Background: Circular RNAs (circRNA) play an essential role in the tumorigenesis of non-small cell lung cancer (NSCLC). CircDTL is a novel identified circRNA with little information regarding its biological role. However, the role of circDTL in NSCLC has not been investigated yet.Method: In this study, the levels of circDTL in tissues and cells were measured by RT-PCR. Cell viability was measured by the CCK-8 assay. Cell migration and invasion were evaluated using the wound healing assay and transwell assay, respectively. Cell death was measured by the cell death ELISA kit. The levels of Fe2+, ROS, MDA and GSH were measured using the commercial kits. The interactions between miR-1287-5p and circDTL/3′UTR GPX4 were verified by dual-luciferase activity assay. The effects of circDTL on tumor growth were evaluated in vivo.Results: CircDTL was found to be upregulated and acted as an oncogene in NSCLC cells. Knockdown of circDTL promoted both apoptosis and ferroptosis of NSCLC cells. It was identified that circDTL exerts its oncogenic effects via the circDTL/miR-1287-5p/GPX4 axis and GPX4 inhibits both ferroptosis and apoptosis. Finally, this study showed that silencing of circDTL promoted the sensitivity of NSCLC cells to chemotherapeutic agents and inhibited the growth of tumors in vivo.Conclusion: CircDTL acts as an oncogene and exerts its effects via the miR-1287-5p/GPX4 axis in NSCLC, providing a potential therapeutic target for NSCLC cancer therapy.

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Published data on the association between vascular endothelial growth factor (VEGF) -2578C/A polymorphism and cancer risk is inconclusive. To derive a more precise estimation of association between VEGF -2578C/A polymorphism and the risk of cancer, we performed a meta-analysis of 5415 cancer cases and 5848 controls from 16 published case-control studies. We used odds ratios (ORs) with 95% confidence intervals (CIs) to assess the strength of the association. Our meta-analysis indicated that VEGF -2578C/A polymorphism was associated with the risk of colorectal cancer under homozygote comparison (OR=0.70, 95% CI=0.53-0.92), dominant model (OR=0.72, 95% CI=0.57-0.92), and recessive model (OR=0.82, 95% CI=0.67-1.01), although no evidence of association between VEGF -2578C/A polymorphism and cancer risk was observed as we compared in the pooled analyses (homozygote comparison: OR=0.97, 95% CI=0.81-1.16). More studies are needed to detect VEGF -2578C/A polymorphism and its association with cancer in different ethnic populations incorporated with environmental exposures in the susceptibility of different kinds of cancer.

The present study aimed to determine the underlying mechanism of toll‑like receptor (TLR) agonist polyinosinic:polycytidylic acid (Poly I:C)‑induced apoptosis in THP‑1 cells following silencing the expression of tumor necrosis factor α‑induced protein 8‑like 2 (TIPE2). THP‑1 cells were incubated with different concentrations of the TLR agonist. Following incubation, reverse transcription‑quantitative polymerase chain reaction was performed to quantify the mRNA expression of TIPE2. Lentiviral technology was used to silence the expression of TIPE2. MTT assay was performed to assess cell proliferation, Annexin V/PI double staining was used to evaluate the apoptosis and western blotting was used to determine the expression levels of caspase‑8 following TIPE2 silencing. The TLRs agonist Poly I:C increased the expression level of TIPE2. During the incubation, Poly I:C also inhibited the proliferation of THP‑1 cells and induced apoptosis. Following silencing of TIPE2 in THP‑1 cells, the Poly I:C‑induced TIPE2 expression was significantly downregulated. Additionally, the Poly I:C‑induced proliferation inhibition and apoptosis in THP‑1 cells were significantly reduced following silencing of TIPE2. The findings of the western blot analysis indicated that the active form of caspase‑8, p18, was downregulated following silencing of TIPE2. In conclusion, the expression of TIPE2 in THP‑1 cells may be upregulated by Poly I:C, which may also inhibit cell proliferation and induce apoptosis. Following the downregulation of TIPE2 the aforementioned effect of Poly I:C treatment was reversed and may be associated with the reduced activity of caspase‑8 that was observed in the TIPE2 silenced group.

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