文章：

CEACAM6通过上调SLC27A2促进胃癌进展

CEACAM6 facilitates gastric cancer progression through upregulating SLC27A2 

原文发布日期：2024-11-19 

英文摘要：

Gastric cancer (GC) is one of the most lethal cancers. However, the underlying mechanisms are not yet fully understood. Here, we investigated the role of carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) in tumor initiation and progression in GC and proposed therapeutic strategies for CEACAM6-positive patients. In this article, we found that CEACAM6 overexpression promoted GC initiation and progression by overactivating FAO. CEACAM6 promotes SLC27A2 expression, contributing to enhanced fatty acid incorporation. CEACAM6 interacts with both SLC27A2 and USP29, facilitating the deubiquitination of USP29 on SLC27A2. Pharmacological inhibition of SLC27A2 attenuates the tumor-initiating ability of GC. Taken together, CEACAM6 overexpression facilitates GC progression by upregulating fatty acid uptake through SLC27A2, thereby contributing to FAO. Genetic ablation of SLC27A2 is a promising therapeutic strategy for patients with CEACAM6-positive GC. 

摘要翻译：

胃癌（GC）是最致命的恶性肿瘤之一，但其发生机制尚未完全阐明。本研究探讨了癌胚抗原相关细胞 adhesion 分子6（CEACAM6）在胃癌发生发展中的作用，并针对CEACAM6阳性患者提出治疗策略。我们发现CEACAM6过表达通过过度激活脂肪酸氧化（FAO）促进胃癌的发生发展。CEACAM6通过促进SLC27A2表达增强脂肪酸摄取，同时与SLC27A2和USP29相互作用，促进USP29对SLC27A2的去泛素化修饰。SLC27A2的药理学抑制可显著降低胃癌的肿瘤起始能力。综上所述，CEACAM6过表达通过SLC27A2上调脂肪酸摄取进而促进FAO，最终加速胃癌进展。针对SLC27A2的基因靶向治疗是CEACAM6阳性胃癌患者的潜在治疗策略。

原文链接：

CEACAM6 facilitates gastric cancer progression through upregulating SLC27A2