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Article ; Online: Protein kinase C delta enhances the diagnostic performance of hepatocellular carcinoma.

Nakagawa, Chika / Oikawa, Tsunekazu / Yamada, Kohji / Tsubota, Akihito / Saeki, Chisato / Katagiri, Kuniko / Tago, Naoko / Kamioka, Hiroshi / Ueda, Kaoru / Haruki, Koichiro / Furukawa, Kenei / Nakano, Masanori / Torisu, Yuichi / Ikegami, Toru / Yoshida, Kiyotsugu / Saruta, Masayuki

Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals

2024 Volume 29, Issue 2, Page(s) 55–67

Abstract: ... to assess the usefulness of serum protein kinase C delta (PKCδ) for detecting these HCCs.: Methods: PKCδ ... with early-stage HCC; low sensitivity for AFP with HCC after eliminating hepatitis C virus (HCV); low ... Background: The conventional markers for hepatocellular carcinoma (HCC), α-fetoprotein (AFP) and ...

Abstract	Background: The conventional markers for hepatocellular carcinoma (HCC), α-fetoprotein (AFP) and des-γ-carboxy prothrombin (DCP), have several limitations; both have low sensitivity in patients with early-stage HCC; low sensitivity for AFP with HCC after eliminating hepatitis C virus (HCV); low specificity for DCP in patients with non-viral HCC, which is increasing worldwide; low specificity for AFP in patients with liver injury; and low specificity for DCP in patients treated with warfarin. To overcome these issues, the identification of novel biomarkers is an unmet need. Objective: This study aimed to assess the usefulness of serum protein kinase C delta (PKCδ) for detecting these HCCs. Methods: PKCδ levels were measured using a sandwich enzyme-linked immunosorbent assay in 363 chronic liver disease (CLD) patients with and without HCC. Results: In both viral and non-viral CLD, PKCδ can detect HCCs with high sensitivity and specificity, particularly in the very early stages. Notably, the value and sensitivity of PKCδ were not modified by HCV elimination status. Liver injury and warfarin administration, which are known to cause false-positive results for conventional markers, did not modify PKCδ levels. Conclusions: PKCδ is an enhanced biomarker for the diagnosis of HCC that compensates for the drawbacks of conventional markers.
MeSH term(s)	Humans ; Carcinoma, Hepatocellular/diagnosis ; Carcinoma, Hepatocellular/pathology ; alpha-Fetoproteins ; Biomarkers, Tumor ; Liver Neoplasms/diagnosis ; Liver Neoplasms/pathology ; Protein Kinase C-delta ; Warfarin ; Sensitivity and Specificity ; Protein Precursors ; Biomarkers ; Hepatitis C ; Prothrombin/metabolism
Chemical Substances	alpha-Fetoproteins ; Biomarkers, Tumor ; Protein Kinase C-delta (EC 2.7.11.13) ; Warfarin (5Q7ZVV76EI) ; Protein Precursors ; Biomarkers ; Prothrombin (9001-26-7)
Language	English
Publishing date	2024-02-15
Publishing country	England
Document type	Journal Article
ZDB-ID	1324372-x
ISSN	1366-5804 ; 1354-750X
ISSN (online)	1366-5804
ISSN	1354-750X
DOI	10.1080/1354750X.2024.2312990
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Zs.A 4864: Show issues

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Article ; Online: The metabolomics of a protein kinase C delta (PKCδ) knock-out mouse model.

Loots, Du Toit / Adeniji, Adetomiwa Ayodele / Van Reenen, Mari / Ozturk, Mumin / Brombacher, Frank / Parihar, Suraj P

Metabolomics : Official journal of the Metabolomic Society

2022 Volume 18, Issue 11, Page(s) 92

Abstract: Introduction: PKCδ is ubiquitously expressed in mammalian cells and its dysregulation plays a key role in the onset of several incurable diseases and metabolic disorders. However, much remains unknown about the metabolic pathways and disturbances ... ...

