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Downregulation of FAM134B suppresses thyroid cell carcinoma development by modulating endoplasmic reticulum stress

Tingting Cheng1, Jiao Shu2, Cheng Zhou1

  • 1Department of Pathology, Puren Hospital affiliated to Wuhan University of Science and Technology, 1 Benxi street, Jianshe Si Road, Qingshan District, Wuhan City, Hubei Province 430080, China.

Cancer Genetics
|April 25, 2026
PubMed

Insights

FAM134B acts as an oncogene in thyroid carcinoma (THCA). Silencing FAM134B inhibits THCA cell proliferation and promotes apoptosis by inducing endoplasmic reticulum stress (ERS) and autophagy.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Biology

Background:

  • Thyroid carcinoma (THCA) is a common endocrine malignancy.
  • The molecular mechanisms driving THCA progression require further elucidation.
  • FAM134B's role in THCA pathogenesis is not well understood.

Purpose of the Study:

  • To investigate the molecular mechanism of FAM134B in regulating endoplasmic reticulum stress (ERS) and autophagy in THCA.
  • To determine the role of FAM134B as an oncogene in THCA development.

Main Methods:

  • Examined FAM134B expression in clinical THCA samples.
  • Performed FAM134B knockdown in TPC-1 cells and overexpression in KTC-1 cells.
  • Assessed cell proliferation, apoptosis, ERS markers (PERK, IRE1α, CHOP), and autophagy markers (LC3B, p62, Calnexin-LAMP1 co-localization).

Main Results:

  • FAM134B was highly expressed in THCA and associated with advanced T staging.
  • FAM134B knockdown reduced proliferation and increased apoptosis in THCA cells.
  • FAM134B knockdown induced ERS and enhanced autophagy, while ERS inhibition partially reversed these effects.

Conclusions:

  • FAM134B functions as an oncogene in THCA.
  • Silencing FAM134B inhibits THCA cell proliferation and promotes apoptosis via induction of ERS and autophagy.
  • FAM134B is a potential therapeutic target for THCA.
Keywords:
ApoptosisAutophagyER stressFAM134BProliferationThyroid carcinoma

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