FSHR Gene Editing

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FSHR Gene Editing    

Follicle-stimulating hormone receptor (FSHR) is a glycosylated transmembrane protein that belongs to the G protein-coupled receptor (GPCR) family. Upon binding follicle stimulating hormone (FSH), FSHR transduces signal primarily through the adenylyl cyclase-cAMP-protein kinase A pathway. FSH is a central hormone of mammalian reproduction, which is produced by the gonadotroph cells in the anterior pituitary gland. The target organs for FSH are the testis and ovary. In males, FSHR is expressed in testicular Sertoli cells and regulates their metabolic functions necessary for germ cell survival and proper spermatogenesis. In females, FSHR is expressed in granulosa cells and regulates the granulosa cell proliferation, maturation of Graafian follicles and estrogen production. Recent studies have indicated the expression of FSHR in many normal extragonadal tissues, as well as in the tumors and tumor vessel endothelial cells (TVECs).

FSHR in Cancer and TVECs

Many studies have shown the expression of FSHR in different types of tumor cells suggesting a potential role of FSH in tumorigenesis and FSHR as a potential target for cancer therapy. FSHR expression was suggested to be present in prostate, ovarian, neuroendocrine pancreatic, thyroid, and pituitary cancer cells and soft tissue sarcomas. A breakthrough in the study of extragonadal FSHR expression was, when the receptor expression was proposed in TVECs of different types of tumors (prostate, breast, pancreas, colon, urinary bladder, liver, kidney, lung, stomach, testis, and ovary), including their metastases.

The major body of research on FSH/FSHR expression in cancerous tissues is related to ovarian cancer. Indeed, FSH appears to inhibit apoptosis in epithelial ovarian cancer cell lines by increased expression of survivin and suppressed expression of programmed cell death gene 6 (PDCD6) and death receptor 5 (DR5); this observation could correlate FSH with disease progression. In the prostate cancer FSHR-positive arterioles, capillaries and venules were located at the periphery of the tumor core. Endothelial cells of the vessels present in normal-appearing tissues at a distance >10 mm outside the tumors or normal prostate were FSHR-negative. The presence of FSHR on tumor blood vessels raises the possibility that FSHR contributes to neoangiogenesis. FSH has been shown to induce vascular endothelial growth factor (VEGF) in granulosa cells and conceivably, a similar role of FSH-FSHR signaling could exist in the tumor endothelium. FSHR may also contribute to the development of metastatic disease. Thus, concerning cancer cells and TVECs (primary and metastatic), it was indicated that FSHR might serve as a potential cellular marker of different tumors and provide a novel approach for targeted cancer therapy. If extragonadal FSHR expression and function could be proven by additional independent studies in the TVECs, as well as in the cancer cells, the finding would suggest for FSHR a great utility as a biomarker and medicinal target.

Therapeutics targeting FSHR

As FSHR plays a key role in human reproductive biology, efforts have been made to target the receptor with small molecules. Several classes of compounds that antagonize FSHR signaling have been identified. Usually, these molecules are negative allosteric modulators of FSHR. Based on the presumed antiangiogenic effects by blocking the FSHR signaling pathway, clinicians from an institution used degarelix for a multi-treated metastatic colon cancer patient. Degarelix is a new gonadotropin-releasing hormone receptor antagonist developed for patients with prostate cancer, which presents antiangiogenic capacity through blockage of FSH production. When combined with standard palliative chemotherapy, degarelix induced a rapid decrease in the FSH level and also radiological and carcinoembryonic antigen stabilization during 1 year of follow-up, while contrast-enhanced ultrasonography demonstrated reduction of tumor vasculature. Recently, Urbanska and colleagues published encouraging data on FSHR-targeted immune therapy. They constructed and evaluated a novel redirected T cell-based immunotherapy targeting FSHR; further exploration is warranted.

FSHR Gene Editing Service

CRISPR/Cas9 PlatformCB, one of the leading biotechnological companies specializing in gene editing, is dedicated to offering comprehensive CRISPR/Cas9 gene-editing services to a wide range of genomics researchers. Based on our platform, we can help you effectively FSHR gene deleted, inserted or point mutated in cells or animals by CRISPR/Cas9 technology.

  • FSHR Gene Knockout: We offer FSHR gene knockout cell line and knockout animal model generation service with high quality. Typically, we develop CRISPR-mediated gene editing cell lines including HEK239T, Hela, HepG2, U87, but we can use other cell lines according to your requirements. Our one-stop KO animal model generation service that covers from sgRNA design and construct, pronuclear microinjection to Founders genotyping and breeding.
  • FSHR Gene Knockin: CRISPR/Cas9 PlatformCB provides the one-stop FSHR knock-in cell line and knockout animal model generation services, including point mutation and gene insertion. Our expert staff has succeeded in dozens of FSHR knock-in cell line generation projects, including stem cells, tumor cells and even difficult-to-handle cells. We also have extensive experience in incorporating CRISPR/Cas9 technology into animal models, which have been fully recognized by our clients.

If you have any questions, please feel free to contact us.

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References

  1. Papadimitriou K, et al. Follicle-stimulating hormone receptor (FSHR): a promising tool in oncology?. Molecular diagnosis & therapy, 2016, 20(6): 523-530.
  2. Gartrell B A, et al. The follicle-stimulating hormone receptor: a novel target in genitourinary malignancies. Urologic Oncology: Seminars and Original Investigations. Elsevier, 2013, 31(8): 1403-1407.
  3. Chrusciel M, et al. Extragonadal FSHR Expression and Function—Is It Real?. Frontiers in endocrinology, 2019, 10.
For research use only. Not intended for any clinical use.

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