GHRH antagonist peptide JV-1-36 induces autophagy in cancer cells through a receptor-dependent mechanism
The GHRH antagonist peptide JV-1-36 induces autophagy in breast (MDA-MB-468) and lung (A549) cancer cells by elevating autophagy-related proteins ATG-5, ATG-3, ATG-7, and ATG-16L1, but only in cells expressing GHRH receptors.
Quick Facts
What This Study Found
JV-1-36 elevated ATG-5, ATG-3, ATG-7, ATG-16L1 in GHRH receptor-positive MDA-MB-468 and A549 cells. No effect in GHRH receptor-negative MCF-7 cells. Confirms receptor-dependent autophagy induction.
Key Numbers
How They Did This
In vitro treatment of breast (MDA-MB-468, MCF-7) and lung (A549) cancer cell lines with GHRH antagonist JV-1-36. GHRH receptor expression confirmed. Autophagy marker protein levels assessed.
Why This Research Matters
GHRH antagonists are anti-cancer peptides with known anti-inflammatory and anti-oxidative effects. Discovering that autophagy is another mechanism adds to understanding of their multi-modal anti-cancer activity.
The Bigger Picture
GHRH antagonists represent a peptide-based approach to cancer treatment distinct from GLP-1 drugs. Understanding that they induce autophagy provides new insight into their mechanism and could guide combination strategies.
What This Study Doesn't Tell Us
In vitro only. Limited to 3 cell lines. Functional significance of autophagy (pro-death vs pro-survival) not determined. No in vivo validation.
Questions This Raises
- ?Is GHRH antagonist-induced autophagy pro-death or pro-survival for cancer cells?
- ?Could combining GHRH antagonists with autophagy modulators enhance anti-cancer effects?
- ?Do GHRH antagonists induce autophagy in non-cancerous cells?
Trust & Context
- Key Stat:
- Receptor-dependent autophagy GHRH antagonist JV-1-36 induces autophagy only in cancer cells expressing GHRH receptors, confirming a specific peptide-mediated mechanism
- Evidence Grade:
- In vitro study with appropriate receptor-negative control. Provides mechanistic insight but limited scope.
- Study Age:
- Published in 2025.
- Original Title:
- Growth hormone - releasing hormone antagonists induce autophagy in cancer cells.
- Published In:
- Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society, 82, 101668 (2025)
- Database ID:
- RPEP-13598
Evidence Hierarchy
Frequently Asked Questions
What is GHRH and why block it in cancer?
Growth hormone-releasing hormone (GHRH) stimulates growth hormone release but also promotes cancer cell growth through receptors expressed on many tumors. GHRH antagonist peptides block these receptors, suppressing tumor growth. This study found they also trigger autophagy—a cellular cleanup process that may contribute to cancer cell death.
What is autophagy in cancer?
Autophagy is a process where cells digest and recycle their own damaged components. In cancer, it can be either protective (helping cancer cells survive stress) or destructive (causing cell death). Understanding which role GHRH antagonist-induced autophagy plays is crucial for developing effective treatments.
Read More on RethinkPeptides
Related articles coming soon.
Cite This Study
https://rethinkpeptides.com/research/RPEP-13598APA
Sigdel, Madan; Fakir, Saikat; Sarker, Md Matiur Rahman; Barabutis, Nektarios. (2025). Growth hormone - releasing hormone antagonists induce autophagy in cancer cells.. Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society, 82, 101668. https://doi.org/10.1016/j.ghir.2025.101668
MLA
Sigdel, Madan, et al. "Growth hormone - releasing hormone antagonists induce autophagy in cancer cells.." Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society, 2025. https://doi.org/10.1016/j.ghir.2025.101668
RethinkPeptides
RethinkPeptides Research Database. "Growth hormone - releasing hormone antagonists induce autoph..." RPEP-13598. Retrieved from https://rethinkpeptides.com/research/sigdel-2025-growth-hormone-releasing-hormone
Access the Original Study
Study data sourced from PubMed, a service of the U.S. National Library of Medicine, National Institutes of Health.
This study breakdown was produced by the RethinkPeptides research team. We analyze and report published research findings without making health recommendations. All interpretations are based solely on the published abstract and study data.