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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.
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Somatic to iPS Cell Reprogramming01:29

Somatic to iPS Cell Reprogramming

Reprogramming alters the gene expression in somatic cells, transforming them into induced pluripotent stem (iPS) cells over several generations. Scientists can reprogram cells by introducing genes for four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) by viral or non-viral methods. These factors are also known as Yamanaka factors after Shinya Yamanaka, who first generated iPS cells using mouse skin cells. Yamanaka was awarded the Nobel Prize in Physiology or Medicine in 2012 for this...
Abnormal Proliferation02:23

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
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Rous Sarcoma Virus (RSV) and Cancer

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Related Experiment Video

Updated: Jun 24, 2026

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

Published on: June 21, 2016

RHEBL1 expression is activated by the Oct4-Sox2 complex in oral squamous cell carcinoma.

Feng Qiu1,2, Yaqiu Chen2, Peibo Li1

  • 1The Department of Stomatology, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe East Road, Erqi District, Zhengzhou City, China.

Functional & Integrative Genomics
|June 22, 2026
PubMed
Summary

Stem cell factors Oct4 and Sox2 promote oral squamous cell carcinoma (OSCC) by regulating RHEBL1 expression. This study reveals RHEBL1

Keywords:
Oct4RHEBL1Sox2Cancer stem cellsOral squamous cell carcinoma

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Live Imaging of Innate Immune and Preneoplastic Cell Interactions Using an Inducible Gal4/UAS Expression System in Larval Zebrafish Skin

Published on: February 3, 2015

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Live Imaging of Innate Immune and Preneoplastic Cell Interactions Using an Inducible Gal4/UAS Expression System in Larval Zebrafish Skin
08:52

Live Imaging of Innate Immune and Preneoplastic Cell Interactions Using an Inducible Gal4/UAS Expression System in Larval Zebrafish Skin

Published on: February 3, 2015

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • RHEBL1 (Ras homolog enriched in brain-like 1) is implicated in tumor promotion via mTOR and NF-κB pathways.
  • The specific role of RHEBL1 in oral squamous cell carcinoma (OSCC) and its regulation by Oct4 and Sox2 remain uncharacterized.

Purpose of the Study:

  • To investigate the function and regulatory mechanisms of RHEBL1 in OSCC development.
  • To analyze the influence of Oct4 and Sox2 on RHEBL1 expression in OSCC.

Main Methods:

  • Immunohistochemistry and immunofluorescence to assess protein expression in tissues.
  • Generation of RHEBL1-overexpressing and knockout cell lines for in vitro and in vivo studies.
  • Bioinformatics, dual-luciferase reporter assays, and ChIP-PCR to validate promoter binding and transcriptional activity.

Main Results:

  • RHEBL1, Oct4, and Sox2 were highly expressed in OSCC tissues, particularly at the invasive front and basal layer.
  • RHEBL1 overexpression enhanced cancer cell proliferation, self-renewal, and in vivo tumorigenicity.
  • RHEBL1 knockout suppressed these cancer-promoting phenotypes.
  • Oct4-Sox2 complexes directly bind and activate the RHEBL1 promoter.

Conclusions:

  • Oct4 and Sox2 promote OSCC initiation and progression by upregulating RHEBL1 expression.
  • RHEBL1 is a key mediator in Oct4/Sox2-driven OSCC development.
  • Targeting the Oct4/Sox2-RHEBL1 axis may offer therapeutic strategies for OSCC.