Mechanism of methyltransferase like 3 in epithelial-mesenchymal transition process, invasion, and metastasis in esophageal cancer.
Mechanism of methyltransferase like 3 in epithelial-mesenchymal transition process, invasion, and metastasis in esophageal cancer.
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甲基转移酶样蛋白3在食管癌上皮间质转化及侵袭转移中的作用机制。
DOI：
10.1080/21655979.2021.1994721
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发表时间：
2021-12
期刊：
影响因子：
4.9
通讯作者：
Lv S
中科院分区：
文献类型：
--
作者：
Liang X;Zhang Z;Wang L;Zhang S;Ren L;Li S;Xu J;Lv S
甲基转移酶样 3 (METTL3) 已被确定为癌症进展的决定性诱导剂。本研究旨在分析METTL3在食管癌（ESCA）上皮间质转化（EMT）、侵袭和转移中的调节机制。检测癌组织和细胞中METTL3的表达，并广泛分析其与临床基线数据的相关性。用sh-RNA-METTL3和microRNA (miR)-20a-5p模拟物转染细胞，然后评估侵袭、迁移和EMT。观察了 DiGeorge Critical Region 8 (DGCR8) 和 m6A 的 N6-甲基腺苷 (m6A) 水平和富集。验证miR-20a-5p与核因子I-C（NFIC）之间的结合关系，然后进行Pearson相关分析。在观察肺转移之前进行皮下肿瘤形成测定。我们的结果显示 METTL3 在 ESCA 患者中高表达，并与严重淋巴结受累和远处转移相关。 METTL3 下调从根本上抑制了侵袭性、迁移性和 EMT。 METTL3 通过改善 m6A 修饰来提高 miR-20a-5p 的表达。 METTL3 抑制下调 miR-20a-5p 表达。此外，miR-20a-5p 上调通过靶向 NFIC 转录促进 ESCA 细胞的侵袭和迁移。 METTL3 抑制可抑制体内肿瘤生长和肺转移。总体而言，METTL3促进m6A修饰以及DGCR8与miR-20a-5p的结合，进一步提高miR-20a-5p的表达并抑制NFIC转录，从而促进EMT、侵袭和迁移。
Methyltransferase like 3 (METTL3) has been identified to serve as a definitive inducer in cancer progression. This study sought to analyze the regulatory mechanism of METTL3 in epithelial-mesenchymal transition (EMT), invasion, and metastasis in esophageal cancer (ESCA). The METTL3 expressions in cancer tissues and cells were detected with extensive analysis of its correlation with clinical baseline data. The cells were transfected with sh-RNA-METTL3 and microRNA (miR)-20a-5p mimic, followed by evaluation of invasion, migration, and EMT. The N6-methyladenosine (m6A) level and enrichment of DiGeorge Critical Region 8 (DGCR8) and m6A were observed. The binding relationship between miR-20a-5p and Nuclear Factor I-C (NFIC) was verified, followed by Pearson correlation analysis. A subcutaneous tumor formation assay was conducted prior to observation of lung metastases. Our results revealed that METTL3 was highly expressed in ESCA patients and associated with severe lymph node involvement and distant metastasis. METTL3 downregulation radically inhibited the invasiveness, migration, and EMT. METTL3 elevated the miR-20a-5p expression via improving m6A modification. METTL3 inhibition downregulated the miR-20a-5p expression. Moreover, miR-20a-5p upregulation facilitated ESCA cell invasiveness and migration by targeting NFIC transcription. METTL3 inhibition suppressed tumor growth and lung metastasis in vivo. Overall, METTL3 promoted m6A modification and the binding of DGCR8 to miR-20a-5p to further elevate the miR-20a-5p expression and inhibit NFIC transcription, thus promoting EMT, invasion and migration.
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影响因子：
8
作者：
通讯作者：
--
影响因子：
3.8
作者：
Cheng Y;Li Y;Nian Y;Liu D;Dai F;Zhang J
通讯作者：
Zhang J
Mir-20a-5p诱导的WTX缺乏通过调节PI3K/AKT信号通路促进胃癌进展
DOI：
10.1186/s13046-020-01718-4
发表时间：
2020-10-08
期刊：
Journal of experimental & clinical cancer research : CR
影响因子：
--
作者：
Li J;Ye D;Shen P;Liu X;Zhou P;Zhu G;Xu Y;Fu Y;Li X;Sun J;Xu J;Zhang Q
通讯作者：
Zhang Q
影响因子：
--
作者：
Pandompatam, Govind;Kashani, Kianoush;Vallabhajosyula, Saraschandra
通讯作者：
Vallabhajosyula, Saraschandra
影响因子：
3.7
作者：
Liang, Xin;Gao, Jiangang;Wu, Changli
通讯作者：
Wu, Changli