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Updated: Sep 27, 2026

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
Published on: January 7, 2013
[Expressions of five protein kinase C isoforms in salivary adenoid cystic carcinoma]
1Department of Oral and Maxillofacial Surgery, First Hospital, China Medical University.
Objective:
The protein kinase C (PKC) family of isoforms plays the key role in the regulation of cellular events, including cell proliferation, differentiation and canceration. Previous work from our laboratory has shown the alteration of PKC and its inhibitor activities in salivary adenoid cystic carcinoma (SACC) [Sun Changfu, et al. West China Journal of Stomatology, 1998, 16(3): 201-203]. This study aimed to further explore the relationship between PKC isoforms and canceration of SACC.
Methods:
Expressions of five isoforms of PKC (alpha, beta I, beta II, epsilon and delta) were examined in cytosolic and membranous fraction of specimen homogenates from SACCs and were compared with the adjacent normal tissues by immunoblotting. Equal amounts of cytosolic and membrane protein from control and experimental groups were simultaneously subjected to sodium dodecyl sulfatepolyacrylamide gel electrophoresis (SDS-PAGE), transferred to nitrocellulose membranes, and reacted with first and second antibodies; Color development and image analysis were performed.
Results:
1. Cytosolic PKC-alpha, PKC-beta I, and PKC-beta II were expressed in SACCs and adjacent normal tissues. The Expressions of these three cytosolic isoforms were reduced significantly in SACCs compared with the adjacent normal tissues; 2. Membranous PKC-alpha was only detected in SACCs and the membranous translocation of cytosolic PKC-alpha was also seen. 3. The expressions of PKC-epsilon and PKC-delta were not detected in both SACCs and adjacent normal tissues.
Conclusion:
There was close relationship between changes of expression of PKC isoforms (alpha, beta I, beta II) and carcinogenesis of SACC. We postulated that there may be relationship between the membranous translocation of PKC-alpha and hematogenous lung metastasis in SACC.
Insights
Protein kinase C (PKC) isoforms alpha, beta I, and beta II expression decreased in salivary adenoid cystic carcinoma (SACC). Membranous translocation of PKC-alpha suggests a role in SACC canceration and potential metastasis.
Area of Science:
- Molecular Biology
- Oncology
- Cell Signaling
Context:
- Salivary adenoid cystic carcinoma (SACC) is a malignant salivary gland tumor.
- Protein Kinase C (PKC) isoforms are crucial regulators of cellular processes, including cancer development.
- Previous studies indicated altered PKC activity in SACC.
Purpose:
- To investigate the expression patterns of specific PKC isoforms (alpha, beta I, beta II, epsilon, delta) in SACC.
- To compare PKC isoform expression in SACC tissues with adjacent normal tissues.
- To explore the relationship between PKC isoform alterations and SACC carcinogenesis.
Summary:
- Cytosolic PKC-alpha, beta I, and beta II expression were significantly reduced in SACC tissues compared to normal tissues.
- Membranous PKC-alpha was detected exclusively in SACC, indicating translocation from the cytosol.
- PKC-epsilon and PKC-delta were not detected in either SACC or normal tissues.
Impact:
- Findings suggest a correlation between altered expression of PKC-alpha, beta I, and beta II and SACC development.
- The membranous translocation of PKC-alpha may be linked to hematogenous lung metastasis in SACC.
- This research provides insights into the molecular mechanisms underlying SACC progression.
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