Hsa_circ_0008133 contributes to lung cancer progression by promoting glycolysis metabolism through the miR-760/MEX3A axis.

BACKGROUND: Lung cancer is a very common cancer with poor prognosis and high mortality. Circular RNAs (circRNAs) have been confirmed to be related to the occurrence of lung cancer, and circ_0008133 has been found to be possibly related to lung cancer. METHODS: Expression of circ_0008133, miR-760, and mex-3 RNA binding family member A (MEX3A) messenger RNA (mRNA) was detected using quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability, colony number, migration, and invasion were assessed using cell counting kit-8 (CCK8), colony formation, wound healing, and transwell assays. Glucose consumption and lactate production were detected using commercial kits. Protein expression was measured using western blot. Dual-luciferase reporter assay and RNA pull-down assay were used to analyze the relationships between miR-760 and circ_0008133 or MEX3A. The effects of circ_0008133 knockdown on tumor growth in vivo were examined by the nude mice expriment. Immunohistochemistry (IHC) assay analyzed Ki-67 expression. RESULTS: Circ_0008133 and MEX3A were markedly boosted in lung cancer tissues and cells. Circ_0008133 knockdown decreased lung cancer cell viability, glucose consumption, lactate production, colony formation, migration, and invasion. In mechanism, circ_0008133 might positively regulate MEX3A expression by sponging miR-760. Additionally, knockdown of circ_0008133 inhibited tumor growth in vivo. CONCLUSION: Circ_0008133 accelerated the progression of lung cancer by promoting glycolysis metabolism through the miR-760/MEX3A axis.

Systematic review of the perioperative immunotherapy in patients with non-small cell lung cancer: evidence mapping and synthesis.

Objectives: This study aimed to use evidence mapping to provide an overview of immune checkpoint inhibitors (ICIs) as perioperative treatments for non-small cell lung cancer (NSCLC) and to identify areas of this field where future research is most urgently needed. Methods: Multiple databases (PubMed, EMBASE, Cochrane Library, and Web of Science) were searched to identify clinical trials published up to November 2021 that examined the effect of perioperative ICIs for perioperative treatment of NSCLC. Study design, sample size, patient characteristics, therapeutic regimens, clinical stages, short-term and long-term therapeutic outcomes, surgery associated parameters, and therapeutic safety were examined. Results: We included 66 trials (3564 patients) and used evidence mapping to characterize the available data. For surgery associated outcomes, sixty-two studies (2480 patients) provided complete information regarding the use of surgery after neoadjuvant immunotherapy and data on R0 resection were available in 42 studies (1680 patients); for short-term clinical outcomes, 57 studies (1842 patients) evaluated pathologic complete response (pCR) after neoadjuvant immunotherapy and most of included studies achieved pCR in the range of 30 to 40%; for long-term clinical outcomes, 15 studies (1932 patients) reported DFS, with a median range of 17.9-53.6 months; and only a few studies reported the safety profiles of perioperative immunotherapies. Conclusion: Our evidence mapping systematically summarized the results of all clinical trials and studies that examined ICIs as perioperative treatments for NSCLC. The results indicated more studies that evaluate long-term patient outcomes are needed to provide a stronger foundation for the use of these treatments.

CircRIP2 promotes NSCLC progression by sponging for miR-671-5p to regulate FOXM1 expression.

Lot of attention had been paid to the role of circular RNAs (circRNAs) in carcinogenesis recently. However, knowledge about circRNAs in NSCLC development is far from satisfactory. In this study, we aimed to provide a novel insight into the circRIP2 in NSCLC development. We used NSCLC tissues, as well as cell lines to elucidate the expression and location of circRIP2 in NSCLC. We also established the circRIP2 overexpression cells A549-circRIP2 and repression cells HCC827-shcircRIP2 for further functional and mechanism studies. The pro-tumorigenic role of circRIP2 was tested by using CCK-8, BrdU and transwell assays. The interaction between circRIP2 and miR-671-5p were validated by luciferase reporter assay, RIP assay, as well as RNA pull down assay. We showed circRIP2 is differentially expressed NSCLC, and acted as a predictor for overall survival (OS) and disease-free survival (DFS). CircRIP2 promoted NSCLC progression by acting as a miRNA sponge for miR-671-5p, thus facilitating its target gene FOXM1 expression. Targeting circRIP2 could be potentially beneficial for NSCLC patients in the future.