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Updated: Dec 11, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
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LncRNA CDKN2B-AS1/miR-141/cyclin D network regulates tumor progression and metastasis of renal cell carcinoma

Pritha Dasgupta1, Priyanka Kulkarni1, Shahana Majid1

  • 1Department of Urology, Veterans Affairs Medical Center, San Francisco and University of California San Francisco, San Francisco, CA, USA.

Cell Death & Disease
|August 21, 2020
PubMed

Insights

This study reveals that the long non-coding RNA CDKN2B-AS1 and microRNA miR-141-3p regulate kidney cancer progression. Targeting this CDKN2B-AS1/miR-141/Cyclin D axis offers a potential therapeutic strategy for renal cell carcinoma (RCC) metastasis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Renal cell carcinoma (RCC) presents management challenges due to its molecular heterogeneity and metastatic potential.
  • Understanding the molecular mechanisms driving RCC progression and metastasis is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the role of the long non-coding RNA CDKN2B-AS1 and microRNA miR-141-3p in renal cell carcinoma (RCC) progression and metastasis.
  • To elucidate the regulatory network involving CDKN2B-AS1, miR-141-3p, and Cyclin D1/D2 in RCC.

Main Methods:

  • Analysis of CDKN2B-AS1 and miR-141 expression in RCC tissues and cell lines.
  • In vitro assays (proliferation, clonogenicity, migration, invasion, apoptosis) and in vivo xenograft mouse models.
  • RNA immunoprecipitation and luciferase reporter assays to confirm molecular interactions.

Main Results:

  • CDKN2B-AS1 was overexpressed, while miR-141 was downregulated in RCC tissues.
  • CDKN2B-AS1 acts as a competing endogenous RNA (ceRNA) for miR-141, targeting CCND1 and CCND2.
  • Inhibition of CDKN2B-AS1 or overexpression of miR-141 suppressed RCC cell proliferation, migration, invasion, and tumor growth, correlating with poor patient survival.
  • The CDKN2B-AS1/miR-141/Cyclin D axis regulates epithelial-mesenchymal transition (EMT) via the RAC1/pPXN pathway.

Conclusions:

  • The CDKN2B-AS1/miR-141/Cyclin D axis is a key regulator of EMT-driven metastasis in RCC.
  • This molecular network represents a promising therapeutic target for managing advanced and metastatic RCC.

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