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Epigenetic activation of SIN1 promotes NSCLC cell proliferation and metastasis by affecting the

Zhongwu Hu1, Yaqin Wang2, Yuemei Wang3

  • 1Department of Thoracic Surgery, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu, 223300, PR China.

Biochemical and Biophysical Research Communications
|December 21, 2016
PubMed

Insights

Stress-activated protein kinase (SAPK) interacting protein 1 (SIN1) promotes non-small cell lung cancer (NSCLC) growth and migration. SIN1 upregulation involves H3K4me3, and it induces epithelial-mesenchymal transition (EMT), making it a potential NSCLC therapeutic target.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Biology

Background:

  • Stress-activated protein kinase (SAPK) interacting protein 1 (SIN1) is a crucial component of mTORC2.
  • SIN1 regulates the Akt pathway, implicated in various cancers.
  • The role of SIN1 in non-small cell lung cancer (NSCLC) progression is not well understood.

Purpose of the Study:

  • To investigate the role and mechanism of SIN1 in NSCLC progression.
  • To determine if SIN1 influences NSCLC cell growth, migration, and invasion.
  • To explore the potential of SIN1 as a therapeutic target in NSCLC.

Main Methods:

  • Cell proliferation assays (MTT, colony formation) in A549 and H1299 cells with SIN1 overexpression and knockdown.
  • Transwell assays to assess cell migration and invasion.
  • Tumor xenograft models in vivo to evaluate tumor growth.
  • Analysis of histone modifications (H3K4me3) and epithelial-mesenchymal transition (EMT) markers (E-cadherin, N-cadherin, Vimentin).

Main Results:

  • SIN1 overexpression significantly enhanced NSCLC cell proliferation and migration in vitro.
  • SIN1 knockdown inhibited NSCLC cell proliferation and migration.
  • Overexpression of SIN1 promoted tumor growth in vivo, while knockdown suppressed it.
  • A mechanistic link was found between SIN1 and H3K4me3, with H3K4me3 involved in SIN1 upregulation.
  • SIN1 promoted NSCLC cell migration and invasion by inducing EMT, downregulating E-cadherin and upregulating N-cadherin and Vimentin.

Conclusions:

  • SIN1 plays a significant role in promoting NSCLC growth, migration, and invasion.
  • SIN1 upregulation is mechanistically linked to H3K4me3.
  • SIN1 induces EMT, contributing to NSCLC progression.
  • SIN1 represents a potential biomarker and a promising therapeutic target for NSCLC treatment.
Keywords:
EMTH3K4 trimethylationMigrationNSCLCSIN1

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