Abstract
BackgroundTo analyze the relative expression of PELI3 and its mechanistic involvement in the non-small cell lung cancer (NSCLC).MethodsPELI3 expression in NSCLC tissue samples was determined by the immunohistochemistry. The transcripts abundance of PELI3 was measured with real-time PCR. The protein intensity was analyzed by western blot. The overall survival in respect to PELI3 or miR-365a-5p expression was plotted by the Kaplan–Meier’s analysis. Cell growth was determined by colony formation assay. Cell viability was measured by MTT assay. The migration and invasion were evaluated by wound healing and transwell assay respectively. The regulatory effect of miR-365a-5p on PELI3 was interrogated with luciferase reporter assay. The direct binding between miR-365a-5p and PELI3 was analyzed by pulldown assay.ResultsPELI3 was aberrantly up-regulated in NSCLC both in vivo and in vitro. High level of PELI3 associated with poor prognosis. PELI3-deficiency significantly inhibited cell viability, colony formation, migration and invasion. We further identified that miR-365a-5p negatively regulated PELI3 in this disease. Ectopic expression of miR-365a-5p in both A549 and H1299 phenocopied PELI3-deficiency. Meanwhile, PELI3-silencing significantly abolished the pro-tumoral effect elicited by miR-365a-5p inhibition.ConclusionOur results highlighted the importance of dysregulated miR-365a-5p-PELI3 signaling axis in NSCLC.
Highlights
Lung cancer is the most common human malignancy and the first cause of cancer-related death in men and second after breast cancer in women [1]
The expression of protein ligase family member 3 (PELI3) is up‐regulated in non-small cell lung cancer (NSCLC) and increased PELI3 expression predicts poor prognosis in NSCLC patients We first determined the relative expression of PELI3 in NSCLC clinical tissue samples; the significantly intensive signal was detected in the tumor samples in comparison with the benign control (Fig. 1a)
The relative high expression of PELI3 protein was observed in all tested NSCLC cell lines including H1299, PC9, A549, SPCA1 and H358 compared to the immortalized human bronchial epithelial cell 16HBE (Fig. 1b)
Summary
Lung cancer is the most common human malignancy and the first cause of cancer-related death in men and second after breast cancer in women [1]. The most frequent risk factor related to the vast majority of lung cancer is long-term tobacco. He et al Biol Res (2019) 52:24 activator of nuclear factor kappa-B ligand (RANKL) [7]. Pellino E3 ubiquitin protein ligase family member 3 (PELI3) was initially identified as as a scaffolding protein which promotes activation of c-Jun and Elk-1 [8] and an intermediate signaling protein in the innate immune response pathway. The PELI3 protein has been reported to facilitate the transmission of the immune response signaling from Toll-like receptors to IRAK/TRAF6 complex [10]. To analyze the relative expression of PELI3 and its mechanistic involvement in the non-small cell lung cancer (NSCLC)
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