ASB16-AS1 up-regulated and phosphorylated TRIM37 to activate NF-kappa B pathway and promote proliferation, stemness, and cisplatin resistance of gastric cancer
机构:[1]Department of Gastrointestinal Surgery, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Institute, No. 52 Fucheng Road, Haidian District, Beijing 100142, China[2]Department of Radiotherapy, Sichuan Cancer Hospital and Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu 610041, China四川省人民医院四川省肿瘤医院
Background Long non-coding RNA (lncRNA) ASB16 antisense RNA 1 (ASB16-AS1) is recognized as an oncogene in several cancer types, but its relation to GC is unknown. Tripartite motif containing 37 (TRIM37) has been proven to accelerate the development of gastric cancer (GC), whereas the molecular mechanism assisted ASB16-AS1 and TRIM37 in regulating GC progression remains unclear. Methods Differentially expressed lncRNAs in GC samples were analyzed based on Gene Expression Omnibus (GEO) data. CCK-8 and colony formation assays were applied to determine the proliferative ability of GC cells. Stem cell-like phenotype of GC cells was assessed by sphere formation assay and flow cytometry analysis. Luciferase reporter assay, RNA immunoprecipitation (RIP), pulldown, and co-immunoprecipitation (Co-IP) were performed to verify the interplay of RNA molecules. Results ASB16-AS1 was upregulated in GC samples according to GEO data and qRT-PCR analysis. ASB16-AS1 strengthened the proliferative ability and stem cell-like characteristics in GC cells. More importantly, ASB16-AS1 encouraged GC cell growth in vivo. Mechanistically, ASB16-AS1 strengthened TRIM37 expression by sequestering miR-3918 and miR-4676-3p. ASB16-AS1 activated NF-kappa B (NF-kappa B) pathway by cooperating with ATM serine/threonine kinase (ATM) to induce TRIM37 phosphorylation. Conclusion In summary, ASB16-AS1 exerted oncogenic functions in GC through modulating TRIM37 expression at both mRNA and protein levels.
基金:
Science Foundation of Peking University Cancer Hospital [2020-12]
第一作者机构:[1]Department of Gastrointestinal Surgery, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Institute, No. 52 Fucheng Road, Haidian District, Beijing 100142, China
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推荐引用方式(GB/T 7714):
Fu Tao,Ji Ke,Jin Li,et al.ASB16-AS1 up-regulated and phosphorylated TRIM37 to activate NF-kappa B pathway and promote proliferation, stemness, and cisplatin resistance of gastric cancer[J].GASTRIC CANCER.2021,24(1):45-59.doi:10.1007/s10120-020-01096-y.
APA:
Fu, Tao,Ji, Ke,Jin, Li,Zhang, Ji,Wu, Xiaojiang...&Ji, Jiafu.(2021).ASB16-AS1 up-regulated and phosphorylated TRIM37 to activate NF-kappa B pathway and promote proliferation, stemness, and cisplatin resistance of gastric cancer.GASTRIC CANCER,24,(1)
MLA:
Fu, Tao,et al."ASB16-AS1 up-regulated and phosphorylated TRIM37 to activate NF-kappa B pathway and promote proliferation, stemness, and cisplatin resistance of gastric cancer".GASTRIC CANCER 24..1(2021):45-59