Search

Sodium Danshensu, extracted from the root of the Salvia miltiorrhiza, has pleiotropic effects including anti‐oxidation, anti‐inflammation and anti‐tumor. However, whether Sodium Danshensu has an anti‐cancer effect in lung cancer remains to be elucidated. The present study aimed to illustrate the effects of Sodium Danshensu on lung cancer cells and the potential molecular mechanisms. BEAS‐2B, A549, and NCI‐H1299 cells were stimulated with 25, 50, and 100 μM Sodium Danshensu for 24, 48, and 72 h, and then cell viability, apoptosis, migration and invasion were determined using 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT), flow cytometry and Transwell assays, respectively. Moreover, the levels of Proliferating cell nuclear antigen (PCNA), matrix metalloproteinase 9 (MMP9), B‐cell lymphoma‐2 (Bcl‐2) associated X (Bax), Bcl‐2, phosphorylated (p)‐phosphoinositide 3‐kinase (PI3K), and p‐Protein kinase B (AKT) in lung cancer cells were evaluated using quantitative real‐time polymerase chain reaction (qRT‐PCR) and/or Western blot assays. We observed that Sodium Danshensu suppressed cells viability, migration, and invasion, as well as promoted cells apoptosis in A549 and NCI‐H1299 cells in a dose‐dependent manner, while Sodium Danshensu had no cytotoxic effect on the proliferation activity of BEAS‐2B cells. Moreover, the expression of PCNA, MMP9, Bcl‐2 were decreased, but Bax was up‐regulated in Sodium Danshensu‐treated A549 and NCI‐H1299 cells. Our findings also revealed that Sodium Danshensu inhibited PI3K/AKT pathway in A549 and NCI‐H1299 cells. In conclusion, our study provided the first evidence that Sodium Danshensu suppressed the malignant biological behaviors of lung cancer cells, indicating that Sodium Danshensu might be a latent candidate for lung cancer therapy. [ABSTRACT FROM AUTHOR]

Background: Non-small cell lung cancer (NSCLC) is the leading cause of cancer death worldwide. Circular RNAs (circRNAs) have been implicated in the pathogenesis of NSCLC. In this study, we explored the molecular determinants underlying the oncogenic property of circ_0026134 in NSCLC., Methods: The levels of circ_0026134, miR-3619-5p and chromatin assembly factor 1 subunit B axis (CHAF1B) were assessed by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Cell colony formation, migration, invasion and apoptosis were detected by colony formation, Transwell, and flow cytometry assays, respectively. Direct relationships among circ_0026134, miR-3619-5p and CHAF1B were verified by dual-luciferase reporter assays., Results: Our results showed that circ_0026134 was highly expressed in NSCLC tissues and cells. Reduced circ_0026134 expression or miR-3619-5p overexpression inhibited NSCLC cell colony formation, migration, invasion, glycolysis and promoted cell apoptosis in vitro. Moreover, circ_0026134 directly targeted miR-3619-5p, and circ_0026134 regulated CHAF1B expression through miR-3619-5p. CHAF1B was a downstream effector of circ_0026134 in affecting NSCLC cell functional behaviors in vitro. Additionally, circ_0026134 silencing weakened tumor growth in vivo., Conclusions: Our study identified a novel regulatory mechanism, the circ_0026134/miR-3619-5p/CHAF1B axis, for the oncogenic role of circ_0026134 in NSCLC, highlighting circ_00261345 inhibition as a potential therapeutic method against NSCLC., (© 2022 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd.)