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MiR-100 up-regulation enhanced cell autophagy and apoptosis induced by cisplatin in osteosarcoma by targeting mTOR

Z Yu1, N Li, K Jiang

  • 1Department of Medical Oncology, The Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China. qycsuaqeeqimccse@sina.com.

European Review for Medical and Pharmacological Sciences
|October 4, 2018
PubMed
Abstract

Insights

MicroRNA 100 (MiR-100) is down-regulated in osteosarcoma, leading to increased mTOR expression. Restoring MiR-100 enhances autophagy and apoptosis, improving cisplatin sensitivity in osteosarcoma cells.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Mammalian target of rapamycin (mTOR) negatively regulates autophagy and is implicated in osteosarcoma pathogenesis.
  • MicroRNA 100 (MiR-100) down-regulation is linked to osteosarcoma development and chemo-resistance.

Purpose of the Study:

  • To investigate the role of MiR-100 in regulating mTOR expression.
  • To determine the effect of MiR-100 on osteosarcoma cell autophagy and cisplatin sensitivity.

Main Methods:

  • Comparative analysis of MiR-100, mTOR, and Beclin-1 expression in osteosarcoma and normal tissues.
  • Dual luciferase assay to confirm the targeting relationship between MiR-100 and mTOR.
  • Assessment of cell autophagy, apoptosis, and malignancy in MG-63 and MG-63/DDP cells following MiR-100 mimic or si-mTOR treatment.

Main Results:

  • Osteosarcoma tissues showed decreased MiR-100 and Beclin-1, and increased mTOR compared to normal tissues.
  • MiR-100 directly inhibited mTOR expression.
  • MiR-100 mimic and/or si-mTOR treatment increased Beclin-1, autophagy, and apoptosis, while reducing colony formation in osteosarcoma cells.

Conclusions:

  • MiR-100 is downregulated in osteosarcoma, correlating with elevated mTOR.
  • Upregulating MiR-100 enhances cisplatin-induced autophagy and apoptosis by targeting mTOR.
  • MiR-100 represents a potential therapeutic target for improving osteosarcoma treatment.

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