Related Experiment Video
Updated: Jun 22, 2026

Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions
Published on: August 2, 2018
Identification and characterization of demethylase JMJD1A as a gene upregulated in the human cellular response to
Aylin Sar1, Dragana Ponjevic, Monica Nguyen
1The Department of Pathology, University of Calgary, AB, Canada.
Abstract:
Hypoxia is commonly found in human solid cancers and serves as a selective environment for the survival of aggressive cancer cells and as protection from anti-cancer therapies. In addition to a shift to anaerobic metabolism, the cellular response to hypoxia includes cessation of cell division and/or cell death. These mechanisms have still not been defined. Identification of the members of hypoxia-induced growth arrest pathways remain incomplete. We have undertaken an expression microarray analysis of the cellular response to hypoxia in diverse cell lines. An identified cohort of genes is reliably upregulated in various cells in response to hypoxia, as validated by reverse-transcriptase polymerase chain reaction (RT-PCR). One of the upregulated targets corresponds to an expressed sequence tag encoded by JMJD1A (a gene also known as JHDM2A), which has been identified as a histone demethylase that regulates the transcription of androgen receptor targets. We confirm, by RT-PCR, the upregulation of JMJD1A after hypoxia and desferroxamine treatment in multiple cell lines. We also show that JMJD1A is predominantly, but not exclusively, a nuclear protein. Immunofluorescent staining of HeLa cells shows a shift of cytoplasmic JMJD1A into the nucleus on hypoxia treatment. Immunohistochemical staining has revealed that JMJD1A is widely expressed in tissues, even in cells that are not known to express the androgen receptor, and is significantly increased in smooth muscle cells upon hypoxia treatment.
Insights
Hypoxia, a low-oxygen state in cancers, upregulates JMJD1A, a histone demethylase. This gene
Area of Science:
- Molecular Biology
- Cancer Research
- Cellular Biology
Background:
- Hypoxia is prevalent in solid tumors, promoting cancer cell survival and therapy resistance.
- Cellular responses to hypoxia include metabolic shifts, growth arrest, and cell death, with incompletely defined mechanisms.
- Identifying genes involved in hypoxia-induced growth arrest is crucial for understanding cancer progression.
Purpose of the Study:
- To identify genes upregulated in response to hypoxia using expression microarray analysis.
- To investigate the role of JMJD1A (JHDM2A) in the cellular response to hypoxia.
- To characterize the expression and localization of JMJD1A under hypoxic conditions.
Main Methods:
- Expression microarray analysis of diverse cell lines under hypoxic conditions.
- Reverse-transcriptase polymerase chain reaction (RT-PCR) for gene expression validation.
- Immunofluorescence and immunohistochemical staining for protein localization studies.
Main Results:
- A cohort of genes was reliably upregulated by hypoxia across multiple cell lines.
- JMJD1A (JHDM2A), a histone demethylase, was identified as a hypoxia-upregulated gene.
- JMJD1A expression increased upon hypoxia and desferrioxamine treatment; it translocates to the nucleus and is widely expressed in tissues.
Conclusions:
- JMJD1A is a hypoxia-responsive gene involved in cellular responses to low-oxygen environments.
- The nuclear localization and broad tissue expression of JMJD1A suggest a significant role in normal and potentially cancerous tissues.
- Further research is warranted to elucidate JMJD1A's precise function in hypoxia-induced pathways and cancer.
Related Concept Videos
Hypoxia
Types of Hypoxia
There are four primary types of hypoxia, each resulting from a different cause:
1. Anemic hypoxia: This type occurs due to insufficient oxygen delivery caused by a lack of red blood cells (RBCs) or RBCs with abnormal or...
Adaptive Mechanisms in Cancer Cells
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Master Transcription Regulators
Master Transcription Regulators
Cell Specific Gene Expression
Cell Specific Gene Expression

