Hsa_circ_0018818 knockdown suppresses tumorigenesis in non-small cell lung cancer by sponging miR-767-3p

Abstract

To identify potential therapeutic targets in non-small cell lung cancer NSCLC, we conducted a bioinformatics analysis of circRNAs differentially expressed between NSCLC tissues and adjacent normal tissues. Cell proliferation and apoptosis was assessed using CCK-8 and flow cytometry, respectively. A connection between hsa_circ_0018818 and miR-767-3p was confirmed in dual luciferase reporter assays. Gene and protein expression in NSCLC cells were measured using quantitative PCR and Western-blotting, respectively. And a xenograft tumor model was established to assess the function of hsa_circ_0018818 in NSCLC in vivo. Hsa_circ_0018818 was greatly upregulated in NSCLC tumor tissues. Knocking down hsa_circ_0018818 using a targeted shRNA inhibited the proliferation and invasiveness of NSCLC cells and induced their apoptosis via the miR-767-3p/Nidogen 1 (NID1) signaling axis. Hsa_circ_0018818 knockdown also inactivated Epithelialmesenchymal transition (EMT) process and PI3K/Akt signaling. In summary, hsa_circ_0018818 knockdown inhibited NSCLC tumorigenesis in vitro and in vivo, which suggests it could potentially serve as a target for the treatment of NSCLC.

Sterculic Acid Alters Adhesion Molecules Expression and Extracellular Matrix Compounds to Regulate Migration of Lung Cancer Cells

“…Its expression correlates with poor outcomes [76]. miR-767-3p reduces NID1 expression and inactivates the NID1/PI3K/Akt/ EMT pathway to reduce tumor growth in NSCLC [77]. NID1 down-regulation was detected after 30 µM SA treatment in H1299 cells, while the A549 cell line did not modify its NID1 expression.…”

Construction of circRNA-miRNA-mRNA network and identification of novel potential biomarkers for non-small cell lung cancer

“…However, it was reported that miR-767-3p was downregulation in LUAD tissue and cell lines, suppressed the expression of CLDN18, and inhibited the LUAD cell proliferation [ 41 ]. Xu et al found that hsa_circ_0018818 knockdown inhibited NSCLC tumorigenesis by functioning the miR-767-3p/Nidogen 1 signaling axis [ 42 ]. We speculated the mechanisms of miRNAs may vary among different cancers.…”

Crosstalk between circRNAs and the PI3K/AKT signaling pathway in cancer progression

“…241 – 244 The expression of circGFRA1 and circ0018818 is significantly upregulated in NSCLC tissues compared to normal counterparts. 245 , 246 Silencing of circ0018818 expression inhibits proliferation, invasion, and EMT and promotes cell apoptosis. 246 In addition, circGFRA1 activates the PI3K/AKT pathway by downregulating the expression of miR-188-3p in lung cancer.…”

“… 245 , 246 Silencing of circ0018818 expression inhibits proliferation, invasion, and EMT and promotes cell apoptosis. 246 In addition, circGFRA1 activates the PI3K/AKT pathway by downregulating the expression of miR-188-3p in lung cancer. Knockdown of circ100876 reduces cell proliferation, migration, and invasion and facilitates NSCLC cell apoptosis by regulating the miR-636/RET axis and PI3K/AKT signaling.…”