Abstract	Introduction: PKCδ is ubiquitously expressed in mammalian cells and its dysregulation plays a key role in the onset of several incurable diseases and metabolic disorders. However, much remains unknown about the metabolic pathways and disturbances induced by PKC deficiency, as well as the metabolic mechanisms involved. Objectives: This study aims to use metabolomics to further characterize the function of PKC from a metabolomics standpoint, by comparing the full serum metabolic profiles of PKC deficient mice to those of wild-type mice. Methods: The serum metabolomes of PKCδ knock-out mice were compared to that of a wild-type strain using a GCxGC-TOFMS metabolomics research approach and various univariate and multivariate statistical analyses. Results: Thirty-seven serum metabolite markers best describing the difference between PKCδ knock-out and wild-type mice were identified based on a PCA power value > 0.9, a t-test p-value < 0.05, or an effect size > 1. XERp prediction was also done to accurately select the metabolite markers within the 2 sample groups. Of the metabolite markers identified, 78.4% (29/37) were elevated and 48.65% of these markers were fatty acids (18/37). It is clear that a total loss of PKCδ functionality results in an inhibition of glycolysis, the TCA cycle, and steroid synthesis, accompanied by upregulation of the pentose phosphate pathway, fatty acids oxidation, cholesterol transport/storage, single carbon and sulphur-containing amino acid synthesis, branched-chain amino acids (BCAA), ketogenesis, and an increased cell signalling via N-acetylglucosamine. Conclusion: The charaterization of the dysregulated serum metabolites in this study, may represent an additional tool for the early detection and screening of PKCδ-deficiencies or abnormalities.
MeSH term(s)	Mice ; Animals ; Metabolomics/methods ; Protein Kinase C-delta/genetics ; Mice, Knockout ; Metabolome ; Biomarkers ; Fatty Acids ; Mammals
Chemical Substances	Protein Kinase C-delta (EC 2.7.11.13) ; Biomarkers ; Fatty Acids
Language	English
Publishing date	2022-11-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	2250617-2
ISSN	1573-3890 ; 1573-3882
ISSN (online)	1573-3890
ISSN	1573-3882
DOI	10.1007/s11306-022-01949-w
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Zs.A 6361: Show issues

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Article ; Online: Protein kinase C delta regulates mononuclear phagocytes and hinders response to immunotherapy in cancer.

Chaib, Mehdi / Holt, Jeremiah R / Fisher, Emilie L / Sipe, Laura M / Bohm, Margaret S / Joseph, Sydney C / Simmons, Boston W / Eugin Simon, Samson / Yarbro, Johnathan R / Tanveer, Ubaid / Halle, Jessica L / Carson, James A / Hollingsworth, T J / Wei, QingQing / Rathmell, Jeffrey C / Thomas, Paul G / Hayes, D Neil / Makowski, Liza

Science advances

2023 Volume 9, Issue 51, Page(s) eadd3231

Abstract: ... an effective strategy to enhance ICB efficacy. We report that protein kinase C delta (PKCδ ... a serine/threonine kinase, is abundantly expressed by MPs in human and mouse tumors. PKCδ ...

Abstract	Mononuclear phagocytes (MPs) play a crucial role in tissue homeostasis; however, MPs also contribute to tumor progression and resistance to immune checkpoint blockade (ICB). Targeting MPs could be an effective strategy to enhance ICB efficacy. We report that protein kinase C delta (PKCδ), a serine/threonine kinase, is abundantly expressed by MPs in human and mouse tumors. PKCδ
MeSH term(s)	Mice ; Humans ; Animals ; Protein Kinase C-delta/genetics ; Protein Kinase C-delta/metabolism ; Signal Transduction ; Neoplasms/therapy ; Immunotherapy ; Phagocytes
Chemical Substances	Protein Kinase C-delta (EC 2.7.11.13)
Language	English
Publishing date	2023-12-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.add3231
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Article ; Online: Inhibition of protein kinase C delta leads to cellular senescence to induce anti-tumor effects in colorectal cancer.

Shimoyama, Yuya / Yamada, Kohji / Yoshida, Saishu / Kawamura, Akira / Hannya, Yoshito / Imaizumi, Yuta / Kumamoto, Tomotaka / Takeda, Yasuhiro / Shimoda, Masayuki / Eto, Ken / Yoshida, Kiyotsugu

Cancer science

2023 Volume 114, Issue 6, Page(s) 2471–2484

Abstract: Protein kinase C delta (PKCδ) is a multifunctional serine-threonine kinase implicated ... We found that PKCδ activates p21 via a p53-independent pathway and that PKCδ-kinase activity is essential ... detection. Finally, a kinase inhibitor of PKCδ suppressed senescence-dependent tumorigenicity in a dose ...

