ArticleJournal of translational medicine2025
CX26 promotes pancreatic cancer progression by competitively inhibiting interaction of c-Myc with PSMD2 and enhancing c-Myc stability.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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Who cites it
2 citing papers in PubMed.
- Beyond the gap: moonlighting functions of connexins in cancer.Cell communication and signaling : CCS · 2026Review
- Application value of a prognostic risk model based on lactate-related genes in non-small cell lung cancer.Translational cancer research · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundPancreatic cancer (PC) is highly aggressive and fatal and has dismal prognostic outcomes, primarily due to its late-stage diagnosis and limited effective treatments. The molecular mechanisms triggering PC progression are largely unclear. This study investigated how CX26 contributes to pancreatic cancer development and its potential as a therapeutic target.
methodsCX26 expression in PC and its clinical significance were examined through bioinformatics analysis. The biological functions of CX26 in PC cells were explored via colony formation, CCK-8, and proteomic analysis. To explore the mechanisms by which CX26 regulates c-Myc stability, co-immunoprecipitation, immunofluorescence, and molecular docking were utilized to investigate the interactions among CX26, PSMD2, and c-Myc. Additionally, subcutaneous xenografts in nude mice were applied to assess the impact of CX26 on PC progression in vivo.
resultsBioinformatics analysis indicated the upregulation of CX26 in PC tissues. In addition, CX26 expression was closely related to dismal prognostic outcomes. Further study revealed that CX26 promotes PC progression in vitro and in vivo. Proteomic analysis identified c-Myc as the key downstream target of CX26. Mechanistically, CX26 indirectly regulated c-Myc stability via PSMD2 rather than directly interacting with c-Myc. Moreover, CX26 competes with c-Myc to bind to the Armadillo-like helical domain of PSMD2, thereby preventing c-Myc proteasomal degradation.
conclusionsThis study suggests that CX26 facilitates PC progression by stabilizing c-Myc through competitively inhibiting the binding of PSMD2 to c-Myc. Given the challenges in directly inhibiting c-Myc, this novel regulatory mechanism provides valuable insights into PC biology and reveals that targeting CX26 is a possible way to promote c-Myc degradation and suppress PC growth.
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