Hsa_circ_0043278 functions as competitive endogenous RNA to enhance glioblastoma multiforme progression by sponging

Zhi Wu1, Maohua Zheng1, Yonghong Zhang1

  • 1Department of Neurosurgery, The First Hospital of Lanzhou University, Lanzhou 730000, China.

Aging
|November 6, 2020
PubMed

Insights

Circular RNA circ_0043278 promotes glioblastoma multiforme (GBM) progression by sponging miR-638 and upregulating HOXA9. Inhibiting circ_0043278 suppressed GBM cell growth and tumor formation, offering potential diagnostic and therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Circular RNAs (circRNAs) are implicated in disease pathogenesis, acting as competing endogenous RNAs (ceRNAs) or miRNA sponges.
  • The specific role of has_circRNA_0043278 (circ_0043278) in glioblastoma multiforme (GBM) and its downstream targets remain largely uncharacterized.

Purpose of the Study:

  • To investigate the function and mechanism of circ_0043278 in GBM pathogenesis.
  • To identify potential therapeutic targets for GBM based on circ_0043278's role.

Main Methods:

  • Validation of circ_0043278 expression in GBM cell lines and tissues.
  • In vitro and in vivo experiments assessing the effects of circ_0043278 knockdown on GBM.
  • Dual-luciferase reporter assays to confirm the interaction between circ_0043278 and miR-638.
  • Analysis of HOXA9 expression and Wnt/β-catenin signaling pathway activation.

Main Results:

  • Circ_0043278 was highly expressed in GBM.
  • Knockdown of circ_0043278 inhibited GBM cell migration, proliferation, invasion, and in vivo tumorigenesis.
  • Circ_0043278 directly sponged miR-638, leading to increased HOXA9 expression and Wnt/β-catenin pathway activation.
  • Inhibition of miR-638 counteracted the effects of circ_0043278 silencing on GBM malignancy.

Conclusions:

  • The circ_0043278/miR-638/HOXA9 axis plays a crucial role in promoting GBM progression.
  • Circ_0043278 represents a potential diagnostic biomarker and therapeutic target for GBM.

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