Non-small cell lung cancer (NSCLC) is the most common malignant tumor of lung, which seriously threatens the life of people. It has been reported that lncRNA prostate cancer-associated transcript 6 (PCAT6) could facilitate the metastasis of NSCLC cells. However, whether lncRNA PCAT6 in NSCLC cells could affect the tumor microenvironment (TME) remains unclear. In the present study, the level of PCAT6 in NSCLC cells was detected using RT-qPCR. The effects of PCAT6 knockdown on the viability and apoptosis in NSCLC cells were detected with CCK-8 and flow cytometry assay. NSCLC cell-derived exosomes were isolated with ultracentrifugation. Next, transwell assay was conducted to assess the migration and invasion of NSCLC cells. Dual-luciferase reporter assay was performed to verify the relationship among PCAT6, miR-326, and KLF1 in A549 cells. In addition, nanoparticle tracking analysis (NTA) was applied to detect the particle size of isolated exosomes. Moreover, ELISA assay was performed to detect the levels of IL-1β and IL-10 in the supernatant of macrophage. We found knockdown of PCAT6 significantly inhibited the viability, migration, and invasion of NSCLC cells. In addition, dual-luciferase reporter assay illustrated that miR-326 was the target of PCAT6 and KLF1 was the target of miR-326 in NSCLC cells. Moreover, NSCLC cells-derived exosomes could promote macrophages M2 polarization by transporting PCAT6. Meanwhile, macrophages M2 polarization was able to promote the metastasis and epithelial-mesenchymal transition (EMT) process of NSCLC cells via regulating PCAT6/miR-326/KLF1 axis. Taken together, knockdown of lncRNA PCAT6 suppressed the growth of NSCLC cells by inhibiting macrophages M2 polarization via miR-326/KLF1 axis.

BACKGROUND Lung cancer is one of the deadliest cancers in the world with the highest incidence and mortality rate among all cancers. Non-small cell lung cancer (NSCLC) accounts for approximately 80% of primary lung cancer. However, efficacy and safety of the current regimens for NSCLC is unsatisfactory. Therefore, there has been an increasing urgency for development of potential therapeutic therapies for NSCLC. AIM To investigate the therapeutic outcomes and safety of continuous intravenous infusion of recombinant human endostatin (Rh-endostain) using an infusion pump in retreated advanced NSCLC. METHODS Patients with retreated advanced NSCLC who were admitted to Zhejiang Provincial People's Hospital from October 2017 to April 2019 were recruited. These patients received continuous intravenous infusion of Rh-endostain using an infusion pump. Objective response rate (ORR), clinical benefit rate (CBR), median progression-free survival (mPFS), and incidences of adverse events (AEs) were analyzed after treatment. RESULTS A total of 45 patients with retreated advanced NSCLC were included, and all of them were evaluated. In these patients, ORR was 22.2%, CBR was 84.4%, and mPFS was 5.3 mo. The following AEs were observed, decreased hemoglobin (34 cases, 75.6%), nausea/vomiting (32 cases, 71.1%), elevated transaminase (24 cases, 53.3%), leukopenia (16 cases, 35.6%), thrombocytopenia (14 cases, 31.1%), and constipation (1 case, 3.4%). None of the patients had leukopenia, nausea /vomiting, and constipation of grade III and above. CONCLUSION The patients showed improved adherence to 5-d continuous intravenous infusion of Rh-endostain using an infusion pump. Favorable efficacy and safety of this treatment regimen were achieved in retreated advanced NSCLC.

Patients with non-small cell lung cancer (NSCLC) can develop strong drug resistance following long-term treatment with platinum-based drugs. Increasing doses of chemotherapeutic drugs fail to obtain better results, and serious complications occur. It has been demonstrated that upregulation of excision repair cross-complementary 1 (ERCC1) in lung cancer cells is closely associated with cell resistance to platinum-based chemotherapy. In addition, curcumin (CMN) enhances antitumor effects in NSCLC by downregulating ERCC1. The aim of the present study was to investigate the effects of demethoxycurcumin (DMC), a curcuminoid, on the reversal of resistance of NSCLC cells in vitro and in vivo. The present study demonstrated that DMC significantly increased the sensitivity of DDP in DDP-resistant A549 (A549/DDP) cells. The results from an MTT assay demonstrated that DMC combined with DDP significantly attenuated the proliferation of A549/DDP cells. Furthermore, DMC exhibited decreased toxicity in normal lung fibroblast MRC-5 cells. In addition, following treatment of A549/DDP cells with a combination of DMC and DDP, the expression of ERCC1 was reduced, the protein levels of Bcl-2 and Bax were decreased and increased, respectively, whereas caspase-3 was activated, according to results from western blotting. Finally, DDP combined with DMC significantly attenuated A549/DDP cell-derived tumor growth in vivo. Taken together, the findings from the present study suggested that DMC in combination with DDP may be considered as a novel combination regimen for restoring DDP sensitivity in DDP-resistant NSCLC cells.