PIK3R1 Promotes Lung Cancer Proliferation Through Activating PI3K/AKT/mTOR Signaling Pathways

Background: Lung cancer is a common malignant neoplasm worldwide. Phosphoinositide-3-kinase, regulatory subunit 1 (PIK3R1) plays as a therapeutic target in many cancers. The role PIK3R1 plays in lung cancer still remains unclear. Our study aims to explore the role of PIK3R1 in lung cancer. Methods: : We used quantitative real-time PCR (qPCR) to detect the PIK3R1 mRNA expression level in our 20 paired lung cancer patients. We then used A549 sh-PIK3R1 , H1299 sh-PIK3R1 , H1650 LV-PIK3R1 , H292 LV-PIK3R1 , A549 sh-PIK3R1+LV-PIK3R1 and H1299 sh-PIK3R1+LV-PIK3R1 cells for in vitro analysis. Cell viability assay was used to detect the ability of PIK3R1 in regulating proliferation of lung cancer. Western blot analysis was used to detect the PIK3R1 protein expression level and proteins in PI3K/AKT/mTOR signaling pathway. Results: : PIK3R1 mRNA expression level was higher in tumour tissues than the corresponding adjacent noncancerous among the 20 lung cancer patients. Increased PIK3R1 promoted lung cancer proliferation and downregulated PIK3R1 inhibited lung cancer proliferation. Furthermore, PIK3R1 downregulation suppressed p-PI3K, p-Akt, and p-mTOR in A549 sh-PIK3R1 and H1299 sh-PIK3R1 cells. Overexpressed of PIK3R1 upregulated p-PI3K, p-Akt, and p-mTOR in H1650 LV-PIK3R1 and H292 LV-PIK3R1 cells. Cell viability was increased in both A549 and H1299 cells following sh-PIK3R1+LV-PIK3R1 co-transfection, thus reversed the effect of sh-PIK3R1 on cell proliferation. Conclusions: : We identified that overexpressed of PIK3R1 could promote lung cancer proliferation via PI3K/AKT/mTOR signaling pathway, thus may provide PIK3R1 as a therapeutic target for effective strategy in lung cancer.