Related Experiment Video
Updated: Apr 21, 2026
12:13
Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
Published on: November 19, 2019
5.8K
ERG oncoprotein inhibits ANXA2 expression and function in prostate cancer.
Nicholas B Griner1, Denise Young1, Pankaj Chaudhary2
1Center for Prostate Disease Research, Department of Surgery, Uniformed Services University of the Health Sciences, Rockville, Maryland.
Molecular Cancer Research : MCR
|October 26, 2014
Summary
ERG overexpression in prostate cancer represses Annexin A2 (ANXA2), disrupting cell polarity and promoting tumor progression. This inverse relationship between ERG and ANXA2 is crucial for understanding prostate cancer development and targeting therapies.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Prostate cancer development is linked to ERG overexpression.
- Annexin A2 (ANXA2) plays a role in maintaining epithelial cell polarity.
Purpose of the Study:
- To investigate the relationship between ERG and ANXA2 in prostate cancer.
- To elucidate the mechanism by which ERG affects ANXA2 expression and function.
Main Methods:
- Genomic analysis of ERG siRNA-treated prostate cells.
- Mechanistic studies on ANXA2 promoter activity.
- Immunohistochemistry on clinical prostate cancer specimens.
Main Results:
- ERG represses ANXA2 transcription by binding to its promoter.
- ERG overexpression disrupts ANXA2-mediated cell polarity and promotes epithelial-mesenchymal transition (EMT).
- A reciprocal expression pattern of ERG and ANXA2 is observed in prostate tumors, correlating with differentiation status.
Conclusions:
- ANXA2 is a novel component of the ERG regulatory network in prostate cancer.
- The ERG-ANXA2 interaction impacts prostate cancer cell differentiation and EMT.
- Targeting ANXA2 may offer new therapeutic strategies for ERG-stratified prostate cancers.
Related Concept Videos
01:31Adrenergic Receptors: ɑ Subtype
2.7K
Adrenoceptors are classified into α and ꞵ classes based on their potencies to catecholamine agonists. α-adrenoceptors show the following order of catecholamine potency:
Adrenaline ≥ Noradrenaline >> Isoprenaline
α-adrenoceptors are further divided into α1 and α2-adrenoceptors.
α1-Adrenoceptors: These receptors are located postsynaptically on the effector organs and cause constriction of smooth muscle mediated by activation of phospholipase...
Adrenaline ≥ Noradrenaline >> Isoprenaline
α-adrenoceptors are further divided into α1 and α2-adrenoceptors.
α1-Adrenoceptors: These receptors are located postsynaptically on the effector organs and cause constriction of smooth muscle mediated by activation of phospholipase...
2.7K
01:24Regulation of Angiogenesis and Blood Supply
2.9K
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.9K
02:23Abnormal Proliferation
4.0K
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...
4.0K
02:38Mitogens and the Cell Cycle
6.3K
Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
6.3K
01:33Cancer-Critical Genes I: Proto-oncogenes
8.7K
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.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
8.7K
01:09GPCRs Regulate Adenylyl Cylase Activity
6.7K
Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
6.7K