龙海晨
(2022-09-01 12:18):
#paper Luo F, Lin K. N6-methyladenosine (m6A) reader IGF2BP1 accelerates gastric cancer aerobic glycolysis in c-Myc-dependent manner[J]. Experimental Cell Research, 2022, 417(1): 113176. PMID: 35489385
DOI: 10.1016/j.yexcr.2022.113176
该文章研究了N 6-甲基腺苷（m 6 A），RNA m 6 A reader IGF2BP1 在胃癌发生发展中的作用。m 6 A参与调节多种癌症中的癌细胞增殖、转移、形成。文章分析了IGF2BP1在胃癌（gastric cancer，GC）中的功能和机制。研究结果表明，IGF2BP1 在 GC 组织中上调，可作为 GC 患者预后不良的预测因子。在功能上，IGF2BP1 促进体外 GC 细胞迁移和有氧糖酵解。IGF2BP1 敲低抑制了体内肿瘤的生长。文章证明了 IGF2BP1 通过 m6A 依赖性方式直接与 c-MYC mRNA 相互作用。文章发现，m 6 A reader IGF2BP1 以依赖 m 6 A/c-Myc 方式促进了 GC 的致癌性，这可能为 GC 提供治疗策略。
N6-methyladenosine (m6A) reader IGF2BP1 accelerates gastric cancer aerobic glycolysis in c-Myc-dependent manner
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Abstract:
The N-methyladenosine (mA) is involved in the regulation of cell proliferation and metastasis formation in multiple cancers. However, the biological significance of RNA mA reader IGF2BP1 and the modification of IGF2BP1 itself have not been fully investigated. Here, we analyzed the functions and mechanism of IGF2BP1 in gastric cancer (GC). Results showed that IGF2BP1 upregulated in GC tissue and acted as a predictor of poor prognosis for GC patients. Functionally, IGF2BP1 promoted the migration and aerobic glycolysis of GC cells in vitro. Moreover, IGF2BP1 knockdown repressed the tumor growth in vivo. We also demonstrated that IGF2BP1 directly interacted with c-MYC mRNA via m6A-dependent manner to by stabilize its stability. Overall, these findings demonstrated that mA reader IGF2BP1 facilitated the carcinogenic of GC in mA/c-Myc-dependent manner, which might provide critical therapeutic strategy for GC.
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