ArticleCancer gene therapy2025
CEACAM6 facilitates gastric cancer progression through upregulating SLC27A2.
Article in Cancer gene therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Metabolic reprogramming, oxidative stress, and mitophagy in JSRV Env-transformed BEAS-2B cells: insights from integrated transcriptomics and metabolomics.BMC genomics · 2026Article
- COL3A1 promotes gastric cancer progression by activating PI3K/AKT signaling.Cancer gene therapy · 2026Article
- SLC27, solute carrier 27 family, a long-chain fatty acid membrane transporters, in human cancers.Frontiers in cell and developmental biology · 2026Review
- CEACAM6 regulates glycolytic metabolism in bladder cancer cell by controlling ENO1 stability.European journal of medical research · 2025Article
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Authors and funding
6 authors.
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Abstract
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.
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