Abstract	Protein kinase C delta (PKCδ) is a multifunctional serine-threonine kinase implicated in cell proliferation, differentiation, tumorigenesis, and therapeutic resistance. However, the molecular mechanism of PKCδ in colorectal cancer (CRC) remains unclear. In this study, we showed that PKCδ acts as a negative regulator of cellular senescence in p53 wild-type (wt-p53) CRC. Immunohistochemical analysis revealed that PKCδ levels in human CRC tissues were higher than those in the surrounding normal tissues. Deletion studies have shown that cell proliferation and tumorigenesis in wt-p53 CRC is sensitive to PKCδ expression. We found that PKCδ activates p21 via a p53-independent pathway and that PKCδ-kinase activity is essential for p21 activity. In addition, both repression of PKCδ expression and inhibition of PKCδ activity induced cellular senescence-like phenotypes, including increased senescence-associated β-galactosidase (SA-β-gal) staining, low LaminB1 expression, large nucleus size, and senescence-associated secretory phenotype (SASP) detection. Finally, a kinase inhibitor of PKCδ suppressed senescence-dependent tumorigenicity in a dose-dependent manner. These results offer a mechanistic insight into CRC survival and tumorigenesis. In addition, a novel therapeutic strategy for wt-p53 CRC is proposed.
MeSH term(s)	Humans ; Protein Kinase C-delta/genetics ; Protein Kinase C-delta/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Cyclin-Dependent Kinase Inhibitor p21/genetics ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Cellular Senescence/genetics ; Colorectal Neoplasms/pathology ; Carcinogenesis
Chemical Substances	Protein Kinase C-delta (EC 2.7.11.13) ; Tumor Suppressor Protein p53 ; Cyclin-Dependent Kinase Inhibitor p21
Language	English
Publishing date	2023-03-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2115647-5
ISSN	1349-7006 ; 1349-7006
ISSN (online)	1349-7006
ISSN	1349-7006
DOI	10.1111/cas.15768
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Article ; Online: Protein kinase C delta mediates Pasireotide effects in an ACTH-secreting pituitary tumor cell line.

Gentilin, E / Borges De Souza, P / Ambrosio, M R / Bondanelli, M / Gagliardi, I / Zatelli, M C

Journal of endocrinological investigation

2023 Volume 46, Issue 12, Page(s) 2609–2616

Abstract: ... that the delta isoform of protein kinase C (PRKCD) controls viability and cell cycle progression of an in vitro ...

Abstract	Purpose: Clinical control of corticotroph tumors is difficult to achieve since they usually persist or relapse after surgery. Pasireotide is approved to treat patients with Cushing's disease for whom surgical therapy is not an option. However, Pasireotide seems to be effective only in a sub-set of patients, highlighting the importance to find a response marker to this approach. Recent studies demonstrated that the delta isoform of protein kinase C (PRKCD) controls viability and cell cycle progression of an in vitro model of ACTH-secreting pituitary tumor, the AtT-20/D16v-F2 cells. This study aims at exploring the possible PRKCD role in mediating Pasireotide effects. Methods: It was assessed cell viability, POMC expression and ACTH secretion in AtT20/D16v-F2 cells over- or under-expressing PRKCD. Results: We found that Pasireotide significantly reduces AtT20/D16v-F2 cell viability, POMC expression and ACTH secretion. In addition, Pasireotide reduces miR-26a expression. PRKCD silencing decreases AtT20/D16v-F2 cell sensitivity to Pasireotide treatment; on the contrary, PRKCD overexpression increases the inhibitory effects of Pasireotide on cell viability and ACTH secretion. Conclusion: Our results provide new insights into potential PRKCD contribution in Pasireotide mechanism of action and suggest that PRKCD might be a possible marker of therapeutic response in ACTH-secreting pituitary tumors.
MeSH term(s)	Humans ; Pituitary Neoplasms/pathology ; Corticotrophs/metabolism ; Corticotrophs/pathology ; Protein Kinase C-delta/metabolism ; Protein Kinase C-delta/pharmacology ; Protein Kinase C-delta/therapeutic use ; Pro-Opiomelanocortin/genetics ; Pro-Opiomelanocortin/metabolism ; Pro-Opiomelanocortin/pharmacology ; Adrenocorticotropic Hormone/metabolism ; Neoplasm Recurrence, Local/pathology ; Cell Line ; Pituitary ACTH Hypersecretion/metabolism ; Cell Line, Tumor
Chemical Substances	pasireotide (98H1T17066) ; Protein Kinase C-delta (EC 2.7.11.13) ; Pro-Opiomelanocortin (66796-54-1) ; Adrenocorticotropic Hormone (9002-60-2)
Language	English
Publishing date	2023-05-26
Publishing country	Italy
Document type	Journal Article
ZDB-ID	432272-1
ISSN	1720-8386 ; 0391-4097 ; 1121-1369
ISSN (online)	1720-8386
ISSN	0391-4097 ; 1121-1369
DOI	10.1007/s40618-023-02117-0
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Zs.A 1480: Show issues

