SYT7 plays a role in promoting thyroid cancer by mediating HMGB3 ubiquitination

Shuai Dong1, Jun Pan1, Yi-Bin Shen1

  • 1The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.

Endocrine-Related Cancer
|January 24, 2022
PubMed

Insights

SYT7 and HMGB3 are elevated in thyroid cancer, promoting tumor growth. SYT7 targets HMGB3 via BRCA1, inhibiting its ubiquitination and boosting cancer progression. Targeting SYT7 or HMGB3 may offer new thyroid cancer treatments.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Thyroid cancer is a common endocrine malignancy requiring novel therapeutic targets.
  • Understanding molecular mechanisms driving thyroid cancer progression is crucial for effective treatment strategies.

Purpose of the Study:

  • To investigate the role of SYT7 and its downstream target HMGB3 in thyroid cancer.
  • To elucidate the molecular mechanism by which SYT7 influences thyroid cancer progression.

Main Methods:

  • Immunohistochemical staining, qPCR, and Western blot to assess SYT7 and HMGB3 expression.
  • Cell function assays (proliferation, migration, apoptosis) to evaluate SYT7 and HMGB3 effects.
  • In vivo tumor growth studies and molecular analyses (GeneChip, IPA, UbiBrowser, Co-IP) to determine the SYT7-BRCA1-HMGB3 pathway.

Main Results:

  • SYT7 and HMGB3 expression were significantly upregulated in thyroid cancer tissues and cells.
  • SYT7 knockdown inhibited thyroid cancer cell proliferation and migration while promoting apoptosis; overexpression had opposite effects.
  • SYT7 interacted with BRCA1 to inhibit HMGB3 ubiquitination, leading to increased HMGB3 protein levels and promoting thyroid cancer progression.

Conclusions:

  • SYT7 and HMGB3 are key drivers of thyroid cancer progression.
  • The SYT7/BRCA1/HMGB3 axis represents a potential therapeutic target for thyroid cancer treatment.

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