Zhang Liang, Li Mingjiang, Li Xiaoping, Xiao Ting, Zhou Honggang, Zhang Weidong, Wang Ping
Tianjin Medical University Cancer Institute & Hospital, Tianjin, PR China.
Department of Thoracic Surgery, Tianjin First Central Hospital, Tianjin, 300192, PR China.
Heliyon. 2024 Aug 30;10(17):e37063. doi: 10.1016/j.heliyon.2024.e37063. eCollection 2024 Sep 15.
PLCD3 belongs to the phospholipase C delta group and is involved in numerous biological functions, including cell growth, programmed cell death, and specialization. However, the role of PLCD3 in lung cancer still needs further investigation. This research aimed to investigate if PLCD3 influences glycolytic reprogramming and lung cancer development through the PKC-dependent Rap1 signaling pathway. This study found that PLCD3 was increased in lung cancer tissues. PLCD3 promotes the proliferation and invasion of lung cancer cells by activating the PKC-dependent Rap1 pathway. The detailed process involves PLCD3 triggering PKC, which subsequently stimulates the Rap1 pathway, leading to glycolytic reprogramming that supplies adequate energy and metabolic substrates necessary for the growth and spread of lung cancer cells. Moreover, PLCD3 can also promote the metastasis and invasion of lung cancer cells by activating the Rap1 pathway. This study reveals the mechanism of PLCD3 in lung cancer and provides new ideas for the treatment of lung cancer. Inhibiting PLCD3, PKC, and the Rap1 pathway may be an effective strategy for treating lung cancer.
PLCD3属于磷脂酶Cδ家族，参与多种生物学功能，包括细胞生长、程序性细胞死亡和细胞特化。然而，PLCD3在肺癌中的作用仍需进一步研究。本研究旨在探讨PLCD3是否通过蛋白激酶C（PKC）依赖的Rap1信号通路影响糖酵解重编程和肺癌发展。该研究发现肺癌组织中PLCD3表达增加。PLCD3通过激活PKC依赖的Rap1通路促进肺癌细胞的增殖和侵袭。具体过程为PLCD3激活PKC，进而刺激Rap1通路，导致糖酵解重编程，为肺癌细胞的生长和扩散提供充足能量和代谢底物。此外，PLCD3还可通过激活Rap1通路促进肺癌细胞的转移和侵袭。本研究揭示了PLCD3在肺癌中的作用机制，为肺癌治疗提供了新思路。抑制PLCD3、PKC和Rap1通路可能是治疗肺癌的有效策略。
