C Sun1, Z Zong, Y Wang, Z Wang, B Yu. 1. Department of Oral and Maxillofacial Surgery, First Hospital, China Medical University.
Abstract
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.
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.