Related Experiment Video

Updated: May 10, 2026

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)
04:12

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)

Published on: December 19, 2019

RhoB promotes cancer initiation by protecting keratinocytes from UVB-induced apoptosis but limits tumor

Nicolas Meyer1, Alexis Peyret-Lacombe2, Bruno Canguilhem2

  • 1Inserm, UMR 1037-CRCT, Toulouse, France; Université Paul Sabatier, Toulouse, France; Department of Dermatology, Hôpital Larrey, Toulouse, France.

The Journal of Investigative Dermatology
|June 25, 2013
PubMed

Insights

Ras homolog gene family, member B (RhoB) protects against UVB-induced skin cancer by promoting keratinocyte survival. Loss of RhoB increases sensitivity to apoptosis, reducing tumor formation but promoting aggressiveness in advanced squamous cell carcinoma.

Area of Science:

  • Oncology
  • Dermatology
  • Molecular Biology

Background:

  • UVB radiation is a known carcinogen, contributing to skin cancer development.
  • Apoptosis, or programmed cell death, plays a critical role in preventing the proliferation of damaged cells.
  • The RhoB GTPase is an early stress response gene implicated in keratinocyte apoptosis following UVB exposure.

Purpose of the Study:

  • To investigate the in vivo role of RhoB in UVB-induced skin carcinogenesis.
  • To determine the mechanism by which RhoB influences keratinocyte apoptosis and tumor development.
  • To explore the association between RhoB expression and the progression of squamous cell carcinoma (SCC).

Main Methods:

  • Generation of RhoB-deficient (rhob-/-) SKH1 mice for in vivo studies.
  • UVB irradiation of mice and analysis of tumor formation and keratinocyte apoptosis.
  • Downregulation of RhoB in primary human keratinocytes using small interfering RNA (siRNA).
  • Assessment of B-cell lymphoma 2 (Bcl-2) expression and DNA double-strand break markers (γH2AX, 53BP1).

Main Results:

  • RhoB-deficient mice exhibited reduced risk of UVB-induced tumors and actinic keratosis.
  • UVB-exposed keratinocytes from rhob-/- mice showed increased sensitivity to apoptosis, linked to Bcl-2 downregulation.
  • UVB-induced tumors in rhob-/- mice were undifferentiated and highly proliferative.
  • Loss of RhoB expression was observed in human undifferentiated SCCs, correlating with increased DNA double-strand breaks.

Conclusions:

  • UVB-induced RhoB expression promotes keratinocyte survival, playing a role in SCC initiation.
  • RhoB deficiency enhances UVB-induced keratinocyte apoptosis, thereby reducing initial tumor formation.
  • Loss of RhoB expression is associated with more aggressive, undifferentiated SCC and may indicate tumor progression.

More Related Videos

Cell Population Analyses During Skin Carcinogenesis06:53

Cell Population Analyses During Skin Carcinogenesis

Published on: August 21, 2013

Pharmacologic Induction of Epidermal Melanin and Protection Against Sunburn in a Humanized Mouse Model12:37

Pharmacologic Induction of Epidermal Melanin and Protection Against Sunburn in a Humanized Mouse Model

Published on: September 7, 2013

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,...
Skin Cancer01:30

Skin Cancer

Skin cancer is a type of cancer that occurs when there is an abnormal growth of skin cells, usually triggered by damage to the DNA within the skin cells. It is primarily caused by exposure to ultraviolet (UV) radiation from the sun or artificial sources like tanning beds. Skin cancer is the most common type of cancer worldwide, and its incidence continues to rise.
Basal Cell Carcinoma (BCC): BCC is the most common type of skin cancer, accounting for about 80% of cases. It typically develops in...
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
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...
Mutations01:35

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity: