SNHG11 contributes to NSCLC cell growth and migration by targeting miR-485-5p/BSG axis

Ruirui Cheng1, Xinhua Lu2, Chenyang Xu2

  • 1Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, No.1 Jianshe East Road, Zhengzhou, 450052, Henan, China.

Insights

Small nucleolar RNA host gene 11 (SNHG11) promotes non-small cell lung cancer (NSCLC) by sponging miR-485-5p to upregulate Basigin (BSG). Silencing SNHG11 inhibited NSCLC cell growth, migration, and epithelial-mesenchymal transition.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Long noncoding RNAs (lncRNAs) are crucial in cancer development.
  • Small nucleolar RNA host gene 11 (SNHG11) exhibits oncogenic roles in various cancers.
  • The function of SNHG11 in non-small cell lung cancer (NSCLC) requires elucidation.

Purpose of the Study:

  • To investigate the role and regulatory mechanism of SNHG11 in NSCLC.
  • To determine the impact of SNHG11 on NSCLC cell biological behaviors.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) for SNHG11 expression analysis.
  • Functional assays (growth, migration, EMT) following SNHG11 silencing.
  • Subcellular fractionation, FISH, RNA pull down, luciferase reporter, and restoration assays to elucidate the regulatory mechanism.

Main Results:

  • SNHG11 was overexpressed in NSCLC cells.
  • SNHG11 silencing inhibited NSCLC cell growth, migration, and epithelial-mesenchymal transition.
  • SNHG11 acts as a molecular sponge for miR-485-5p, upregulating Basigin (BSG) expression.

Conclusions:

  • SNHG11 is oncogenic in NSCLC.
  • SNHG11 promotes NSCLC progression by regulating the miR-485-5p/BSG axis.
  • SNHG11 represents a potential therapeutic target for NSCLC.