Postępy Dermatologii i Alergologii

Abstract

3/2024 vol. 41
Original paper

miR-22 negatively regulating NOD-like receptor protein 3 gene in the proliferation, invasion, and migration of malignant melanoma cells

  1. Department of Burn Plastic and Aesthetic Surgery, Nanchong Central Hospital, Second Clinical Medical College of North Sichuan Medical College, Nanchong, Sichuan Province, China
  2. Department of Critical Care Medicine, Nanchong Central Hospital, Second Clinical Medical College of North Sichuan Medical College, Nanchong, Sichuan Province, China
  3. Department of Stomatology, Nanchong Central Hospital, Second Clinical Medical College of North Sichuan Medical College, Nanchong, Sichuan Province, China
  4. Department of Thoracic Surgery, Nanchong Central Hospital, Second Clinical Medical College of North Sichuan Medical College, Nanchong, Sichuan Province, China
Adv Dermatol Allergol 2024; XLI (3): 284-291
Online publish date: 2024/04/25
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Introduction:

Malignant melanoma (MM) is a highly aggressive skin tumour.

Aim:

To investigate whether miR-22 is involved in the proliferation, invasion, and migration of melanoma cells (MCs) by negatively regulating NOD-like receptor protein 3 (NLRP3) gene.

Material and methods:

Human MCs (WM239a) and human epidermal melanocytes (HEM) were used as study material. The expression levels of miR-22 and NLRP3 were detected by qRT-PCR. The expression of NLRP3 protein was determined by Western blot (WB) analysis. The effects of miR-22 and NLRP3 on the proliferation, invasion, and migration of MCs were evaluated by cell counting kit-8 (CCK-8), Transwell cell invasion assay, and scratch assay.

Results:

The expression of miR-22 was clearly lower in WM239a than in HEM. Up-regulation of miR-22 expression in WM239a clearly raised the expression of miR-22, Caspase-1, and E-cadherin and the apoptotic rate of WM239a; however, the levels of interleukin-1b (IL-1b) and NLRP3, cell proliferation activity, invasion and migration ability were clearly decreased. The negative regulation of NLRP3 by miR-22 may play a major role in activities of MM.

Conclusions:

Further studies will help to reveal the molecular details of this regulatory mechanism and provide new therapeutic strategies.

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