Prostate Cancer

Prostate cancer is the fourth leading cause of cancer deaths worldwide and the second most common form of cancer and cancer death in men in America. There is a large degree of heterogeneity amongst prostate cancers, both between individual cases and within more specific categories of disease progression, which complicates treatment and further research. Initial diagnosis utilizes immunohistochemistry to determine if a tumor is invasive and if it will respond to androgen therapy.

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Research Areas

Literature (10)

Pathways (1)

Prostate Cancer Product Areas

Localized prostate cancer grows slowly and may not need treatment, or it can be managed with surgery. However, if the cancer grows and metastasizes, primary androgen therapy can be administered to act at androgen receptors and suppress the release of androgens. The same approach can be used in prostate cancer research, for example, Goserelin acetate (Cat. No. 3592) is a synthetic gonadotropin-releasing hormone (GnRH) analog that behaves as an agonist at the GnRH receptors. It stimulates gonadotropin and sex hormone release in the short term and suppresses prostate cancer tumor growth with continued administration. Prostate cancer that is resistant to primary androgen therapy, a state known as metastatic castration resistant prostate cancer (mCRPC), can be treated with second generation androgen deprivation therapy. To simulate this process in research, the enzyme inhibitor Abiraterone acetate (Cat. No. 6520) can be used, which inhibits CYP450 enzymes involved in the synthesis of androgens.

Prostate cancer cells demonstrate many of the same genetic and metabolic changes as other cancer types, such as an increased requirement for nutrients to promote rapid growth. However, there are also some more specific metabolic, enzyme and genetic prostate cancer markers that are the subject of further research. For example, the cells of the most common form of prostate cancer, acinar adenocarcinoma, accumulate large reservoirs of zinc and, unlike other solid tumors, prostate cancer tends to rely more heavily on anaplerosis (TCA cycle) for amino acid metabolism and have elevated TCA cycle intermediates, this compares to a focus solely on energy production from anaplerosis in other cancers.

Other metabolic alterations in prostate cancer include: upregulation of phosophoglycerate dehydrogenase, increased glycolysis due to activation of GLUT1, increased hexokinase 1/2 activity and expression, and the upregulation of G6PD in response to mTOR.

Genetic alterations in prostate cancer include up- and down-regulation of specific genes; for example, AURKA and MYCN are amplified, but there is loss of function of RB1 and TP53/p53 and loss of PTEN. The aurora kinases encoded by AURKA gene are involved in mitosis and MYCN encodes a nuclear protein that drives cell growth and proliferation. RB1 and TP53 are both tumor suppressor genes and PTEN loss leads to hyperactivation of PI3K/AKT/mTOR signaling and is found in almost half of mCRPC tumors.

Prostate Cancer Tumor Progression

Figure 1: Prostate cancer tumor progression Schematic showing the progression of prostate cancer from normal tissue (left) through to metastatic disease (right).

Prostate Cancer Research Targets

Prostate cancer marker	Tumor change or target	Tumor progression and targets for research
Metabolic	Citrate-oriented in normal prostate	Oxidative phosphorylation, lipogenesis (FASN and lipid metabolism), increased glycolysis
Metabolic		Hypoxia – angiogenesis and aggressive tumor growth (HIFs)
Genetic	Loss or loss of function	PTEN loss, loss of function of RB1 and TP53/p53
Genetic	Upregulation	Aurora kinases; MYC
Epigenetic or transcription factors	Methylation, microRNA, histone modifications	EZH2 overexpression, bromodomains
Enzymes	Overexpression	Methyltransferases, hexokinases, G6PD, PI3K, AKT, mTOR, cytochrome P450, matrix metalloproteinases, HDAC1
Androgen receptor	Progressive dysregulation	Receptor downregulation (PROTAC® degraders and targeted protein degradation); Wnt signalling, β-catenin
Other targets		RAF, OCT4, BRD4

