HSD17B2 Antibodies

Estradiol 17-beta-dehydrogenase 2 (HSD17B2)

Capable of catalyzing the interconversion of testosterone and androstenedione, as well as estradiol and estrone. Also has 20-alpha-HSD activity.

Uses NADH while EDH17B3 utilizes NADPH. .

Gene Information

Human
Gene Name:	HSD17B2
Uniprot:	P37059
Entrez:	3294

Family

Belongs to:
short-chain dehydrogenases/reductases (SDR) family

Alternative Names

17-beta-hydroxysteroid dehydrogenase type 2; 20 alpha-hydroxysteroid dehydrogenase; E2DH; EC 1.1.1.62,17-beta-HSD 2; EC 1.1.1.63; EDH17B220-alpha-HSD; estradiol 17-beta-dehydrogenase 2; HSD17; hydroxysteroid (17-beta) dehydrogenase 2; Microsomal 17-beta-hydroxysteroid dehydrogenase; SDR9C2; short chain dehydrogenase/reductase family 9C, member 2; Testosterone 17-beta-dehydrogenase

Molecular Weight

Mass (kDA):
42.785 kDA

Genomic Context

Human
Location:	16q23.3
Sequence:	16; NC_000016.10 (82035253..82098534)

Subcellular Localizations

Membrane; Single-pass type II membrane protein.

Diseases

• Malignant Neoplasms
• Neoplasms
• Malignant Neoplasm Of Breast
• Endometrial Polyp
• Mammary Neoplasms
• Endometriosis, Site Unspecified
• Malignant Neoplasm Of Prostate
• Prostatic Neoplasms
• Endometrial Neoplasms
• Endometrial Carcinoma
• Steroid Sulfatase Deficiency Disease
• Carcinoma

• Adenocarcinoma
• Growth Retardation
• Infertility
• Osteoporosis
• Colorectal Neoplasms
• Inflammation
• Colorectal Cancer

Pathways

• Pathogenesis
• Secretion
• Localization
• Methylation
• Lung Development
• Spermatogenesis
• Cell Proliferation
• Menopause
• Decidualization
• Prolactin Secretion
• Transport
• Tricarboxylic Acid Cycle
• Gene Silencing

• Osteoblast Differentiation
• Aging
• Brain Development
• Hepatocyte Proliferation
• Cell Maturation
• Regulation Of Hepatocyte Proliferation
• Bone Development

PTMs

• Methylation

• Reduction

• Oxidation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/HSD17B2

Best Uses Of The HSD17B2 Marker

This article will cover some of the best uses of the HSD17B2 marker, as well as other potential uses for this gene. If you have a specific condition, you should also read our other article about the use of this gene in clinical trials. We will discuss the use of HSD17B2 in prostate cancer and other potential applications. You will also find out what clinical trials currently exist and how these tests can be used.

HSD17B2 in prostate cancer

This study investigated the relationship between HSD17B2 and prostate cancer. The authors found that the expression of the gene was significantly lower in tumor tissues compared to nontumoral tissues. This association was found in patients with prostate cancer and benign prostate tissue. In addition, there was a significantly lower expression of HSD17B2 in tumors of the stomach and cardia. This finding was further supported by the presence of the gene deletion in patients with primary prostate cancer.

These findings support the role of circulating hormones in prostate cancer progression. These hormones are effect modifiers, rather than direct players. Although the relationship between prostate cancer and circulating hormones is complex, the results of the current study suggest that circulating hormones may play a role. For instance, the gene rs1256049 was associated with prostate cancer, while rs743572 was associated with high-grade disease. However, it remains to be seen how these genes affect prostate cancer.

The HSD17B2 and prostate cancer association was further explored in a prospective cohort study. Patients who had a high HSD17B2 or HMGCS2 expression level were more likely to have poor responses to preoperative chemoradiotherapy. Therefore, HSD17B2 and prostate cancer are closely linked, but the exact mechanism is unknown. But the findings are still important. They suggest that both HSD17B2 and HMGCS2 may play a role in prostate cancer.

Among the findings, two different CRISPR constructs were used to knock out HSD17B2 in the MDA-Pca-2b cell line. Interestingly, the knockout cells produced significantly more DHT than control-HSD17B2-deficient cells. This study suggests that the down-regulation of HSD17B2 facilitates the production of DHT in prostate cancer cell lines. These results indicate a possible mechanism of androgen accumulation in CRPC.

A second study, conducted in Africa, examined the HSD17B2 and prostate cancer relationship. It found that both the HSD17B2 and ETS dependent biomarkers were highly predictive of biochemical recurrence in African American men. The epigenetic modifier HSD17B2 altered the expression of CD146. In a separate study, researchers identified the role of HSD17B2 in prostate cancer by identifying ETS-dependent biomarkers.