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Article ; Online: The Role of Tyrosine Phosphorylation of Protein Kinase C Delta in Infection and Inflammation.

Yang, Qingliang / Langston, Jordan C / Tang, Yuan / Kiani, Mohammad F / Kilpatrick, Laurie E

International journal of molecular sciences

2019 Volume 20, Issue 6

Abstract: Protein Kinase C (PKC) is a family composed of phospholipid-dependent serine/threonine kinases ... and these kinases can be positive or negative regulators of signaling pathways. The delta isoform ...

Abstract	Protein Kinase C (PKC) is a family composed of phospholipid-dependent serine/threonine kinases that are master regulators of inflammatory signaling. The activity of different PKCs is context-sensitive and these kinases can be positive or negative regulators of signaling pathways. The delta isoform (PKCδ) is a critical regulator of the inflammatory response in cancer, diabetes, ischemic heart disease, and neurodegenerative diseases. Recent studies implicate PKCδ as an important regulator of the inflammatory response in sepsis. PKCδ, unlike other members of the PKC family, is unique in its regulation by tyrosine phosphorylation, activation mechanisms, and multiple subcellular targets. Inhibition of PKCδ may offer a unique therapeutic approach in sepsis by targeting neutrophil-endothelial cell interactions. In this review, we will describe the overall structure and function of PKCs, with a focus on the specific phosphorylation sites of PKCδ that determine its critical role in cell signaling in inflammatory diseases such as sepsis. Current genetic and pharmacological tools, as well as in vivo models, that are used to examine the role of PKCδ in inflammation and sepsis are presented and the current state of emerging tools such as microfluidic assays in these studies is described.
MeSH term(s)	Allosteric Regulation ; Animals ; Humans ; Neutrophils/metabolism ; Phosphorylation ; Protein Kinase C-delta/chemistry ; Protein Kinase C-delta/metabolism ; Sepsis/metabolism ; Signal Transduction
Chemical Substances	Protein Kinase C-delta (EC 2.7.11.13)
Language	English
Publishing date	2019-03-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms20061498
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Article ; Online: Ghrelin Represses Thymic Stromal Lymphopoietin Gene Expression through Activation of Glucocorticoid Receptor and Protein Kinase C Delta in Inflamed Skin Keratinocytes.

Jeong, Hayan / Chong, Hyo-Jin / So, Jangho / Jo, Yejin / Yune, Tae-Young / Ju, Bong-Gun

International journal of molecular sciences

2022 Volume 23, Issue 7

Abstract: ... promoter. In addition, ghrelin-induced protein kinase C δ (PKCδ)-mediated phosphorylation of p300 at serine ...

