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Research Paper|Volume 15, Issue 23|pp 13920—13943

Has-miR-300—GADD45B promotes melanoma growth via cell cycle

Long Chen1,2,3,4, Chenglong Fang5, Xiaoxue Yuan2, Mengqi Liu2, Ping Wu1, Li Zhong2, Zhiyong Chen1,2
  • 1Department of Burn Plastic and Cosmetology, Affiliated Fuling Hospital, Chongqing University, Chongqing 408099, China
  • 2College of Bioengineering, Chongqing University, Chongqing 400000, China
  • 3Department of Immunology, School of Basic Medical Sciences, Chengdu Medical College, Chengdu 610500, Sichuan, China
  • 4Non-Coding RNA and Drug Discovery Key Laboratory of Sichuan Province, Chengdu Medical College, Chengdu 610500, Sichuan, China
  • 5Department of Rehabilitation, LinYi People’s Hospital, Linyi 276000, Shandong, China
* Equal contribution
Received: June 15, 2023Accepted: October 16, 2023Published: December 7, 2023
https://doi.org/10.18632/aging.205276

Copyright: © 2023 Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Response to oncogenic factors like UV, GADD45 family in skin participates in scavenging ROS, DNA repair and cell cycle control. Because of this, the previous study of the chronic UVB injury model has found that hsa-miR-300 can conduct intercellular transport by exosomes and target regulation of GADD45B. Whether the hsa-miR-300—GADD45B still regulates tumor development by cell cycle pathway is unclear. Through transcriptomic analysis of primary (n=39) and metastatic (n=102) melanoma, it was confirmed that in metastatic samples, some of the 97 down-regulated genes participate in maintaining skin homeostasis while 42 up-regulated genes were enriched in cancer-related functions. Furthermore, CDKN1A, CDKN2A, CXCR4 and RAD51 in the melanoma pathway, were also differentially expressed between normal skin and melanoma. CDKN1A and CDKN2A were also found to be involved in TP53-dependent cell cycle regulation. In conclusion, it was speculated that CDKN1A, CDKN2A, TP53, GADD45B and hsa-miR-300 may have regulatory relationships. It was demonstrated that there is a bidirectional regulation between hsa-miR-300 and TP53. In addition, miR-300 can regulate CDKN1A by GADD45B/TP53 and promote melanoma growth by accelerating the cell cycle transition from G1/S to G2 phase.