GNA15 facilitates the malignant development of thyroid carcinoma cells via the BTK-mediated MAPK signaling pathway

Yihan Sun1, Yifan Han2

  • 1Neck Surgery Department, The 2nd School of Medicine, WMU/The 2nd Affiliated Hospital and Yuying Children's Hospital of WMU, Longwan District, Wenzhou City, Zhejiang Province, China.

PubMed

Insights

G protein subunit alpha 15 (GNA15) promotes thyroid carcinoma (TC) progression by activating the MAPK pathway via Bruton tyrosine kinase (BTK). Silencing GNA15 inhibits TC cell viability, proliferation, migration, and invasion.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • G protein subunit alpha 15 (GNA15) is implicated as an oncogene in various cancers.
  • The specific role of GNA15 in thyroid carcinoma (TC) remains largely uncharacterized.

Purpose of the Study:

  • To investigate the expression and function of GNA15 in thyroid carcinoma.
  • To elucidate the underlying molecular mechanisms, including its interaction with Bruton tyrosine kinase (BTK) and the MAPK signaling pathway.

Main Methods:

  • Bioinformatic analysis of GNA15 expression in TC.
  • In vitro assays (MTT, colony formation, Transwell) to assess TC cell functions.
  • Western blot analysis for MAPK pathway components (ERK, JNK, p38).
  • BTK knockdown and rescue experiments to determine GNA15's mechanism.

Main Results:

  • GNA15 was significantly overexpressed in TC tissues.
  • GNA15 overexpression enhanced TC cell viability, proliferation, migration, and invasion.
  • GNA15 upregulated the phosphorylation of ERK, JNK, and p38, indicating MAPK pathway activation.
  • BTK deficiency inhibited TC cell malignant behaviors and MAPK signaling, but these effects were reversed by GNA15 overexpression.

Conclusions:

  • GNA15 acts as an oncogene in thyroid carcinoma.
  • GNA15 promotes TC cell malignancy by interacting with BTK and activating the MAPK signaling pathway.
  • Targeting GNA15 may represent a potential therapeutic strategy for thyroid carcinoma.

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