Abstract	Ghrelin, a peptide hormone secreted from enteroendocrine cells of the gastrointestinal tract, has anti-inflammatory activity in skin diseases, including dermatitis and psoriasis. However, the molecular mechanism underlying the beneficial effect of ghrelin on skin inflammation is not clear. In this study, we found that ghrelin alleviates atopic dermatitis (AD)-phenotypes through suppression of thymic stromal lymphopoietin (TSLP) gene activation. Knockdown or antagonist treatment of growth hormone secretagogue receptor 1a (GHSR1a), the receptor for ghrelin, suppressed ghrelin-induced alleviation of AD-like phenotypes and suppression of TSLP gene activation. We further found that ghrelin induces activation of the glucocorticoid receptor (GR), leading to the binding of GR with histone deacetylase 3 (HDAC3) and nuclear receptor corepressor (NCoR) NCoR corepressor to negative glucocorticoid response element (nGRE) on the TSLP gene promoter. In addition, ghrelin-induced protein kinase C δ (PKCδ)-mediated phosphorylation of p300 at serine 89 (S89), which decreased the acetylation and DNA binding activity of nuclear factor- κB (NF-κB) p65 to the TSLP gene promoter. Knockdown of PKCδ abolished ghrelin-induced suppression of TSLP gene activation. Our study suggests that ghrelin may help to reduce skin inflammation through GR and PKCδ-p300-NF-κB-mediated suppression of TSLP gene activation.
MeSH term(s)	Cytokines/metabolism ; Dermatitis, Atopic/drug therapy ; Dermatitis, Atopic/genetics ; Dermatitis, Atopic/metabolism ; Gene Expression ; Ghrelin/genetics ; Ghrelin/metabolism ; Ghrelin/pharmacology ; Humans ; Inflammation/genetics ; Inflammation/metabolism ; Keratinocytes/metabolism ; NF-kappa B/metabolism ; Protein Kinase C-delta/genetics ; Protein Kinase C-delta/metabolism ; Receptors, Glucocorticoid/genetics ; Receptors, Glucocorticoid/metabolism ; Skin/metabolism
Chemical Substances	Cytokines ; Ghrelin ; NF-kappa B ; Receptors, Glucocorticoid ; Protein Kinase C-delta (EC 2.7.11.13) ; thymic stromal lymphopoietin (GT0IL38SP4)
Language	English
Publishing date	2022-04-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23073977
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Article: Reduced protein kinase C delta association with a higher molecular weight complex in mitochondria of Barth Syndrome lymphoblasts.

Mejia, Edgard M / Zegallai, Hana M / Sparagna, Genevieve C / Hatch, Grant M

bioRxiv : the preprint server for biology

2021

Abstract: The protein kinase C delta (PKCδ) signalosome exists as a high molecular weight complex ... protein expression. We hypothesize that the lack of PKCδ within this higher molecular weight complex ...

Abstract	The protein kinase C delta (PKCδ) signalosome exists as a high molecular weight complex in mitochondria and controls mitochondrial oxidative phosphorylation. Barth Syndrome (BTHS) is a rare X-linked genetic disease in which mitochondrial oxidative phosphorylation is impaired due to a mutation in the gene TAFAZZIN which results in reduction in the phospholipid cardiolipin and an accumulation of monolysocardiolipin. Here we examined if PKCδ association with a higher molecular weight complex was altered in mitochondria of BTHS lymphoblasts. Immunoblot analysis of blue native-polyacrylamide gel electrophoresis mitochondrial fractions revealed that PKCδ associated with a higher molecular weight complex in control lymphoblasts but this was markedly reduced in BTHS patient B lymphoblasts in spite of an increase in PKCδ protein expression. We hypothesize that the lack of PKCδ within this higher molecular weight complex may contribute to defective mitochondrial PKCδ signaling and thus to the bioenergetic defects observed in BTHS.
Language	English
Publishing date	2021-07-21
Publishing country	United States
Document type	Preprint
DOI	10.1101/2021.07.21.453087
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Article ; Online: Receptor interacting protein kinase 4 promotes cell proliferation, migration, and invasion in ovarian cancer via targeting protein kinase C delta.

Jin, Aihong / Zhang, Longhui / Fang, Guangguang / Chen, Yinzi

Drug development research

2021 Volume 83, Issue 2, Page(s) 407–415

Abstract: ... performed to detect the expressions of RIPK4 and protein kinase C delta (PRKCD) in OC cells. In addition ... Receptor interacting protein kinase 4 (RIPK4) has been reported to function as an oncogenic role ...

