학술논문
Targeting transient receptor potential canonical 1 reduces non-small cell lung cancer chemoresistance and sternness via inhibition of PI3K/AKT signaling
Document Type
Academic Journal
Author
Source
Oncology Letters. August, 2023, Vol. 26 Issue 2, p1I, p9 p.
Subject
Language
English
ISSN
1792-1074
Abstract
TRPC1 enhances cell proliferation and migration in non-small cell lung cancer (NSCLC); however, its effect on NSCLC chemoresistance and sternness remains to be determined. The aim of the current study was to investigate the effect of TRPC1 on NSCLC chemoresistance and sternness and to determine the underlying mechanism of action. Cisplatin-resistant A549 (A549/CDDP) and H460 (H460/CDDP) cells were first established and were then transfected with negative control small interfering (si)RNA (si-NC) or TRPC1 siRNA (si-TRPC1). Cells were then treated with 740 Y-P, a PI3K/Akt agonist. Subsequently, the sensitivity of A549/CDDP and H460/CDDP cells to CDDP was evaluated. Furthermore, the expression levels of CD133 and CD44, and sphere formation ability were also determined. The results showed that the half-maximal inhibitory concentration ([IC.sub.50]) of CDDP was significantly higher in A549/CDDP cells compared with A549 cells and in H460/CDDP cells compared with H460 cells. TRPC1 silencing decreased the [IC.sub.50] value of CDDP compared with the si-NC group in A549/CDDP (11.78 vs. 21.58 [micro]M; P Key words: transient receptor potential canonical 1, non-small cell lung cancer, stemness, chemoresistance, PI3K/AKT signaling
Introduction Lung cancer is one of the most fatal and common types of cancer globally, accounting for ~11.4% of new cancer cases and 18.0% of cancer-related deaths in 2020. Notably, [...]
Introduction Lung cancer is one of the most fatal and common types of cancer globally, accounting for ~11.4% of new cancer cases and 18.0% of cancer-related deaths in 2020. Notably, [...]