Related Experiment Video

Updated: Jun 2, 2026

Prediction and Validation of Gene Regulatory Elements Activated During Retinoic Acid Induced Embryonic Stem Cell Differentiation
09:07

Prediction and Validation of Gene Regulatory Elements Activated During Retinoic Acid Induced Embryonic Stem Cell Differentiation

Published on: June 21, 2016

Implication of retinoic Acid receptor-Beta in renal-cell carcinoma

B Vanderleede1, T Opdenoordt, C Vandenbrink

  • 1UNIV DUSSELDORF,UROL CLIN,W-4000 DUSSELDORF 1,GERMANY.

International Journal of Oncology
|May 11, 2011
PubMed

Insights

Loss of retinoic acid receptor (RAR) beta in kidney cancer may drive tumor growth. Restoring RAR beta expression inhibited renal cancer cell proliferation, suggesting its role in kidney oncogenesis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The retinoic acid receptor (RAR) beta gene is located on chromosome 3p, a region frequently deleted in renal cell carcinoma.
  • Retinoic acid (RA) inhibits cell proliferation and tumor formation, suggesting RAR beta's loss may contribute to kidney cancer development.

Purpose of the Study:

  • To examine RAR beta expression in primary kidney tumors and renal cancer cell lines.
  • To investigate the role of RARB in retinoic acid-dependent growth control in renal cancer.

Main Methods:

  • Analysis of RAR beta expression in 12 primary kidney tumors and 11 renal cancer cell lines.
  • Stable transfection of RAR beta expression vectors into two renal cancer cell lines (SK-RC-35 and SK-RC-48).
  • Assessment of cell proliferation in response to retinoic acid in transfected cell lines.

Main Results:

  • Five tumors showed severely reduced RAR beta expression; one had an aberrant transcript.
  • Only three renal cancer cell lines exhibited detectable RAR beta expression at low levels.
  • RAR beta-expressing clones showed markedly reduced proliferation with RA; transfectants responded to high RA doses.

Conclusions:

  • Reduced RAR beta expression is observed in a subset of kidney tumors and cell lines.
  • Restoring RAR beta expression can inhibit proliferation of renal cancer cells in the presence of RA.
  • RAR beta is potentially implicated in the pathogenesis of renal cell carcinoma.

More Related Videos

Modeling Spontaneous Metastatic Renal Cell Carcinoma (mRCC) in Mice Following Nephrectomy11:27

Modeling Spontaneous Metastatic Renal Cell Carcinoma (mRCC) in Mice Following Nephrectomy

Published on: April 29, 2014

Related Concept Videos

The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR activation may...
Receptor Tyrosine Kinases01:26

Receptor Tyrosine Kinases

Receptor tyrosine kinases or RTKs are membrane-bound receptors that phosphorylate specific tyrosine on protein substrates. RTKs regulate cellular growth, differentiation, survival, and migration. They contain an extracellular ligand binding domain, a transmembrane domain, and a cytosolic tail with intrinsic kinase activity. Several extracellular signaling molecules activate RTKs in one or more ways and relay the signal downstream. Ligands such as platelet-derived growth factor (PDGF) or...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...