Evidence map›Paper›PMID 40626525›Full record

ArticleCurrent molecular medicine2026

SLC41A2 Suppresses Colon Cancer Progression by Inhibiting GSK3β Ubiquitin-proteasome Degradation.

Yueyao Lu, Ying Shen, Jinsong Liu, Jianzhong Deng, Yue Wang, Qian Liu, Wenbin Lu

Abstract read
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Article in Current molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Yueyao LuDepartment of Oncology, Changzhou Wujin People's Hospital, Changzhou Medical Center, Nanjing Medical University, Jiangsu Province, 213017, China.
Ying ShenDepartment of Oncology, The Wujin Clinical College of Xuzhou Medical University, Jiangsu Province, 213017, China.
Jinsong LiuDepartment of VIP Medical, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Jianzhong DengDepartment of Oncology, The Wujin Clinical College of Xuzhou Medical University, Jiangsu Province, 213017, China.
Yue WangDepartment of Oncology, The Wujin Clinical College of Xuzhou Medical University, Jiangsu Province, 213017, China.
Qian LiuDepartment of Oncology, Changzhou Wujin People's Hospital, Changzhou Medical Center, Nanjing Medical University, Jiangsu Province, 213017, China.
Wenbin LuDepartment of Oncology, Changzhou Wujin People's Hospital, Changzhou Medical Center, Nanjing Medical University, Jiangsu Province, 213017, China.

Funding

Basic Youth Program of Changzhou Medical Center of Nanjing Medical University CMCB202452Changzhou High-Level Medical Talents Training Project 2022CZBJ110Changzhou Sci & Tech Program CJ20230007, CJ20245002Innovation Team Project of the Science and Technology Development Fund at the Affiliated Hospital of Xuzhou Medical University XYFC202303Jiangsu Province Key Laboratory of Tumor Biotherapy XZSYSKF2023034Medical Education Collaborative Innovation Fund of Jiangsu University JDY2023017
6 · The paper itself

Abstract

backgroundColon cancer is a highly prevalent tumor with a high mortality rate worldwide. SLC41A2 is a member of the solute carrier family, but its role in colon cancer is still unclear.

methodsThe relationship between the expression level of SLC41A2 and clinicopathological features in colon cancer was investigated using data from the TCGA database. The differential expression genes of SLC41A2 were identified the potential role of SLC41A2 in colon cancer was analysed through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. By transfecting plasmids or siRNA to overexpress or knock down SLC41A2 in colon cancer cells, the effects of SLC41A2 on colon cancer cell proliferation, migration, and apoptosis were detected through EdU, MTT, wound-healing, Transwell, and JC-1 experiments.. Western blot and ubiquitination experiments validated the regulation of GSK3β stability by SLC41A2. Rescue experiments and CCK8 assays confirmed the regulatory effect of SLC41A2 on GSK3β.

resultsCompared to normal tissues, SLC41A2 exhibited a lower expression level in colon cancer, and the expression levels of SLC41A2 were correlated with the stage and Tumor Node Metastasis (TNM) classification. GO and KEGG analyses displayed that SLC41A2 primarily affected the growth factor activity and Wnt signaling pathway. Furthermore, elevated expression of SLC41A2 notably decreased the proliferation, migration and invasion of colon cancer cells, along with increased apoptosis. The overexpression of SLC41A2 and rescue experiments confirmed that SLC41A2 enhances the protein stability of GSK3β by inhibiting its ubiquitin-proteasome degradation and causes the upregulation of GSK3β, thereby suppressing the progression of colon cancer.

conclusionSLC41A2 was lowly expressed in colon cancer tissues or cells. By inhibiting the ubiquitin-proteasome degradation of GSK3β, SLC41A2 can significantly upregulate the expression of GSK3β, which ultimately suppresses the proliferation and migration of colon cancer cells.

Indexed as

Colonic NeoplasmsGlycogen Synthase Kinase 3 betaOrganic Cation Transport ProteinsProteasome Endopeptidase ComplexUbiquitinApoptosisCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleProteolysisUbiquitinationGlycogen Synthase Kinase 3 betaGSK3B protein, humanOrganic Cation Transport ProteinsProteasome Endopeptidase ComplexUbiquitinColon cancerGSK3βmetastasisproliferationSLC41A2Wnt signaling pathway

Identifiers

PMID40626525

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.