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Background <p>Accumulating 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.</p> Methods and results <p>Integrated 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.</p> Conclusions <p>Based 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.</p>

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

  • 期刊论文

  • 发表日期：

    2025年7月16日

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

摘要

Background

Accumulating 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 results

Integrated 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.

Conclusions

Based 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.