The Roles of Noncoding RNAs in the Development of Osteosarcoma Stem Cells and Potential Therapeutic Targets.

Front Cell Dev Biol

Department of Orthopedic Surgery, Shengjing Hospital, China Medical University, Shenyang, China.

Published: February 2022

AI Article Synopsis

  • Osteosarcoma (OS) is the most common bone tumor in kids and teens, and patients often have a poor prognosis due to chemotherapy resistance linked to cancer stem cells (CSCs).
  • CSCs are a small group of tumor cells that can self-renew and contribute to tumor growth, spread, and drug resistance.
  • The review discusses how noncoding RNAs (ncRNAs), especially various types of microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), regulate the development of CSCs in OS and suggests that targeting these ncRNAs may offer new treatment options.

Article Abstract

Osteosarcoma (OS) is the common bone tumor in children and adolescents. Because of chemotherapy resistance, the OS patients have a poor prognosis. The one reason of chemotherapeutic resistance is the development of cancer stem cells (CSCs). CSCs represent a small portion of tumor cells with the capacity of self-renewal and multipotency, which are associated with tumor initiation, metastasis, recurrence and drug resistance. Recently, noncoding RNAs (ncRNAs) have been reported to critically regulate CSCs. Therefore, in this review article, we described the role of ncRNAs, especially miRNAs, lncRNAs and circRNAs, in regulating CSCs development and potential mechanisms. Specifically, we discussed the role of multiple miRNAs in targeting CSCs, including miR-26a, miR-29b, miR-34a, miR-133a, miR-143, miR-335, miR-382, miR-499a, miR-1247, and let-7days. Moreover, we highlighted the functions of lncRNAs in regulating CSCs in OS, such as B4GALT1-AS1, DANCR, DLX6-AS1, FER1L4, HIF2PUT, LINK-A, MALAT1, SOX2-OT, and THOR. Due to the critical roles of ncRNAs in regulation of OS CSCs, targeting ncRNAs might be a novel strategy for eliminating CSCs for OS therapy.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8888953PMC
http://dx.doi.org/10.3389/fcell.2022.773038DOI Listing

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