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Sermorelin

GHRH (1-29), GRF 1-29 NH2, Sermorelin acetate

Quick Stats
Studies 223
Trials 41
2016 pubmed 32 citations

Antagonists of growth hormone-releasing hormone receptor induce apoptosis specifically in retinoblastoma cells.

Chu. Wai Kit WK; Law. Ka Sin KS; Chan. Sun On SO; Yam. Jason Cheuk Sing JC; Chen. Li Jia LJ; Zhang. Hao H; Cheung. Herman S HS; Block. Norman L NL; Schally. Andrew V AV; Pang. Chi Pui CP

Key Findings

  • Retinoblastoma cells have high levels of the GHRH receptor, unlike other retinal cells.
  • Two GHRH‑R antagonists, MIA‑602 and MIA‑690, trigger programmed cell death (apoptosis) specifically in retinoblastoma cells.
  • Treatment with these antagonists down‑regulates genes that drive cell growth and up‑regulates genes that promote apoptosis.

Practical Outcomes

  • For biohackers and self‑experimenters, this study offers no actionable protocol or dosage guidance. The work is focused on a pediatric eye cancer and suggests a potential future therapeutic avenue, not a current health‑optimization strategy.

Summary

Scientists discovered that drugs that block the growth‑hormone‑releasing hormone receptor can kill eye‑cancer cells (retinoblastoma) while leaving normal eye cells unharmed. This finding is specific to a childhood eye tumor and does not translate into any immediate health‑boosting advice for the general public.

Abstract

Retinoblastoma (RB) is the most common intraocular cancer in children worldwide. Current treatments mainly involve combinations of chemotherapies, cryotherapies, and laser-based therapies. Severe or late-stage disease may require enucleation or lead to fatality. Recently, RB has been shown to arise from cone precursor cells, which have high MDM2 levels to suppress p53-mediated apoptosis. This finding leads to the hypothesis that restoring apoptosis mechanisms in RBs could specifically kill the cancer cells without affecting other retinal cells. We have previously reported involvement of an extrapituitary signaling pathway of the growth hormone-releasing hormone (GHRH) in the retina. Here we show that the GHRH receptor (GHRH-R) is highly expressed in RB cells but not in other retinal cells. We induced specific apoptosis with two different GHRH-R antagonists, MIA-602 and MIA-690. Importantly, these GHRH-R antagonists do not trigger apoptosis in other retinal cells such as retinal pigmented epithelial cells. We delineated the gene expression profiles regulated by GHRH-R antagonists and found that cell proliferation genes and apoptotic genes are down- and up-regulated, respectively. Our results reveal the involvement of GHRH-R in survival and proliferation of RB and demonstrate that GHRH-R antagonists can specifically kill the RB cells.

Study Information

Provider

pubmed

Year

2016

Date

2016-11-23T00:00:00.000Z

DOI

10.1073/pnas.1617427113

Citations

32

References

33