Downregulation of PRKCI inhibits osteosarcoma cell growth by inactivating the Akt/mTOR signaling pathway

Area of Science:

• Oncology
• Molecular Biology
• Biochemistry

Background:

• Protein kinase C iota (PRKCI) exhibits abnormal expression in various cancers.
• The specific role of PRKCI in osteosarcoma pathogenesis remains largely unexplored.

Purpose of the Study:

• To investigate the biological function and molecular mechanisms of PRKCI in osteosarcoma.
• To assess PRKCI as a potential therapeutic target for osteosarcoma.

Main Methods:

• PRKCI expression analysis in osteosarcoma cell lines via Western blot and RT-PCR.
• Functional assays including CCK-8, colony formation, flow cytometry, Transwell, and wound-healing assays to evaluate cell proliferation, colony formation, cell cycle, migration, and invasion.
• Immunoprecipitation to explore PRKCI and SQSTM1 interaction.
• Analysis of Akt/mTOR signaling pathway activation following PRKCI knockdown.

Main Results:

• PRKCI was found to be significantly overexpressed in osteosarcoma cell lines.
• Overexpression of PRKCI enhanced osteosarcoma cell proliferation and colony formation.
• Silencing PRKCI inhibited proliferation, colony formation, migration, and invasion, and induced G2/M cell cycle arrest.
• PRKCI and SQSTM1 were co-overexpressed in osteosarcoma, with PRKCI expression correlating with histological type.
• Knockdown of PRKCI suppressed osteosarcoma cell proliferation through inactivation of the Akt/mTOR signaling pathway.

Conclusions:

• PRKCI plays a crucial role in promoting osteosarcoma cell proliferation, migration, and invasion.
• PRKCI exerts its oncogenic effects partly by activating the Akt/mTOR signaling pathway.
• PRKCI represents a promising molecular target for the development of novel osteosarcoma therapies.