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N6-甲基腺苷修饰 REG1α 通过 β-连环蛋白/原癌基因 c-Myc/乳酸脱氢酶 A 轴介导的糖酵解重编程促进结直肠癌的进展。

N-methyladenosine modification of REG1α facilitates colorectal cancer progression via β-catenin/MYC/LDHA axis mediated glycolytic reprogramming.

机构信息

Department of Gastroenterology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.

Department of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.

出版信息

Cell Death Dis. 2023 Aug 25;14(8):557. doi: 10.1038/s41419-023-06067-6.

DOI:10.1038/s41419-023-06067-6
PMID:37626036
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10457312/
Abstract

Aerobic glycolysis has been considered as a hallmark of colorectal cancer (CRC). However, the potential functional regulators of glycolysis in CRC remains to be elucidated. In the current study, we found that Regenerating islet-derived protein 1-alpha (REG1α) was significantly increased in both CRC tissues and serum, and positively associated with CRC patients' lymph node metastasis, advanced tumor stage, and unfavorable prognosis. Ectopic expression of REG1α contributed to various tumorigenic properties, including cell proliferation, cell cycle, migration, invasion, and glycolysis. In contrast, REG1α deficiency in CRC cells attenuated malignant properties and glucose metabolism. Mechanically, REG1α promoted CRC proliferation and metastasis via β-catenin/MYC axis-mediated glycolysis upregulation. Moreover, the malignant behaviors governed by REG1α could be effectively abolished by silencing of Wnt/β-catenin/MYC axis or glycolysis process using specific inhibitors. Besides, REG1α expression was mediated by METTL3 in an mA-dependent manner. Overall, our work defines a novel regulatory model of the METTL3/REG1α/β-catenin/MYC axis in CRC, which indicates that REG1α could function as a novel biomarker and a potential therapeutic target for patients with CRC.

摘要

有氧糖酵解被认为是结直肠癌（CRC）的一个标志。然而，CRC 中糖酵解的潜在功能调节剂仍有待阐明。在本研究中，我们发现再生胰岛衍生蛋白 1-α（REG1α）在 CRC 组织和血清中均显著增加，并且与 CRC 患者的淋巴结转移、晚期肿瘤分期和不良预后呈正相关。REG1α 的异位表达有助于多种致瘤特性，包括细胞增殖、细胞周期、迁移、侵袭和糖酵解。相比之下，CRC 细胞中 REG1α 的缺失会减弱恶性特性和葡萄糖代谢。在机制上，REG1α 通过β-catenin/MYC 轴介导的糖酵解上调促进 CRC 增殖和转移。此外，通过沉默 Wnt/β-catenin/MYC 轴或使用特定抑制剂抑制糖酵解过程，可以有效消除 REG1α 调控的恶性行为。此外，METTL3 以 mA 依赖的方式介导 REG1α 的表达。总的来说，我们的工作定义了 CRC 中 METTL3/REG1α/β-catenin/MYC 轴的新调控模型，表明 REG1α 可以作为 CRC 患者的新型生物标志物和潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d2a/10457312/1607562f2619/41419_2023_6067_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d2a/10457312/ac39358d052c/41419_2023_6067_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d2a/10457312/0252c89dd3da/41419_2023_6067_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d2a/10457312/efcefa9e7a3f/41419_2023_6067_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d2a/10457312/89fd3f5c6e62/41419_2023_6067_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d2a/10457312/1ec9d6b41379/41419_2023_6067_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d2a/10457312/2c71717882d1/41419_2023_6067_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d2a/10457312/71ea7ad1cb8b/41419_2023_6067_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d2a/10457312/1607562f2619/41419_2023_6067_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d2a/10457312/ac39358d052c/41419_2023_6067_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d2a/10457312/0252c89dd3da/41419_2023_6067_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d2a/10457312/efcefa9e7a3f/41419_2023_6067_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d2a/10457312/89fd3f5c6e62/41419_2023_6067_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d2a/10457312/1ec9d6b41379/41419_2023_6067_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d2a/10457312/2c71717882d1/41419_2023_6067_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d2a/10457312/71ea7ad1cb8b/41419_2023_6067_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d2a/10457312/1607562f2619/41419_2023_6067_Fig8_HTML.jpg

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本文引用的文献

[1]
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Oncogenesis. 2021-1-5

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