The two RNAs were inserted into the CRISPR plasmid. The resulting constructs were derived from lentiCRISPR v2 provided by Dr. Feng Zhang. The two plasmids were cotransfected with 293T cells. The transfections were carried out for 48 hours. Mission RNAi provided the shRNA and puromycin. It was also necessary to check whether the shRNA worked.

Although the role of HSD17B2 in prostate cancer remains unclear, there are some promising results. The gene suppresses the conversion of androgens from testis to DHT. This, in turn, suppresses the growth of tumors in men. This inactivation inhibits the AR signaling pathway. While this is an important factor in prostate cancer, it should not be considered in isolation. For the time being, more studies are needed.

Other uses for HSD17B2

Other uses for HSD17B2 include inhibiting the conversion of androgens to DHT and to 5a-dione. HSD17B2 is highly expressed in different prostate cancer cell lines, such as PC3 and LNCaP. Overexpression of the protein resulted in inactivation of T and DHT. Induction of HSD17B2 was achieved using Dox and the adrenal precursor AD in MDA-Pca-2b cells.

Moreover, the gene is responsible for the conversion of androgens into estradiol and testosterone. Its function is crucial for maintaining intracellular levels of these hormones. In addition, HSD17B2 catalyzes the interconversion of testosterone and androstenedione with estradiol. The enzyme exhibits 17-b HSD activity and 20a-HSD activity toward 20a-dihydroprogesterone.

The genes encoding HSD17B2 are also called 17bHSD. There are two isoforms of 17bHSD, the M and the S. In mice, overexpression of both isoforms increases the risk of developing cancer. Similarly, in humans, HSD17B2 is used for genetic studies. There are new uses for HSD17B2 and its isoforms.

There are multiple mechanisms involved in the regulation of HSD17B2, including cancer prevention and detection. HSD17B2 is reduced in prostate cancer, and its expression decreases with the progression of the disease. This gene also plays a role in cancer therapy, as it is associated with decreased incidence of prostate cancer. In addition, HSD17B2 is induced by estrogen in men with advanced prostate cancer. It is also involved in the progression of breast cancer and has a role in the development of fibrosis.

The regulation of HSD17B2 can reveal novel strategies for prostate cancer treatment. DNA methylation in the HSD17B2 promoter inhibits SP1 binding, reducing its protein abundance. The results also demonstrate the importance of epigenetic regulation in prostate cancer treatment. These studies highlight the need for HSD17B2 as a novel therapeutic target. The next step is the discovery of anti-cancer drugs.

Studies have shown that mRNA transcription of HSD17B2 regulates the availability of ligands for several nuclear receptors. It inactivates estradiol and testosterone, activates 20a-hydroxyprogesterone 1 (progesterone), and regulates retinoids. Furthermore, HSD17B2 is potentially involved in the metabolism of retinoids. For this reason, HSD17B2 has several other uses.

Clinical trials

The HSD17B2 gene is expressed in breast cancer cells, and detection of this gene is essential to developing treatments. In a recent study, researchers identified two miRNAs that regulate the expression of the gene: miR-205-3p and miR-75-1. The researchers found that miR-17 upregulated HSD17B1 and HSD17B2 in both breast cancer cell lines. Although further studies are needed to determine whether miR-205-3p and miR-17p can influence the expression of HSD17B1, this work provides a starting point.

The HSD17B2 gene is expressed in two types of breast cancer cell lines: MCF7 and T-47D. In this study, cells were treated with five-nM estradiol or ethanol for six hours. Treatment with the five-nM estradiol lowered the level of HSD17B1.

The two miRNAs, miR-210 and miR-205, both inhibit the expression of HSD17B1. MiR-210 resulted in a mixed response. Other miRNAs tested, including miR-214-3p, resulted in reduced HSD17B2 expression. Clinical trials of the HSD17B2 gene are ongoing and will reveal how it affects tumor growth.

ERa-dependent regulation of HSD17B2 expression in breast cancer cell lines, such as MCF7, shows an estradiol-dependent effect. Estradiol has a limited effect on the expression of HSD17B2, but increases it in cells that lack estrogen receptor-a. The ERa-negative cell line, SK-BR-3, had no effect on HSD17B2 expression.

GREB1 and EPHB6 are known tumor suppressors, which promote HSD17B2 expression. HSD17B2 and GREB1 are downregulated in metastases, while KLK5 and TP63 are downregulated in LG and CRPC cells. The UGT2B16 and TP63 downregulated cells showed reduced HSD17B2 expression. This study also showed a relationship between CRPC and HG.

In a study with a dummy model of DH, dihydrotestosterone treatment increased HSD17B1 and HSD17B2 expression in three breast cancer cell lines. In contrast, dihydrotestosterone did not have an effect on the HSD17B2 gene in DH cells, but did increase it in T-47D and MCF7.