EIF3J-AS1 promotes glioma cell growth via up-regulating ANXA11 through sponging miR-1343-3p

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Cancer Cell International Open Access

PRIMARY RESEARCH

EIF3J‑AS1 promotes glioma cell growth via up‑regulating ANXA11 through sponging miR‑1343‑3p Jianguo Qi1†, Zhengrui Wang2†, Zhensheng Zhao3 and Lijun Liu4* 

Abstract  Background:  Glioma is one prevalent malignant tumor originates from the central nervous system. Dysregulation of long non-coding RNAs (lncRNAs) has been found to be a molecular signature behind the pathology of a variety of cancers, including glioma. EIF3J antisense RNA 1 (EIF3J-AS1) is a novel lncRNA, whose performance in carcinogenesis has been unfolded. Nevertheless, the role of EIF3J-AS1 has never been investigated in glioma. Methods:  qRT-PCR analysis was adopted to evaluate the relative levels of RNAs. In vitro functional assays, including colony formation, EdU, TUNEL and caspase-3/8/9 activity assays were conducted to study the impacts of EIF3J-AS1 on glioma. Dual-luciferase activity assays, RNA pull down assay and RIP assay were performed to elucidate molecular interplay among genes. Results:  EIF3J-AS1 was overexpressed in glioma cell lines. Knockdown of EIF3J-AS1 hampered glioma malignant phenotypes. MiR-1343-3p could bind to EIF3J-AS1. Moreover, miR-1343-3p targeted Annexin A11 (ANXA11) in its 3′UTR region. Mechanistically, EIF3J-AS1 relieved ANXA11 from miR-1343-3p silencing in the EIF3J-AS1/miR-1343-3p/ ANXA11 RNA induced silencing complex (RISC), thus eliciting promoting effects on glioma progression. MiR-1343-3p inhibitor and ANXA11 overexpression offset the inhibitory impacts of EIF3J-AS1 silencing on glioma development. Conclusion:  EIF3J-AS1/miR-1343-3p/ANXA11 axis significantly affected biological behaviors in glioma, suggesting new therapeutic target for glioma treatment. Keywords:  Glioma, EIF3J-AS1, miR-1343-3p, ANXA11 Background Glioma remains the most frequently diagnosed primary tumor and lethal form of brain tumors [1]. The most common histologic subtypes of glioma are astrocytoma and oligodendroglioma [2]. Despite multimodal therapeutic strategy, such as chemotherapy, radiotherapy and other adjuvant therapy have been combined to combat glioma *Correspondence: [email protected] † Jianguo Qi and Zhengrui Wang—co-first authors 4 Department of Neurosurgery, Xiangyang No.1 People’s Hospital Affiliated to Hubei University of Medicine, NO.15 Jiefang Road, Fancheng District, Xiangyang 441000, Hubei, China Full list of author information is available at the end of the article

over the last decade, the prognosis of glioma patients remains unoptimistic [3, 4]. Lack of efficient and novel molecular target in clinical treatment is a vital reason for the unsatisfactory outcome [5]. Therefore, exploring molecular mechanism of glioma is of vital significance. Cancer transcriptome is featured in aberrant expression of both protein-coding and non-coding transcripts. Numerous evidence have indicated that long non-coding RNAs (lncRNAs) played important part in regulating the development of human diseases, even the malignant progression of cancers, including glioma [6–8]. Recently, emerging r