New and Top Products for Prostate Cancer Research

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Target	Top Products	New Products
AKT1	Akti-1/2, SC 79	AT 7867
AR	Cl-4AS-1, GSK 650394	ARCC 4 (PROTAC^®)
AURKA	Lestaurtinib, Anacardic acid
CTNNB1	endo-IWR 1, XAV 939 (GMP version available)	FzM1.8
CYP17A1	Abiraterone acetate
ERG	ERGi-USU
EZH2	3-Deazaneplanocin A hydrochloride, UNC 1999	JQEZ5
NR3C1	Gap 27, Hydrocortisone	Alsterpaullone
GSK-3B	CHIR 99021, SB 216763
HSPA5	Pifithrin-μ, VER 155008
MYC	10058-F4, KJ Pyr 9
NCOA1	Lys-CoA
PIK3CA/PIK3CB	LY 294002 hydrochloride, Wortmannin	Omipalisib
TMPRSS2	Nafamostat mesylate
FOXM1		RCM 1
BRD4	MZ 1, (+)-JQ1	AT 1 (PROTAC^®)
CUL3		WS 383
BMI1	PRT 4165
Asah1	Oleylethanolamide
FOXA1	(+)-JQ1
ABCG2		Kyoto Probe-1
NR2F2		CIA 1
SPOP	SPOP-i-6lc

PROTAC® is a registered trademark of Arvinas Operations, Inc., and is used under license.

Literature for Prostate Cancer

Tocris offers the following scientific literature for Prostate Cancer to showcase our products. We invite you to request* or download your copy today!

*Please note that Tocris will only send literature to established scientific business / institute addresses.

Cell Cycle and DNA Damage Research Product Guide

This product guide provides a review of the cell cycle and DNA damage research area and lists over 150 products, including research tools for:

Cell Cycle and Mitosis
DNA Damage Repair
Targeted Protein Degradation
Ubiquitin Proteasome Pathway
Chemotherapy Targets

Stem Cell Research Product Guide

This product guide provides a background to the use of small molecules in stem cell research and lists over 200 products for use in:

Self-renewal and Maintenance
Differentiation
Reprogramming
Organoid Generation
GMP and Ancillary Material Grade Products

TPD and Induced Proximity Research Product GuideUpdated

This brochure highlights the tools and services available from Bio-Techne to support your Targeted Protein Degradation and Induced Proximity research, including:

Active Degraders
TAG Degradation Platform
Degrader Building Blocks
Assays for Protein Degradation
Induced Proximity Tools

Autophagy Scientific Review

Written by Patricia Boya and Patrice Codogno, this review summarizes the molecular mechanisms, physiology and pathology of autophagy. The role of autophagy in cell death and its links to disease are also discussed. Compounds available from Tocris are listed.

MAPK Signaling Scientific Review

MAP kinase signaling is integral to the regulation of numerous cellular processes such as proliferation and differentiation, and as a result is an important focus of cancer and immunology research. Updated for 2016, this review discusses the regulation of the MAPK pathway and properties of MAPK cascades. Compounds available from Tocris are listed.

Angiogenesis in Cancer Poster

This poster summarizes the pathogenesis of angiogenesis in cancer, as well as some of the main angiogenesis therapeutic targets.

Autophagy Poster

Autophagy is a cellular process used by cells for degradation and recycling. Written by Patricia Boya and Patrice Codogno, this poster summarizes the molecular machinery, physiology and pathology of autophagy. Compounds available from Tocris are listed.

Cancer Metabolism Poster

This poster summarizes the main metabolic pathways in cancer cells and highlights potential targets for cancer therapeutics. Genetic changes and epigenetic modifications in cancer cells alter the regulation of cellular metabolic pathways providing potential cancer therapeutic targets.

Epigenetics in Cancer Poster

This poster summarizes the main epigenetic targets in cancer. The dysregulation of epigenetic modifications has been shown to result in oncogenesis and cancer progression. Unlike genetic mutations, epigenetic alterations are considered to be reversible and thus make promising therapeutic targets.

Programmed Cell Death Poster

There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.

Pathways for Prostate Cancer

Akt Signaling Pathway

The Akt signaling pathway plays a key role in the mediation of protein synthesis, metabolism, proliferation and cell cycle progression. It may be referred to as a 'prosurvival' pathway.