Background: Previous genome-wide transcriptome profiling found circ_ZNF124 was highly expressed in lung adenocarcinoma, however, the role of circ_ZNF124 in non-small cell lung cancer (NSCLC) is still unknown. The purpose of this study was to investigate the role and molecular mechanism of circ_ZNF124 in NSCLC development. Methods: The expression of circ_ZNF124, miR-337-3p and JAK2 (Janus Kinase 2) in lung cancer cell lines and normal epithelial cells were detected by qRT-PCR (quantitative real-time PCR). siRNA was used to knockdown circ_ZNF124 expression in cells. The effects of circ_ZNF124 in NSCLC cells were determined by cell growth, cell migration, cell cycle analysis and colony formation. Bioinformatics analysis, RNA immunoprecipitation, luciferase assay and western blots were used to study the molecular mechanism of circ_ZNF124 in NSCLC. Results: The results showed that circ_ZNF124 expression was highly upregulated in NSCLC cells than in normal epithelial cells. Knockdown of circ_ZNF124 by using siRNA significantly decreased cell growth, promoted cell cycle arrested in sub-G1 phase, impaired cell migration and colony formation. Bioinformatic analysis discovered that miR-337-3p was a direct target of circ_ZNF124. In contrast to circ_ZNF124, miR-337-3p expression was significantly downregulated in NSCLC cells. Biotin labeled circ_ZNF124 immunoprecipitation and luciferase assay showed that miR-337-3p could directly bind to and affect circ_ZNF124 activity. The regulation of circ_ZNF124 on miR-337-3p was also investigated. Further analysis showed that despite STAT3 (signal transducer and activator of transcription 3), JAK2 was also a target of miR-337-3p, overexpression of miR-337-3p greatly downregulated JAK2, STAT3 and JAK2/STAT3 downstream regulated oncogenes HIF1a (Hypoxia-inducible factor 1-alpha), BCL2 (B cell lymphoma 2) and c-FOS expression, however, the roles of miR-337-3p in JAK2/STAT3 signaling pathway were greatly inhibited in the presence of circ_ZNF124. Conclusion: In NSCLC, highly expressed circ_ZNF124 promoted the activation of JAK2/STAT3 signaling pathway by acting as a sponge of miR-337-3p, thus promoting the occurrence and development of NSCLC. Circ_ZNF124 could be a potential biomarker or target for the treatment of NSCLC patients in the future.

This paper aims to explore the lncRNA PROX1-AS1 effect on proliferation, migration, invasion, and apoptosis of lung cancer cells together with its targeted regulation on miR-1305. To adopt qRT-PCR to test PROX1-AS1 and miR-1305 expression levels in lung cancer tissues and adjacent tissues. Lung cancer cells A549 were cultured in vitro and randomly divided into several groups, which are si-NC, si-PROX1-AS1, miR-NC, miR-1305, si-PROX1-AS1 plus anti-miR-NC, and si-PROX1-AS1 plus anti-miR-1305. To adopt the CCK-8 method to test cell proliferation and to adopt the Transwell chamber experiment to test cell migration and invasion. To adopt the flow cytometry method to test the apoptosis rate. Through a dual luciferase experiment, we decided to find out the targeting relationship between PROX1-AS1 and miR-1305. Then we adopted the western blot method to test CyclinD1, MMP-2, MMP-9, Bcl-2, p21, and Bax expression levels. Compared with adjacent tissues ( P < 0.05 ), the expression of PROX1-AS1 in lung cancer tissue was remarkably higher, while the expression of miR-1305 was remarkably lower ( P < 0.05 ). After PROX1-AS1 knockdown expression or miR-1305 overexpression, cell activity, migration, and invasion ability were outstandingly lowered ( P < 0.05 ), but the apoptosis rate was obviously raised ( P < 0.05 ), CyclinD1, MMP-2, Bcl-2, and MMP-9 protein data were remarkably reduced ( P < 0.05 ), but p21 and Bax protein conditions were outstandingly enhanced ( P < 0.05 ). The dual luciferase experiment confirmed that PROX1-AS1 had a targeting relationship with miR-1305. After cotransfection with si-PROX1-AS1 and anti-miR-1305, the cell viability, migration and invasion ability were remarkably enhanced ( P < 0.05 ), the apoptosis rate was remarkably reduced ( P < 0.05 ), CyclinD1, MMP-2, Bcl-2, and MMP-9 protein were increased remarkably ( P < 0.05 ), and p21 or Bax protein was lowered remarkably ( P < 0.05 ). On the one hand, PROX1-AS1 can promote lung cancer proliferation, migration, and invasion. On the other hand, it may restrain apoptosis, possibly through inhibiting miR-1305 expression.

Aim: To investigate the effects of SKA3 on cell proliferation and metastasis in non-small-cell lung cancer (NSCLC) and its underlying mechanism. Methods: Immunohistochemistry was employed to analyze the expression of SKA3 in NSCLC. CCK-8 assay, EdU assay, Transwell assay and flow cytometry analysis were employed to assess cell proliferation, metastatic potential and apoptosis in vitro, respectively. A lung metastasis model was used to evaluate metastasis of NSCLC cells in vivo. A luciferase reporter gene assay was conducted to verify the targeting relationship. Results: SKA3 exhibited high expression in NSCLC tissues and cells. Overexpression of SKA3 remarkably accelerated cell proliferation and metastasis and suppressed apoptosis of NSCLC cells and promoted lung metastasis in a mouse model. miR-128-3p repressed SKA3 expression by targeting it. Conclusion: miR-128-3p inhibited the progression of NSCLC through targeting SKA3.

Tracheal reconstruction after extensive resection remains a challenge in thoracic surgery. Aortic allograft has been proposed to be a potential tracheal substitute. However, clinically, its application is limited for the shortage of autologous aortic segment. Whether xenogeneic aortic biosheets can be used as tracheal substitutes remains unknown. In the present study, we investigated the possibility in dog model. The results show that all dogs were survived without airway symptoms at 6 months after tracheal reconstruction with gently decellularized bovine carotid arteries. In the interior of engrafted areas, grafted patch integrated tightly with the residual native tracheal tissues and tracheal defects in the lumen were repaired smoothly without obvious inflammation, granulation, anastomotic leakage, or stenosis. In addition, histological and scanning electron microscopy examination showed that grafted patches were covered with ciliated columnar epithelium similar to epithelium in native trachea, which indicated successfully re-epithelialization of decellularized bovine carotid arteries in dogs. These findings provide preclinical investigation of xenogeneic aortic biosheets in serving as tracheal substitute in a dog model, which proposes that decellularized biosheets of bovine carotid may be a potential material for bioartificial tracheal graft.