CircRNA B cell linker regulates cisplatin sensitivity in nonsmall cell lung cancer via microRNA-25-3p/BarH­like homeobox 2 axis.

Cisplatin (DDP) was a commonly used drug in the treatment of nonsmall cell lung cancer (NSCLC). However, the current resistance of patients to DDP seriously affected its therapeutic effect. Circular RNAs (circRNAs) have been reported to regulate drug resistance in cells. The purpose of this paper is to study the effect of circRNA B cell linker (circ_BLNK) in DDP resistance of NSCLC. The abundances of circ_BLNK, microRNA-25-3p (miR-25-3p) and BarH­like homeobox 2 (BARX2) were examined by quantitative real-time PCR and western blot analysis. Cell proliferation and apoptosis were detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay, EdU assay and flow cytometry. Transwell assay was applied to assess cell migration and invasion. Protein levels were quantified by western blot analysis. Dual-luciferase reporter assay was enforced to confirm the links among circ_BLNK, miR-25-3p and BARX2. The mice models were enforced to evaluate tumorigenicity. Herein, circ_BLNK and BARX2 were lower-expressed, whereas miR-25-3p was higher-expressed in A549/DDP and H1299/DDP cells than their homologous parental NSCLC cells. Circ_BLNK increases improved DDP sensitivity of NSCLC cells by promoting cell apoptosis and inhibiting proliferation, migration and invasion. Moreover, we confirmed that circ_BLNK regulated BARX2 by inhibiting miR-25-3p. Accordingly, overexpression of circ_BLNK improved DDP sensitivity of NSCLC cells via miR-25-3p/BARX2 axis. Besides, circ_BLNK reduced cell resistance to DDP, thereby inhibiting tumor development in mice. Circ_BLNK promoted the DDP sensitivity of NSCLC via regulating miR-25-3p/BARX2 axis.

The optimal neoadjuvant regimen for nonsmall cell lung cancer: A meta-analysis.

OBJECTIVE: To compare the efficacy and complications of different neoadjuvant to determine the optimal regimens for nonsmall cell lung cancer (NSCLC) patients. METHODS: A systematic search of the Web of Science, and PubMed databases was conducted through June 3, 2021, reporting a comparison of chemotherapy, chemoradiotherapy, and immunotherapy. RESULTS: Of 3462 studies, 25 were considered for evidence synthesis. 1035 patients who received chemotherapy or radiotherapy before surgery did not prolong the overall survival (OS) compared with 1038 patients who received surgery alone (hazard ratio [HR] 1.13, 95% CI 1·00-1·28, P = 0·05). 1192 patients received chemoradiotherapy and 864 patients received chemotherapy or radiotherapy; chemoradiotherapy prolonged the OS compared with chemotherapy (HR 0.52, 95% CI 0·29 to 0.95, P = .03). Compared with 110 patients who received other therapy, 93 patients who received immunotherapy had prolonged the OS (HR 1.56, 95% CI 1·08-2·25, P = .02). Chemoradiotherapy increased the pathological response rate (HR 1.68, 95% CI 1·33-2·12, P < .0001), and grade 3 and 4 adverse effects were not increased (HR 5.90, 95% CI 0.88 to 39.60, P = .007). Immunotherapy increased the pathological response (HR 2.79, 95% CI 1·71-4·54, P < .0001), with no significant effects on grades 3 and 4 adverse(HR 0.71, 95% CI 0·19-2·64, P = .61). CONCLUSION: Our data showed that chemotherapy may prolong OS and PFS, but not statistically significant; however, the combination of chemotherapy and radiation did show an advantage, and immunotherapy may be also the choice for neoadjuvant therapy.

Long non­coding RNA SLNCR1 regulates non­small cell lung cancer migration, invasion and stemness through interactions with secretory phospholipase A2.

Long non­coding RNA (lncRNA) SRA­like non­coding RNA (SLNCR1; also known as linc00673) is a recently identified oncogenic lncRNA. The role of SLNCR1 in non­small cell lung cancer (NSCLC), a common malignancy, remains poorly understood. The present study aimed to investigate the involvement of long non­coding RNA SLNCR1 in the pathogenesis of NSCLC. Reverse transcription­quantitative PCR (RT­qPCR) and ELISA were performed to measure the levels of lncRNA SLNCR1 and secretory phospholipase A2 (sPLA2) in lung biopsies, respectively. Correlations between expression levels of lncRNA SLNCR1 and sPLA2 were analyzed by Pearson's correlation analysis. Diagnostic value of lncRNA SLNCR1 for NSCLC was evaluated by receiver operating characteristic curve analysis. lncRNA SLNCR1 small interfering (si)RNA and sPLA2 overexpression vector were transfected into NSCLC cells. Cell migration, invasion and stemness were examined by Transwell migration assay, Matrigel invasion assay and flow cytometric assay, respectively. Following transfection, expression of lncRNA SLNCR1 and sPLA2 was detected by RT­qPCR and western blotting, respectively. The results demonstrated that lncRNA SLNCR1 expression levels were upregulated in tumor tissues compared with adjacent healthy tissues of patients with NSCLC. Plasma lncRNA SLNCR1 and sPLA2 expression levels were upregulated in patients with NSCLC compared with healthy controls. Plasma lncRNA SLNCR1 and sPLA2 were positively correlated in patients with NSCLC, but not in healthy controls. lncRNA SLNCR1 siRNA silencing inhibited, whereas sPLA2 overexpression promoted cell migratory and invasive abilities and stemness. lncRNA SLNCR1 siRNA silencing led to downregulated sPLA2 expression, whereas sPLA2 overexpression did not significantly affect lncRNA SLNCR1 expression. sPLA2 overexpression attenuated the inhibitory effects of lncRNA SLNCR1 siRNA silencing on cell migration, invasion and stemness. In conclusion, lncRNA SLNCR1 may regulate cancer cell migration, invasion and stemness in NSCLC through interactions with sPLA2.