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Related Concept Videos

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...
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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.
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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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Abnormal Proliferation02:23

Abnormal Proliferation

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...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Such genes that act...

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Related Experiment Video

Updated: Jun 10, 2026

Detection of Lung Tumor Progression in Mice by Ultrasound Imaging
04:43

Detection of Lung Tumor Progression in Mice by Ultrasound Imaging

Published on: February 27, 2020

HIF-2alpha deletion promotes Kras-driven lung tumor development.

Jolly Mazumdar1, Michele M Hickey, Dhruv K Pant

  • 1Abramson Family Cancer Research Institute, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.

Proceedings of the National Academy of Sciences of the United States of America
|July 28, 2010
PubMed
Summary

Inhibiting hypoxia-inducible factor-2alpha (HIF-2alpha) in non-small cell lung cancer (NSCLC) unexpectedly increased tumor growth by downregulating the tumor suppressor Scgb3a1. This suggests HIF-2alpha levels must be carefully considered for effective NSCLC therapy.

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Published on: July 21, 2018

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Non-small cell lung cancer (NSCLC) remains a leading cause of cancer mortality globally.
  • Hypoxia-inducible factors (HIFs), specifically HIF-1alpha and HIF-2alpha, are often overexpressed in NSCLC.
  • Constitutive HIF-2alpha activity is implicated in promoting lung tumor progression, positioning HIFs as potential therapeutic targets.

Purpose of the Study:

  • To investigate the role of HIF-1alpha and HIF-2alpha in Kras(G12D)-driven murine NSCLC.
  • To determine the downstream targets and regulatory mechanisms of HIF-2alpha in lung cancer.
  • To assess the therapeutic implications of HIF-2alpha inhibition in NSCLC.

Main Methods:

  • Genetic deletion of Hif-1alpha and Hif-2alpha in a Kras(G12D)-driven mouse model of NSCLC.
  • Analysis of tumor burden, gene expression (including Scgb3a1), and AKT pathway activity.
  • Validation in human NSCLC cell lines and xenografts, and analysis of human NSCLC patient samples.

Main Results:

  • Hif-1alpha deletion had no significant effect on tumor growth.
  • Hif-2alpha deletion led to increased tumor burden, associated with decreased Scgb3a1 expression.
  • Scgb3a1 was identified as a direct HIF-2alpha target gene, and its downregulation by HIF-2alpha deficiency enhanced AKT pathway activity.
  • A positive correlation between HIF-2alpha and SCGB3a1 expression was observed in ~70% of human NSCLC samples.

Conclusions:

  • HIF-2alpha plays a complex role in NSCLC, regulating the expression of the tumor suppressor Scgb3a1.
  • Therapeutic strategies targeting HIF-2alpha in NSCLC require careful consideration, as complete inhibition may paradoxically promote tumor growth.
  • Maintaining HIF-2alpha activity above a certain threshold may be crucial for suppressing tumor progression via Scgb3a1-mediated mechanisms.