Park Hyun-Ji, Park Shin-Hyung
Department of Pathology, College of Korean Medicine, Dong-eui University, Busan, Republic of Korea.
Nat Prod Res. 2023 Aug-Sep;37(17):2924-2928. doi: 10.1080/14786419.2022.2137503. Epub 2022 Oct 28.
The aim of this study was to investigate the anticancer effect of var. (AT) root extract on human non-small cell lung cancer (NSCLC) cells and the mechanism involved in such effect. Among three fractions of AT root extract, hexane fraction (HAT) significantly decreased the proliferation of NSCLC cells. Besides, HAT treatment dose-dependently inhibited colony formation of NSCLC cells. These effects were associated with apoptosis induction evidenced by increased chromatin condensation, accumulation of sub-G1 DNA content and annexin V-positive cells, and enhanced expression of apoptotic proteins, including cleaved-caspases and cleaved-poly (ADP-ribose) polymerase (PARP). Notably, phosphorylation levels of signal transducer and activator of transcription 3 (STAT3) and Src were decreased by HAT. Transfection with STAT3 or Src for constitutive activation reversed the anti-proliferative effect of HAT on H1299 cells. Taken together, our findings suggest that HAT-induced apoptosis in NSCLC cells is mediated by inhibition of Src/STAT3 pathway.
本研究的目的是探讨变种（AT）根提取物对人非小细胞肺癌（NSCLC）细胞的抗癌作用及其相关机制。在AT根提取物的三个组分中，己烷组分（HAT）显著降低了NSCLC细胞的增殖。此外，HAT处理剂量依赖性地抑制了NSCLC细胞的集落形成。这些作用与凋亡诱导有关，表现为染色质浓缩增加、亚G1期DNA含量积累、膜联蛋白V阳性细胞增多，以及凋亡蛋白表达增强，包括裂解的半胱天冬酶和裂解的聚（ADP-核糖）聚合酶（PARP）。值得注意的是，HAT降低了信号转导和转录激活因子3（STAT3）和Src的磷酸化水平。用STAT3或Src进行组成型激活转染可逆转HAT对H1299细胞的抗增殖作用。综上所述，我们的研究结果表明，HAT诱导NSCLC细胞凋亡是通过抑制Src/STAT3途径介导的。
