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Updated: Nov 12, 2025

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
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Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells

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MiR-125b acts as a tumor suppressor of melanoma by targeting NCAM

Tao Wang1, Wei Li, Shuang Yin

  • 1Department of Plastic and Aesthetic Surgery, the Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.

Journal of B.U.ON. : Official Journal of the Balkan Union of Oncology
|March 15, 2021
PubMed
Abstract

Insights

MicroRNA-125b (miR-125b) acts as a tumor suppressor in malignant melanoma (MM). Lower miR-125b levels correlate with increased MM cell growth and migration, while targeting neural cell adhesion molecule (NCAM).

Area of Science:

  • Molecular Oncology
  • Biochemistry

Background:

  • Malignant melanoma (MM) is an aggressive skin cancer with complex regulatory mechanisms.
  • MicroRNAs (miRNAs) play crucial roles in cancer development and progression.

Purpose of the Study:

  • To investigate the role of microRNA-125b (miR-125b) in malignant melanoma (MM) cell growth and apoptosis.
  • To elucidate the underlying molecular mechanisms involving neural cell adhesion molecule (NCAM).

Main Methods:

  • Quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry were used to assess miR-125b and NCAM expression in MM tissues and cells.
  • Exogenous overexpression of miR-125b in MM A375 cells was performed.
  • In vitro functional assays (proliferation, migration, apoptosis) and dual-luciferase reporter assays were conducted.

Main Results:

  • MiR-125b was significantly downregulated in MM tissues and cells.
  • NCAM isoforms (NCAM-120, NCAM-140, NCAM-180) were significantly upregulated in MM.
  • Overexpression of miR-125b inhibited MM cell proliferation and migration while promoting apoptosis.
  • MiR-125b directly targets the 3'-untranslated region (3'-UTR) of NCAM mRNA.

Conclusions:

  • MiR-125b functions as a tumor suppressor in malignant melanoma.
  • The tumor-suppressive effects of miR-125b are mediated through its targeting of NCAM.

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