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TGFBR3 inhibits progression of papillary thyroid cancer by inhibiting the PI3K/AKT pathway and EMT

Hanrong Zhang1, Junxin Chen1, Xin Chen1

  • 1Department of Endocrinology and Diabetes Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.

Endocrine Connections
|October 15, 2024
PubMed
Abstract

Insights

Transforming growth factor beta receptor III (TGFBR3) is down-regulated in papillary thyroid cancer (PTC), suppressing tumor growth. Its low expression correlates with poor prognosis, but restoring TGFBR3 inhibits PTC progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genomics

Background:

  • Transforming growth factor beta receptor III (TGFBR3) exhibits tumor-suppressive functions in various cancers.
  • The specific role of TGFBR3 in papillary thyroid cancer (PTC) has not been previously elucidated.

Purpose of the Study:

  • To investigate the expression levels and functional role of TGFBR3 in papillary thyroid cancer (PTC).
  • To explore the underlying molecular mechanisms by which TGFBR3 influences PTC progression.

Main Methods:

  • Analysis of TGFBR3 expression in PTC using The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases.
  • In vitro assays including Edu, wound healing, and Transwell assays to assess cell proliferation, migration, and invasion.
  • Transcriptome sequencing, qRT-PCR, and Western blotting to elucidate molecular mechanisms.

Main Results:

  • TGFBR3 expression is significantly downregulated in PTC tissues compared to normal thyroid tissues.
  • Low TGFBR3 expression is associated with poorer patient prognosis and reduced thyroid differentiation.
  • Overexpression of TGFBR3 inhibited PTC cell proliferation, migration, and invasion, and suppressed the PI3K/AKT pathway and epithelial-mesenchymal transition.

Conclusions:

  • TGFBR3 functions as a tumor suppressor in PTC.
  • TGFBR3 inhibits PTC progression by downregulating the PI3K/AKT pathway and epithelial-mesenchymal transition.
  • TGFBR3 influences tumor immune infiltration in the PTC microenvironment.
Keywords:
EMTPI3K/AKT pathwayTGFBR3invasionpapillary thyroid cancer

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