AP003352.1/miR-141-3p axis enhances the proliferation of osteosarcoma by LPAR3

PeerJ. 2023 Sep 15:11:e15937. doi: 10.7717/peerj.15937. eCollection 2023.

Abstract

Osteosarcoma (OS) is a highly malignant tumor with a poor prognosis and a growing incidence. LncRNAs and microRNAs control the occurrence and development process of osteosarcoma through ceRNA patterns. The LPAR3 gene is important in cancer cell proliferation, apoptosis and disease development. However, the regulatory mechanism of the ceRNA network through which LPAR3 participates in osteosarcoma has not been clarified. Herein, our study demonstrated that the AP003352.1/miR-141-3p axis drives LPAR3 expression to induce the malignant progression of osteosarcoma. First, the expression of LPAR3 is regulated by the changes in AP003352.1 and miR-141-3p. Similar to the ceRNA of miR-141-3p, AP003352.1 regulates the expression of LPAR3 through this mechanism. In addition, the regulation of AP003352.1 in malignant osteosarcoma progression depends to a certain degree on miR-141-3p. Importantly, the AP003352.1/miR-141-3p/LPAR3 axis can better serve as a multi-gene diagnostic marker for osteosarcoma. In conclusion, our research reveals a new ceRNA regulatory network, which provides a novel potential target for the diagnosis and treatment of osteosarcoma.

Keywords: CeRNA; Cell proliferation; LPAR3; Osteosarcoma.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / genetics
  • Bone Neoplasms* / genetics
  • Cell Proliferation / genetics
  • Humans
  • MicroRNAs* / genetics
  • Osteosarcoma* / genetics

Substances

  • MicroRNAs
  • MIRN141 microRNA, human

Grants and funding

This research was funded by the Liaoning Provincial Natural Science Foundation of China, grant number 2019-ZD-1010 and 2023-MS-343, and the Dalian Science and Technology Innovation Foundation, Grant Number 2022JJ13SN088 and 2020JJ27SN087. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.