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Updated: Feb 5, 2026

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Fibronectin-1 modulated by the long noncoding RNA OIP5-AS1/miR-200b-3p axis contributes to doxorubicin resistance of

Zhu Kun-Peng1,2, Zhang Chun-Lin1,2, Ma Xiao-Long1,2

  • 1Department of Orthopedics, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.

Journal of Cellular Physiology
|September 12, 2018
PubMed

Insights

Fibronectin-1 (FN1) promotes chemoresistance in osteosarcoma (OS) by interacting with OIP5-AS1 and miR-200b-3p. Targeting this pathway may improve osteosarcoma treatment outcomes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Chemoresistance significantly hinders osteosarcoma (OS) patient survival.
  • The molecular mechanisms driving OS chemoresistance are not fully understood.

Purpose of the Study:

  • To investigate the role of fibronectin-1 (FN1) in osteosarcoma chemoresistance.
  • To elucidate the regulatory pathway involving long noncoding RNA OIP5-AS1, miR-200b-3p, and FN1 in OS chemoresistance.

Main Methods:

  • Microarray analysis of chemo-resistant and sensitive OS cell lines.
  • Functional assays (in vitro and in vivo) to assess FN1's effect on chemoresistance.
  • Mechanistic studies including luciferase reporter gene assays, RNA immunoprecipitation, RNA pull-down, and rescue assays.

Main Results:

  • Fibronectin-1 (FN1) was significantly upregulated in chemoresistant OS cells and tissues, correlating with poor prognosis.
  • Inhibition of FN1 enhanced OS cell sensitivity to doxorubicin, while overexpression decreased sensitivity.
  • FN1 expression is regulated by the long noncoding RNA (lncRNA) OIP5-AS1 via sponging of miR-200b-3p.

Conclusions:

  • The lncRNA OIP5-AS1/miR-200b-3p/FN1 pathway plays a crucial role in osteosarcoma chemoresistance.
  • This regulatory pathway represents a potential therapeutic target for overcoming chemoresistance in osteosarcoma.
Keywords:
FN1chemoresistancelncRNA OIP5-AS1miR-200b-3posteosarcoma

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