Evidence map›Paper›PMID 40668324›Full record

ArticleMolecular biology reports2025

Mechanism of ABCD3 inhibiting colorectal cancer progression by regulating Wnt/β-catenin.

Huali Luo, Mengxing Li, Xiaojing Lin, Shu Zhao, Qinshan Li

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Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

5 authors.

Huali LuoClinical Laboratory Center, Guizhou Institute of Precision Medicine, Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, China.
Mengxing LiDepartment of Hematology, Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, China.
Xiaojing Lin *Department of Obstetrics and Gynecology, Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, China.
Shu Zhao *Department of Obstetrics, Guizhou People's Hospital, Guiyang, 550002, China.
Qinshan LiClinical Laboratory Center, Guizhou Institute of Precision Medicine, Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, China. liqinshan@gmc.edu.cn.

Funding

Guizhou Medical University Science and Technology Plan Project 21NSFCP12National Natural Science Foundation of China 81760039National Natural Science Foundation of China 81960476
6 · The paper itself

Abstract

backgroundAccumulating evidence highlights the critical role of dysregulated Wnt/β-catenin signaling in colorectal cancer (CRC) pathogenesis. However, the clinical translation of therapeutics targeting this pathway remains challenging. While ABCD3 is known to modulate the Wnt/β-catenin signaling pathway and influence CRC progression, its precise molecular regulatory mechanisms and prognostic significance require further elucidation. This study further elucidates the mechanism by which the ABCD3 gene mediates CRC progression through regulation of the Wnt/β-catenin pathway. METHODS AND

resultsIntegrated analysis of TCGA transcriptomic data using weighted gene co-expression network analysis (WGCNA) identified ABCD3 as a hub gene within the CRC prognostic model. ABCD3 downregulation in CRC was systematically validated through three complementary approaches: Western blot for protein quantification, RT-PCR for transcriptional profiling, and immunohistochemical evidence from the Human Protein Atlas database. To investigate its functional role, ABCD3 knockdown was performed using siRNA in HT29 and HCT15 cell lines. Subsequent functional characterization revealed that ABCD3 suppression significantly attenuated cellular proliferation (CCK-8 assay) and concomitantly reduced invasive and migratory capacities in Transwell assays.

conclusionsBased on the CRC prognostic model, ABCD3 was identified as a significant prognostic factor, with low expression associated with poorer prognosis. Functional analysis demonstrated an anti-tumor role for ABCD3 in CRC pathogenesis, mediated through suppression of Wnt/β-catenin signaling, which effectively mitigates malignant CRC behavior. These findings suggest that targeting this ABCD3-Wnt/β-catenin regulatory axis represents a novel strategy for precision treatment of CRC.

Indexed as

Colorectal NeoplasmsWnt Signaling Pathwaybeta CateninCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHT29 CellsHumansPrognosisbeta CateninATP-binding cassette subfamily D member 3Colorectal cancerInvasionMigrationProliferationWnt/β-catenin signaling pathway

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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.