Bystin-like protein forms a functional complex with DDX49 to enhance thyroid cancer progression

Yue Wang1, Xiaoxiao Xing1, Dongpo Zhang1

  • 1Department of Surgery, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.

Neoplasma
|December 18, 2025
PubMed

Insights

Bystin-like protein (BYSL) drives thyroid cancer by inhibiting tumor suppressor miR-145-5p. Targeting the BYSL-DDX49 complex offers a promising therapeutic strategy for aggressive thyroid malignancies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Thyroid cancer incidence is increasing globally, necessitating new therapeutic targets for aggressive forms.
  • Identifying novel oncogenic drivers is crucial for advancing thyroid cancer treatment.

Purpose of the Study:

  • To identify and characterize Bythin-like protein (BYSL) as a novel oncogenic driver in thyroid carcinoma.
  • To elucidate the molecular mechanism by which BYSL contributes to thyroid cancer progression.

Main Methods:

  • Analysis of clinical thyroid cancer specimens and cell lines.
  • In vitro functional assays (proliferation, migration, invasion, apoptosis).
  • Investigation of protein-protein interactions and microRNA biogenesis pathways.

Main Results:

  • BYSL is significantly upregulated in thyroid malignancies and correlates with poor patient outcomes.
  • BYSL promotes tumor cell proliferation, migration, invasion, and inhibits apoptosis.
  • BYSL interacts with DDX49, impairing miR-145-5p biogenesis and suppressing its tumor-suppressive function.

Conclusions:

  • The BYSL-DDX49 complex is a key regulator of thyroid cancer progression.
  • Targeting the BYSL-DDX49 complex may represent a novel therapeutic strategy for thyroid cancer.
  • Restoring tumor-suppressive pathways via miR-145-5p modulation is a potential therapeutic avenue.

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