The function of long non-coding RNA SNHG11 and its working mechanism in triple-negative breast cancer

Tahani Mohamed Ibrahim Al-Hazani1, Wedad Saeed Al-Qahtani2, Maha Abdulla Alwaili3

  • 1Department of Biology, College of Sciences and Humanities, Prince Sattam Bin Abdulaziz University, PO Box 83, Al-Kharj 11940, Saudi Arabia.

Insights

Long non-coding RNA SNHG11 promotes triple-negative breast cancer (TNBC) progression by upregulating specificity protein 2 (SP2) and mucin 1 (MUC-1), while downregulating microRNA-7-5p. This study reveals SNHG11

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Triple-negative breast cancer (TNBC) poses a significant health challenge for women.
  • The molecular mechanisms underlying TNBC progression require further elucidation.

Purpose of the Study:

  • To investigate the role and mechanism of long non-coding RNA (lncRNA) SNHG11 in TNBC.
  • To explore the regulatory network involving SNHG11, microRNA-7-5p (miR-7-5p), specificity protein 2 (SP2), and mucin 1 (MUC-1) in TNBC.

Main Methods:

  • Detection of SNHG11, miR-7-5p, SP2, and MUC-1 expression in TNBC tissues and cells.
  • Evaluation of the impact of SNHG11 and SP2 on TNBC cell malignant behaviors.
  • Prediction and verification of molecular interactions using bioinformatics and experimental approaches.
  • Analysis of SP2 binding to the MUC-1 promoter.

Main Results:

  • Elevated expression of SNHG11, SP2, and MUC-1 was observed in TNBC.
  • SNHG11 knockdown inhibited TNBC cell progression.
  • SP2 silencing attenuated the promoting effect of SNHG11 on TNBC.
  • SNHG11 negatively regulated miR-7-5p and positively regulated SP2.
  • SP2 directly bound to the MUC-1 promoter, suppressing MUC-1 expression.

Conclusions:

  • lncRNA SNHG11 promotes TNBC cell malignant behaviors and facilitates tumor progression.
  • The SNHG11/miR-7-5p/SP2/MUC-1 axis represents a novel regulatory pathway in TNBC.
  • SNHG11 holds potential as a therapeutic target for TNBC.

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