More and more circular RNAs (circRNAs) revealed to play a critical role in the initiation and progression of cancer, however, the effects of circRNAs on non-small cell lung cancer (NSCLC) remain largely undetermined. In the present study, we screened the dysregulated circRNAs in paired NSCLC and normal samples from GEO database and identified circ_0043278 was to be significantly up-regulated in NSCLC and demonstrated it promotes NSCLC progression in vitro and in vivo. Then, we revealed the expression of miR-520f, a downstream factor of circ_0043278, was significantly down-regulated in NSCLC and acted as a tumor inhibitor. In addition, we revealed that circ_0043278 sponged miR-520f, which was demonstrated to target ROCK1, CDKN1B, and AKT3 in NSCLC cells. In conclusion, circ_0043278 promoted NSCLC cell proliferation, invasion, and migration by increasing ROCK1, CDKN1B, and AKT3 expressions through direct inhibition of miR-520f.
Background: Immune checkpoint inhibitors (ICIs) combined with chemotherapy have been applied as a first-line treatment for lung cancer, but consistent beneficial results have not been documented. Therefore, our meta-analysis aimed to evaluate the effectiveness and safety of combination therapy to promote its application. Methods: We searched electronic databases for studies that estimated the safety and efficacy of combined therapy. The objective response rate (ORR) and disease control response (DCR) parameters were evaluated with odds ratio (OR) values of the combination arm over the non-combination arm. Hazard ratios (HR) and its 95% confidence intervals (95% CI) were used to calculate progression-free survival (PFS) and overall survival (OS) in the combination and non-combination arms. All treatment-related adverse events (TRAEs) and 3 to 5 TRAEs were expressed as relative risk (RR) values of the combination arm over the noncombination arm. Results: Ten eligible studies involving 4,887 patients were identified. The pooled ORs for ORR and DCR were 1.85 (95% CI: 1.30-2.63, P<0.01) and 1.14 (95% CI: 0.70-1.86, P<0.01), respectively. The pooled HRs for PFS and OS were 0.67 (95% CI: 0.58-0.79, P<0.001) and 0.76 (95% CI: 0.65-0.88, P<0.001), respectively. In subgroup analysis, ORR and DCR were significantly improved in the programmed cell death-1/L1 (PD-1/L1) blockade for non-small cell lung cancer (NSCLC) group (subgroup A), with a combined OR values of 2.36 (95% CI: 1.79-3.13, P<0.001) and 1.92 (95% CI: 1.10-3.35, P<0.001), respectively. However, no significant benefits were observed in the cytotoxic T lymphocyte antigen-4 (CTLA-4) blockade for small cell lung cancer (SCLC) (subgroup B) and CTLA-4 blockade for NSCLC groups (subgroup C). In addition, a significant improvement in PFS was observed in subgroup A, subgroup B and subgroup C, with pooled HR values of 0.58 (95% CI: 0.52-0.63, P<0.001), 0.86 (95% CI: 0.76-0.97, P<0.05) and 0.83 (95% CI: 0.68-1.00, P<0.05), respectively. Only subgroup A exhibited an OS benefit, with a combined HR value of 0.67 (95% CI: 0.55-0.81, P<0.001). Moreover, as the expression of PD-L1 increased, the PFS and OS benefits were more significantly. Furthermore, patients without central nervous system (CNS) metastasis who were treated with PD-1/L1 inhibitors had a longer OS than patients with CNS metastasis (HR:
Lung cancer is among the most frequently occurring cancers and the leading cause of cancer‐related deaths worldwide. Nonsmall cell lung cancer is accountable for 85% to 90% of all lung cancer cases and develops distant metastases with high mortality. In this work, we elucidated the role of activating transcription factor 1 (ATF1) in migration and invasion of lung cancer cells. We found that the migration and invasion were inhibited with ATF1 silencing in lung cancer cells. By contrast, ATF1 overexpression led to promotion in migration and invasion. The alteration in ATF1 expression induced a change in the epidermal growth factor receptor (EGFR) and matrix metalloproteinases (MMP)‐2 expression level in the same tendency. Thus, we provided a potential new candidate for therapies against lung cancer, showing the possible mechanism underlying the invasion and migration of lung cancer cells.
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