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METTL3‐mediated m6A modification of EPPK1 to promote the development of esophageal cancer through regulating the PI3K/AKT pathway

基因敲除 下调和上调 PI3K/AKT/mTOR通路 细胞生长 癌症研究 蛋白激酶B 细胞迁移 免疫印迹 化学 免疫沉淀 癌细胞 庆大霉素保护试验 细胞 癌症 信号转导 生物 细胞生物学 细胞凋亡 生物化学 遗传学 基因
作者
Jun Jia,Longhai Yu
出处
期刊:Environmental Toxicology [Wiley]
卷期号:39 (5): 2830-2841 被引量:4
标识
DOI:10.1002/tox.24158
摘要

Abstract Methyltransferase like 3 (METTL3) has been proved to be involved in the progression of various cancers. In this study, we explored the role of METTL3 and its underlying mechanism in esophageal cancer progression. The mRNA and protein levels of METTL3 and epiplakin1 (EPPK1) were determined using qRT‐PCR and western blot. The proliferative ability was evaluated through 3‐(4,5)‐dimethylthiahiazo (‐z‐y1)‐3,5‐di‐ phenytetrazoliumromide (MTT), colony formation, and EdU assays. Transwell invasion assay and wound‐healing assay were employed for detecting cell invasion and migration, respectively. Cell stemness was evaluated by sphere‐formation assay. Xenograft tumor experiments and immunohistochemistry (IHC) were performed to explore the effects of METTL3 knockdown on tumor growth in vivo. The N6‐methyladenosine (m6A) modification of EPPK1 was analyzed using MeRIP. RNA‐protein immunoprecipitation (RIP) and dual‐luciferase reporter assays were used to verify the relationship between EPPK1 and METTL3. METTL3 was upregulated in esophageal cancer tissues and cells, which was related to the poor prognosis of esophageal cancer patients. Knockdown of METTL3 overtly decreased the proliferative, invasive, migrated abilities, and cell stemness of esophageal cancer cells in vitro. Moreover, depletion of METTL3 also observably suppressed the growth of tumor in vivo. EPPK1 was a direct target of METTL3, and METTL3 could mediate the m6A modification of EPPK1. EPPK1 was downregulated in esophageal cancer tissues and cells, and EPPK1 depletion markedly repressed cell proliferation, invasion, migration, and stemness of esophageal cancer cells. The inhibition effects of METTL3 deficiency on these malignant behaviors were harbored by EPPK1 upregulation in esophageal cancer cells. In addition, METTL3 deficiency reduced EPPK1 expression to inactivate the PI3K/AKT pathway. Our results revealed that METTL3 deficiency regulated the m6A modification of EPPK1 to inhibit the PI3K/AKT pathway, thereby restraining the progression of esophageal cancer.
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