Protein kinase Cε makes the life and death decision

Abstract

Cancer is caused by dysregulation in cellular signaling systems that control cell proliferation, differentiation and cell death. Protein kinase C (PKC), a family of serine/threonine kinases, plays an important role in the growth factor signal transduction pathway. PKCε, however, is the only PKC isozyme that has been considered as an oncogene. It can contribute to malignancy by enhancing cell proliferation or by inhibiting cell death. This review focuses on how PKCε collaborates with other signaling pathways, such as Ras/Raf/ERK and Akt, to regulate cell survival and cell death. We have also discussed how PKCε mediates is antiapoptotic signal by altering the level or function of proand antiapoptotic Bcl-2 family members.

Intracellular Interaction of Interleukin (IL)-32α with Protein Kinase Cϵ (PKCϵ) and STAT3 Protein Augments IL-6 Production in THP-1 Promonocytic Cells

“…A variety of tissues, such as those of the nervous, cardiac, and immune systems, express PKC⑀, and the role of PKC⑀ is important for their proper function (19 -22). PKC⑀ may be a useful therapeutic target to treat disease conditions, such as inflammation (19), ischemia (23), addiction (24), pain (25), anxiety (26,27), and cancer (28,29).…”

PKC and Cancer: Time for a Comeback?

“…Preneoplastic lesions observed in prostate PKCe transgenic mice display high levels of phosphoAkt, and overexpression of PKCe in non-transformed prostate epithelial cells leads to growth advantage as well as enhanced phospho-Erk and phospho-Akt levels. PKCe-depleted cells lose their ability to form tumors in nude mice or display reduced tumor growth kinetics, as shown using breast, lung and prostate cancer cellular models (4,8,14,15).…”

“…RNAi-mediated silencing of PKCe reduces the ability of cancer cells to migrate and invade. The loss of aggressive phenotype may reflect impaired ability to activate small GTPases implicated in migration, such as Rac, as well as reduced secretion of metalloproteinases involved in the degradation of the extracellular matrix (4,13,(15)(16)(17).…”

Protein Kinase Cε Regulates Proliferation and Cell Sensitivity to TGF-1β of CD4+ T Lymphocytes: Implications for Hashimoto Thyroiditis

“…P rotein kinase C (PKC) is a family of phospholipiddependent serine/threonine kinases that regulate a wide variety of cellular functions (1). The PKC family consists of at least 11 members that have been categorized into three groups based on their structure and biochemical properties, and named conventional, novel, and atypical PKCs.…”

“…The PKC family consists of at least 11 members that have been categorized into three groups based on their structure and biochemical properties, and named conventional, novel, and atypical PKCs. Conventional PKCs (a, bI, bII, and g) require Ca 2+ and diacylglycerol (DAG) for their activation, novel PKCs (d, ε, h, u) are dependent on DAG but not Ca 2+ , whereas atypical PKCs (z, l/i) are independent of both Ca 2+ and DAG (1).…”