Cyclic long noncoding RNAs have recently become major players in cancer biology and can serve as biomarkers for cancer diagnosis and prognosis, and as potential therapeutic targets. We explored circulating LINC00342 as a predictor of non–small cell lung cancer (NSCLC). The expression of LINC00342 in tissues, serum, PBMC, and NSCLC cell lines were screened by reverse transcription quantitative polymerase chain reaction. A multistage validation and risk score formula detection analysis was used. The effect of LINC00342 on proliferation was assessed by MTT, p53, and PTEN pathways, which were analyzed by Western blot analysis. We found that LINC00342 was upregulated in the tissues, serum, and PBMC of patients with NSCLC. In addition, patients with higher LINC00342 expression levels were associated with poor overall survival. For the diagnosis of NSCLC, the specificity and sensitivity of LINC00342 were significantly higher than that of CYFRA 21‐1. Moreover, LINC00342 promoted proliferation by inhibiting the expression of p53 and PTEN proteins in NSCLC cell lines. Our study demonstrates that LINC00342 is involved in the development, and LINC00342 may be a potential diagnostic factor and a target for new therapies for future patients with NSCLC.

MicroRNAs (miRNAs) are short non-coding RNAs, which generally regulate gene expression at the post-transcriptional level. Dysregulation of miRNAs has been reported in numerous cancer types, including lung cancer. In the present study, the role of miR-505 in non-small cell lung cancer (NSCLC) cells was investigated. miR-505 served a tumor suppressor role in NSCLC cells. By reverse transcriptase-quantitative polymerase chain reaction detection, it was demonstrated that miR-505 was downregulated in NSCLC tissues and cell lines, which is negatively associated with large tumor size, Tumor-Node-Metastasis stage and distant metastasis in patients with NSCLC. Functional studies revealed that miR-505 inhibited cell proliferation, migration, invasion and epithelial-mesenchymal transition progress in vitro and tumor growth in vivo. Mechanically, mitogen-activated protein kinase kinase kinase 3 (MAP3K3) was identified as a direct target of miR-505 by binding to its 3′untranslated region and demonstrated to mediate the tumor suppressor roles of miR-505 in NSCLC cells. The effect of miR-505 on the activation of AKT/nuclear factor-κB (NFκB) pathway, which was downstream targets of MAP3K3, was further analyzed by western blot analysis and immunofluorescence analyses. The data demonstrated the inhibition of the AKT/NFκB pathway upon overexpressing miR-505 and the activation of AKT/NFκB pathway upon silencing miR-505. Collectively, the data revealed the novel role and target of miR-505 in NSCLC cells, which may provide novel insights regarding its role in the carcinogenesis of NSCLC and its potential values for clinical applications.

No abstract

BackgroundThe study was conducted to evaluate the efficacy and safety of weekly intravenous nanoparticle albumin‐bound paclitaxel (NAB‐paclitaxel) treatment in patients with advanced non‐small‐cell lung cancer (NSCLC) who have undergone multi‐line therapy, and to investigate the association of secreted protein acidic and rich in cysteine (SPARC) expression status with clinical outcome.MethodsSixty‐four patients who received NAB‐paclitaxel treatment (130 mg/m2 on days 1 and 8 of a 21 day cycle) as third line or further systemic treatment from 1 May 2011 to 30 June 2014 were included in this retrospective analysis. Tumor tissue was available in 28 patients for analysis of SPARC expression by immunohistochemistry.ResultsSixty‐two patients had response evaluation and complete survival follow‐up data; 83.9% received the weekly NAB‐paclitaxel as fourth‐line treatment or beyond. The objective response and disease control rates (n = 62) were 16.1% (10/62) and 64.5% (40/62), respectively. The median progression‐free and overall survival rates were 3.7 (95% confidence interval 2.6–4.8) and 9.8 months (95% confidence interval 6.9–12.8), respectively. Previous treatment with taxane did not affect the response to NAB‐paclitaxel. The main grade 3–4 toxicities experienced were neutropenia (9.4%) and leukopenia (7.8%). Patients with SPARC expression in tumor stroma but not in cancer cells had poorer progression‐free survival compared with those with negative SPARC expression in tumor stroma cells (3.3 vs. 5.0 months, P = 0.036).ConclusionWeekly NAB‐paclitaxel might be effective for heavily pretreated NSCLC patients. SPARC expression in tumor stroma cells might be a potential negative predictor of NAB‐paclitaxel.

No abstract