Qu Liujing, Xin Yu, Feng Jieni, Ren Xiaolei, Li Zuming, Chen Xueru, Miao Guangyan, Chen Jiankun, Sun Chengming, Lu Yue
Department of Clinical Laboratory, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China.
Department of Medical Laboratory, Qingdao Sixth People's Hospital, Qingdao, China.
Front Oncol. 2024 Jul 2;14:1389136. doi: 10.3389/fonc.2024.1389136. eCollection 2024.
PRKCI is abnormally expressed in various cancers, but its role in osteosarcoma is unknown. This study aimed to explore the biological function of PRKCI in osteosarcoma and its potential molecular mechanism. PRKCI expression was evaluated in osteosarcoma cell lines using Western blot analysis and reverse transcription PCR. The CCK-8 assay, colony formation assay, flow cytometry, Transwell assay, and wound-healing assay were used to detect the proliferation, colony-forming capacity, cell cycle, migration, and invasion of osteosarcoma cells when PRKCI was overexpressed or knocked down. The interaction between PRKCI and SQSTM1 was explored using immunoprecipitation. Finally, the protein molecule expression of the Akt/mTOR signaling pathway in osteosarcoma was detected when PRKCI was knocked down. Our study found that PRKCI was overexpressed in osteosarcoma cell lines. The overexpression of PRKCI promoted the proliferation and colony-forming capacity of osteosarcoma cells, while silencing PRKCI inhibited the proliferation, colony-forming capacity, migration, and invasion of osteosarcoma cells and arrested the cell cycle at the G2/M phase. Both PRKCI and SQSTM1 were overexpressed in osteosarcoma. The expression of PRKCI was only related to histological type, while that of SQSTM1 was not related to clinical characteristics. The expression of PRKCI and SQSTM1 in osteosarcoma was higher than that in chondrosarcoma. Knockdown of PRKCI inhibited the proliferation of osteosarcoma cells by inactivating the Akt/mTOR signaling pathway, suggesting that PRKCI was a potential target for osteosarcoma therapy.
蛋白激酶Cι型（PRKCI）在多种癌症中异常表达，但其在骨肉瘤中的作用尚不清楚。本研究旨在探讨PRKCI在骨肉瘤中的生物学功能及其潜在的分子机制。采用蛋白质免疫印迹分析和逆转录聚合酶链反应评估骨肉瘤细胞系中PRKCI的表达。当PRKCI过表达或敲低时，使用细胞计数试剂盒-8（CCK-8）检测法、集落形成检测法、流式细胞术、Transwell检测法和伤口愈合检测法来检测骨肉瘤细胞的增殖、集落形成能力、细胞周期、迁移和侵袭。采用免疫沉淀法探究PRKCI与Sequestosome 1（SQSTM1）之间的相互作用。最后，当PRKCI被敲低时，检测骨肉瘤中Akt/mTOR信号通路的蛋白质分子表达。我们的研究发现，PRKCI在骨肉瘤细胞系中过表达。PRKCI的过表达促进了骨肉瘤细胞的增殖和集落形成能力，而沉默PRKCI则抑制了骨肉瘤细胞的增殖、集落形成能力、迁移和侵袭，并使细胞周期停滞在G2/M期。PRKCI和SQSTM1在骨肉瘤中均过表达。PRKCI的表达仅与组织学类型有关，而SQSTM1的表达与临床特征无关。骨肉瘤中PRKCI和SQSTM1的表达高于软骨肉瘤。敲低PRKCI可通过使Akt/mTOR信号通路失活来抑制骨肉瘤细胞的增殖，这表明PRKCI是骨肉瘤治疗的一个潜在靶点。
