LINC02535 + miR-30a-5p combination enhances proliferation and inhibits apoptosis in metastatic breast Cancer cells

Toxicol In Vitro. 2024 Jun:98:105845. doi: 10.1016/j.tiv.2024.105845. Epub 2024 May 14.

Abstract

Current clinical therapies for metastatic breast cancer (MBC) have limited therapeutic efficacy and induce significant systemic side effects, leading to poor patient compliance. To address this challenge, this investigation focuses on the design of LINC02535 + miR-30a-5p for treating breast cancer. In vitro cytotoxicity studies confirmed that LINC02535 + miR-30a-5p was more effective in 4 T1 cells, with reduced toxicity in NIH3T3 cells. Further verification of cellular morphology was achieved through various biochemical staining methods. Additionally, the antimetastatic attributes of LINC02535 + miR-30a-5p have been evaluated using both migration scratch and Transwell migration assays, which have collectively revealed excellent antimetastatic potential. The DNA fragmentation of the 4 T1 cells was assessed using a comet assay. LINC02535 + miR-30a-5p improved ROS levels and caused mitochondrial membrane potential alterations and DNA damage, which resulted in apoptosis. Therefore, we propose that LINC02535 + miR-30a-5p could be an alternative therapeutic strategy for breast cancer therapy.

Keywords: Antimetastasis; Apoptosis; Breast cancer; DNA fragmentation; LINC02535.

MeSH terms

  • Animals
  • Apoptosis* / drug effects
  • Breast Neoplasms* / genetics
  • Breast Neoplasms* / pathology
  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation* / drug effects
  • DNA Damage
  • Female
  • Humans
  • Membrane Potential, Mitochondrial / drug effects
  • Mice
  • MicroRNAs* / genetics
  • NIH 3T3 Cells
  • RNA, Long Noncoding* / genetics
  • Reactive Oxygen Species / metabolism

Substances

  • MicroRNAs
  • RNA, Long Noncoding
  • Reactive Oxygen Species