MAFG-AS1 aggravates the progression of pancreatic cancer by sponging miR-3196 to boost NFIX
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Cancer Cell International Open Access
PRIMARY RESEARCH
MAFG‑AS1 aggravates the progression of pancreatic cancer by sponging miR‑3196 to boost NFIX Liqing Ye†, Weijian Feng†, Hanqin Weng* , Chongde Yuan, Jia Liu and Zaiguo Wang
Abstract Background: A host of researches have demonstrated the regulation of long non-coding RNAs (lncRNAs) in the progression of pancreatic cancers (PC). In this study, our main task was to analyze the function of MAF bZIP transcription factor G antisense RNA 1 (MAFG-AS1) in PC. Methods: RT-qPCR measured gene expression. Functional experiments, including EdU assay, flow cytometry analysis, TUNEL assay and transwell assay, assessed the biological changes of PC cells. RNA pull down assay, luciferase reporter assay and RIP assay verified the interaction between RNAs. Results: MAFG-AS1 was lowly expressed in normal pancreatic samples but up-regulated in PC tissues and cell lines. Besides, MAFG-AS1 silence suppressed cell proliferation and migration whereas promoted cell apoptosis in PC. Mechanism assays verified that miR-3196 could bind with MAFG-AS1. Moreover, miR-3196 was discovered to be lowly expressed in PC cell lines, and its overexpression inhibited PC cell growth and migration. Importantly, nuclear factor I X (NFIX), overexpressed in PC cell lines, was validated to be positively modulated by MAFG-AS1 through absorbing miR-3196. Moreover, overexpression of NFIX could countervail the restraining effects of MAFG-AS1 knockdown on the growth and migration of PC cells. Conclusion: MAFG-AS1 had an oncogenic function in the progression of PC via regulating miR-3196/NFIX pathway, and decreasing MAFG-AS1 expression could attenuate PC progression. Keywords: MAFG-AS1, miR-3196, NFIX, Pancreatic cancer Background Pancreatic cancer (PC) is a common tumor in the digestive system around the globe, characterized by intensive migration and high invasion [1]. Though great achievements have been made in comprehensive therapies of cancers, the morbidity and mortality of PC are still increasing, which makes it a great threat to human life and health [2]. The prognosis of PC is rather dismal in *Correspondence: [email protected] † Liqing Ye and Weijian Feng Co-first author Department of Hepato‑Billiary Surgery, Dongguan People’s Hospital, Southern Medical University, Guangming Road, Dongcheng District, Dongguan 523059, Guangdong, China
the past decade [3]. Surgery is a routine treatment for PC patients, but the recurrence rate is extremely high due to frequent metastasis [4]. The detailed cause of PC is still a riddle. Hence, it is necessary to study the pathological feature of PC and figure out the underlying mechanism to find out effective therapeutic ways. Long non-coding RNAs (lncRNAs) are widely identified to modulate biological progression in multiple cancers. For instance, lncRNA PCAT-1 accelerated NSCLC progression by targeting miR-149-5p to regulate LRIG2 [5]. MALAT1 promoted the progression of ovarian cancer through modulating miR-506 and iASPP [6]. Lnc-ATB facilitated cell proliferation
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