Review Article Open Access

MicroRNA-92a: The Administrator of Certain Diseases

Zhiyuan Sun1, Qing Xu2, Xiaoyi Tian1, Yingjie Yang1, Qinglu Wang3 and Xuewen Tian1
  • 1 Shandong Sport University, China
  • 2 Shandong Sports Rehabilitation Research Center, China
  • 3 Qilu Medical University, China

Abstract

MicroRNA-92a (miR-92a) is an evolutionarily conserved noncoding small RNA that can regulate gene expression after transcription. Previous studies have found that miR-92a is overexpressed in many tumors and can regulate numerous tumor suppressor genes negatively, with relevant effects on the development of different tumors, by regulating the DUSP10/c-Jun N-terminal kinase (JNK), phosphatase and tensin homologs (PTEN)/AKT, Wnt and EP4/Notch1 signaling axes. MiR-92a also promotes the proliferation and migration of vascular smooth muscle cells (VSMCs) through the Rho-associated coiled-coil-forming kinase/myosin light chain kinase signaling pathway and inhibits VSMC apoptosis through the MKK4/JNK signaling pathway. Moreover, miR-92a affects endothelial functions; mediates endothelial dysfunction in chronic kidney diseases; mediates THBS1 inhibition; promotes the migration, proliferation and angiogenesis of neighboring endothelial cells (ECs); mediates the Nrf2/KEAP1/ARE signaling pathway to regulate vascular endothelial aging; and is involved in immune responses to activate ECs. This review summarizes the potential role and pathogenic mechanism of the miR-92a gene in certain diseases to provide possible new treatment options.

American Journal of Biochemistry and Biotechnology
Volume 16 No. 2, 2020, 235-243

DOI: https://doi.org/10.3844/ajbbsp.2020.235.243

Submitted On: 27 March 2020 Published On: 21 May 2020

How to Cite: Sun, Z., Xu, Q., Tian, X., Yang, Y. & Wang, Q. (2020). MicroRNA-92a: The Administrator of Certain Diseases. American Journal of Biochemistry and Biotechnology, 16(2), 235-243. https://doi.org/10.3844/ajbbsp.2020.235.243

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Keywords

  • microRNA-92a
  • Cancer
  • Signaling Pathway
  • Endothelial Damage
  • Vascular Smooth Muscle Cell