-53
Weichert W, Gekeler V, Denkert C, Dietel M, Hauptmann S.
Protein kinase C isoform expression in ovarian carcinoma
correlates with indicators of poor prognosis. Int J Oncol. 2003
Sep;23(3):633-9
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This article should be referenced as such:
Justilien V, Fields AP. PRKCI (protein kinase C, iota). Atlas
Genet Cytogenet Oncol Haematol. 2012; 16(12):913-917.
Yang YL, Chu JY, Luo ML, Wu YP, Zhang Y, Feng YB, Shi ZZ,
Xu X, Han YL, Cai Y, Dong JT, Zhan QM, Wu M, Wang MR.
Atlas Genet Cytogenet Oncol Haematol. 2012; 16(12)
917