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TGF-beta induced RBL2 expression in renal cancer cells by down-regulating miR-93

J Shi1, Y Zhuang, X K Liu

  • 1Department of Urology, Tangshan Gongren Hospital, Hebei Medical University, No. 27, Wenhua Road, Lubei District, Tangshan, 063000, China.

Clinical & Translational Oncology : Official Publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
|September 4, 2014
PubMed
Abstract

Insights

Transforming growth factor-beta (TGF-beta) upregulates Retinoblastoma-like protein 2 (RBL2) in renal cancer by inhibiting microRNA-93 (miR-93). This TGF-beta/miR-93/RBL2 pathway halts cancer cell growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Transforming growth factor-beta (TGF-beta) is known to induce cell cycle arrest in various cell types.
  • Mechanisms include the upregulation of proteins like p21, p27, and Retinoblastoma (Rb).
  • The role of RBL2, another member of the Rb family, in TGF-beta-induced cell cycle arrest was previously uncharacterized.

Purpose of the Study:

  • To investigate whether TGF-beta treatment induces RBL2 expression in renal cancer cells.
  • To elucidate the molecular mechanisms underlying the regulation of RBL2 by TGF-beta.
  • To identify the role of RBL2 in TGF-beta-mediated growth inhibition and cell cycle arrest.

Main Methods:

  • Quantitative real-time PCR and Western blot were used to measure RBL2 and miR-93 expression.
  • Cell proliferation was assessed using CCK-8 assays.
  • Cell cycle analysis was performed via PI staining.
  • The interaction between miR-93 and RBL2 3'-UTR was confirmed using a dual-luciferase reporter assay.

Main Results:

  • TGF-beta treatment dose- and time-dependently increased RBL2 expression in renal cancer cells.
  • RBL2 mediated the growth inhibitory and cell cycle arrest effects of TGF-beta.
  • miR-93 directly targets RBL2, with miR-93 overexpression decreasing RBL2 levels and miR-93 knockdown increasing them.
  • TGF-beta treatment suppressed miR-93 expression, leading to increased RBL2 levels.

Conclusions:

  • TGF-beta induces RBL2 expression in renal cancer cells by downregulating miR-93.
  • A novel signaling pathway, TGF-beta/miR-93/RBL2, has been identified.
  • This pathway provides a new molecular mechanism for TGF-beta-induced growth arrest in renal cancer.

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