CBLB inhibits papillary thyroid cancer malignancy via negatively regulating MYCBP/c-Myc axis

Yanli Yang1, Xiaoyan Pei1, Qingqing Yang1

  • 1Department of Endocrinology, The First Affiliated Hospital of Bengbu Medical University, Bengbu 233004, China.

Cellular Signalling
|May 26, 2026
PubMed

Insights

CBLB functions as a tumor suppressor in papillary thyroid carcinoma (PTC). It targets MYCBP for degradation, inhibiting the c-Myc pathway and suppressing PTC progression, indicating therapeutic potential.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Papillary thyroid carcinoma (PTC) incidence is rising globally, but its molecular drivers are not fully understood.
  • Identifying novel tumor suppressors is crucial for understanding PTC pathogenesis.

Purpose of the Study:

  • To investigate the role of CBLB as a tumor suppressor in papillary thyroid carcinoma.
  • To elucidate the molecular mechanism by which CBLB regulates PTC progression.

Main Methods:

  • Analysis of public databases (GEPIA, UALCAN) and PTC cell lines to assess CBLB expression.
  • Functional experiments involving CBLB knockdown and overexpression to evaluate its impact on PTC phenotypes.
  • Mechanistic studies to determine CBLB's interaction with MYCBP and its effect on the c-Myc pathway.

Main Results:

  • CBLB expression is significantly reduced in PTC tissues compared to normal thyroid tissues.
  • CBLB knockdown enhances PTC malignant phenotypes, while CBLB overexpression suppresses them.
  • CBLB directly binds to MYCBP, promoting its ubiquitination and degradation, which subsequently inhibits the c-Myc pathway and affects oncogenic targets.

Conclusions:

  • The CBLB/MYCBP/c-Myc axis is a critical regulator of PTC progression.
  • CBLB acts as a tumor suppressor by targeting MYCBP and inhibiting oncogenesis.
  • CBLB presents therapeutic potential for targeting MYCBP-driven oncogenesis in PTC.

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