Abstract	Receptor interacting protein kinase 4 (RIPK4) has been reported to function as an oncogenic role in several types of cancers. The aim of this study was to evaluate the role of RIPK4 in ovarian cancer (OC) cells and to elucidate the mechanism behind this effect. In this study, the GEPIA database was used to analyze the RIPK4 expressions in OC tissues and overall survival. qRT-PCR and western blot assay were performed to detect the expressions of RIPK4 and protein kinase C delta (PRKCD) in OC cells. In addition, cell proliferation was assessed by CCK-8 and colony formation assay while cell invasion and migration were evaluated by transwell, wound healing and western blot assay. The interaction of RIPK4 and PRKCD was analyzed by the STRING database and the bioGRID database, and verified with co-immunoprecipitation. Herein, we describe that RIPK4 expression was upregulated in OC tissues and cells and was associated with poor overall survival. RIPK4 silencing repressed the proliferation, migration, and invasion of OC cells. Mechanistically, PRKCD was highly expressed in OC cells and was combined with RIPK4. PRKCD was highly positively associated with RIPK4 in OC and was regulated by RIPK4. Moreover, PRKCD overexpression reversed the inhibitory effects of RIPK4 silencing on OC cell proliferation, migration, and invasion. RIPK4 functions as an oncogene in OC cells via at least partially binding to PRKCD, which might represent a novel therapeutic strategy for improving survival for patients with OC.
MeSH term(s)	Carcinoma, Ovarian Epithelial/metabolism ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Female ; Humans ; Ovarian Neoplasms/genetics ; Protein Kinase C-delta/genetics ; Protein Serine-Threonine Kinases/metabolism
Chemical Substances	RIPK4 protein, human (EC 2.7.1.-) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Protein Kinase C-delta (EC 2.7.11.13)
Language	English
Publishing date	2021-08-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	604587-x
ISSN	1098-2299 ; 0272-4391
ISSN (online)	1098-2299
ISSN	0272-4391
DOI	10.1002/ddr.21871
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Zs.B 2542: Show issues

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Article ; Online: Role of alternatively spliced, pro-survival Protein Kinase C delta VIII (PKCδVIII) in ovarian cancer.

Patel, Rekha S / Rupani, Rea / Impreso, Sabrina / Lui, Ashley / Patel, Niketa A

FASEB bioAdvances

2021 Volume 4, Issue 4, Page(s) 235–253

Abstract: Ovarian cancer is the deadliest malignant disease in women. Protein Kinase C delta (PRKCD; PKCδ) is ... serine/threonine kinase extensively linked to various cancers. In humans, PKCδ is alternatively spliced to PKCδI and ... signaling kinase PKCδVIII is a viable target to develop therapeutics to combat progression of ovarian cancer. ...

Abstract	Ovarian cancer is the deadliest malignant disease in women. Protein Kinase C delta (PRKCD; PKCδ) is serine/threonine kinase extensively linked to various cancers. In humans, PKCδ is alternatively spliced to PKCδI and PKCδVIII. However, the specific function of PKCδ splice variants in ovarian cancer has not been elucidated yet. Hence, we evaluated their expression in human ovarian cancer cell lines (OCC): SKOV3 and TOV112D, along with the normal T80 ovarian cells. Our results demonstrate a marked increase in PKCδVIII in OCC compared to normal ovarian cells. Therefore, we elucidated the role of PKCδVIII and the underlying mechanism of its expression in OCC. Using overexpression and knockdown studies, we demonstrate that PKCδVIII increases cellular survival and migration in OCC. Further, overexpression of PKCδVIII in T80 cells resulted in increased expression of Bcl2 and knockdown of PKCδVIII in OCC decreased Bcl2 expression. Using co-immunoprecipitations and immunocytochemistry, we demonstrate nuclear localization of PKCδVIII in OCC and further show increased association of PKCδVIII with Bcl2 and Bcl-xL in OCC. Using PKCδ splicing minigene, mutagenesis, siRNA and antisense oligonucleotides, we demonstrate that increased levels of alternatively spliced PKCδVIII in OCC is regulated by splice factor SRSF2. Finally, we verified that PKCδVIII levels are elevated in samples of human ovarian cancer tissue. The data presented here demonstrate that the alternatively spliced, signaling kinase PKCδVIII is a viable target to develop therapeutics to combat progression of ovarian cancer.
Language	English
Publishing date	2021-12-10
Publishing country	United States
Document type	Journal Article
ISSN	2573-9832
ISSN (online)	2573-9832
DOI	10.1096/fba.2021-00090
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