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Updated: Nov 1, 2025

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microRNA-17 is a tumor suppressor in oral squamous cell carcinoma and is repressed by LSD1

Kaixin Wangzhou1, Wanren Fu2, Mengmeng Li3

  • 1School of Management, Hainan Medical University, Haikou, China.

Oral Diseases
|June 21, 2021
PubMed
Abstract

Insights

Lysine-specific demethylase 1 (LSD1) supports oral squamous cell carcinoma (OSCC) stem cells by regulating miR-17 and the KPNA2/PI3K/AKT pathway, impacting OSCC development.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Epigenetic modifiers influence cellular reprogramming and cancer stem cell (CSC) characteristics.
  • Lysine-specific demethylase 1 (LSD1) is implicated in various cancers.
  • Cancer stem cells (CSCs) drive tumor initiation and progression.

Purpose of the Study:

  • To investigate the role of LSD1 in oral squamous cell carcinoma (OSCC) development.
  • To determine if LSD1 sustains OSCC cancer stem cells (OSCSCs).

Main Methods:

  • RT-qPCR to screen differentially expressed histone-modifying enzymes in OSCSCs.
  • Microarray analysis in cells with low LSD1 expression.
  • In vitro and in vivo experiments to assess cell activity and pathway modulation.

Main Results:

  • OSCSCs exhibit high LSD1 levels; LSD1 inhibition reduces OSCSC viability, migration, invasion, and sphere formation.
  • LSD1 demethylates histone to inhibit microRNA-17 (miR-17) expression.
  • miR-17 targets KPNA2, with downstream genes enriched in the PI3K/AKT pathway.
  • Modulation of LSD1, miR-17, and KPNA2 affects OSCSC activity.

Conclusions:

  • LSD1 promotes OSCC by sustaining OSCSCs.
  • LSD1's mechanism involves miR-17 demethylation and activation of the KPNA2/PI3K/AKT pathway.
  • This study enhances understanding of epigenetic regulation in OSCC.
Keywords:
AKT pathwayKPNA2LSD1PI3Kcancer stem cellsmicroRNA-17oral squamous cell carcinoma

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