PESV represses non-small cell lung cancer cell malignancy through circ_0016760 under hypoxia

Abstract

Background Non-small cell lung cancer (NSCLC) accounts for more than 80% of lung cancers, which is the most common malignant tumor worldwide. Polypeptide extract from scorpion venom (PESV) has been reported to inhibit NSCLC process. The present study aims to reveal the roles of PESV in NSCLC progression under hypoxia and the inner mechanism. Methods The expression levels of circular RNA 0016760 (circ_0016760) and microRNA-29b (miR-29b) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Protein expression was determined by western blot and immunohistochemistry assays. Cell migration, invasion, proliferation and tube formation were investigated by transwell, cell colony formation, 3-(4,5-Dimethylthazol-2-yl)-2,5-diphenyltetrazolium bromide and tube formation assays. The impacts between PESV and circ_0016760 overexpression on tumor growth in vivo were investigated by in vivo tumor formation assay. Results Circ_0016760 expression was dramatically upregulated in NSCLC tissues and cells, compared with adjacent lung tissues and cells, respectively. PESV treatment downregulated circ_0016760 expression. Circ_0016760 silencing or PESV treatment repressed cell migration, invasion, proliferation and tube formation under hypoxia in NSCLC cells. Circ_0016760 overexpression restored the effects of PESV treatment on NSCLC process under hypoxia. Additionally, circ_0016760 acted as a sponge of miR-29b, and miR-29b bound to HIF1A. Meanwhile, miR-29b inhibitor impaired the influences of circ_0016760 knockdown on NSCLC process under hypoxia. Further, ectopic circ_0016760 expression restrained the effects of PESV exposure on tumor formation in vivo. Conclusion Circ_0016760 overexpression counteracted PESV-induced repression of NSCLC cell malignancy and angiogenesis under hypoxia through miR-29b/HIF1A axis.

Astragaloside IV-PESV Repressed T Cell Immunosuppression by Inhibiting PD-L1 Expression in Prostate Cancer through STAT3 Pathway

“…In PCa, astragaloside IV also plays an important role [20,21]. Scorpion has an activating efect, and PESV could inhibit the proliferation of NSCLC cells [33], induce apoptosis in lung cancer cells [34], and inhibit the development of H22 liver cancer transplantation tumors in mice [35]. In addition, PESV could also induce apoptosis in PCa cells DU145 [22].…”

Exosomal circular RNA: a signature for lung cancer progression

“…Because of its ability to behave as a miR-29b sponge, circ 0016760 was able to prevent miR-29b from binding to HIF1A. Furthermore, circ_0016760 silencing inhibited cell proliferation, invasion, and angiogenesis or tube formation [ 113 ].…”

Non-coding RNAs in lung cancer: emerging regulators of angiogenesis

“…Circ_0016760 expression is significantly increased in both NSCLC tissues and cells and can promote the malignant phenotype of NSCLC. Mechanistically, up-regulation of circ_0016760 acts as a sponge of miR-29b and promotes the oncogenic effect of HIF-1α, further inducing malignancy and angiogenesis in NSCLC [ 74 ].…”