Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Psychoneuroimmunology: Diabetes and Cancer

Psychoneuroimmunology: Diabetes and Cancer

Chronic stress has been linked to both the onset and progression of serious health conditions, including Type 2 diabetes and cancer. Type 2 diabetes, a widespread chronic illness, is closely associated with obesity and insulin resistance, both of which often worsen under stress. Studies indicate that men experiencing high levels of chronic stress face a 45% higher risk of developing diabetes compared to those with minimal stress. Stress triggers physiological responses that elevate blood...

Tumor Immunotherapy

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.

Immune Surveillance by NK Cells and Phagocytes

Immune Surveillance by NK Cells and Phagocytes

Immune surveillance is an integral part of the innate immune system, involving the continuous monitoring of peripheral tissues to detect and respond to pathogens, infected cells, or cancerous cells. This surveillance is conducted primarily by natural killer (NK) cells and phagocytes, which employ distinct but complementary mechanisms to identify and eliminate threats.
Natural Killer Cells: The Fast Responders
NK cells are large granular lymphocytes found in the blood and lymphatic system. These...

Adaptive Mechanisms in Cancer Cells

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

Adaptive Mechanisms in Cancer Cells

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy. SP binds and activates these...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Application of the Multi Theory Model to improve self reported determinants of appropriate antibiotic prescribing among veterinary students.

Scientific reports·2026

Same author

Ocular Safety of Intravitreal Engineered Humanized Anti-VEGF Nanobody and Its Efficacy in the Attenuation of Choroidal Neovascularization and Associated Subretinal Fibrosis.

Biomolecules·2026

Same author

Scorpion Venom-Derived Voltage-Gated Potassium Channel Blocker Peptides: A Cutting-Edge Therapeutic Frontier in Breast Cancer Research and Beyond.

Current cancer drug targets·2026

Same author

Exploiting signal transduction pathways for cancer therapy: insights from natural products in preclinical models.

Frontiers in pharmacology·2026

Same author

Kv1.3 Channel inhibition by nanoformulated MeuKTx as a therapeutic strategy in breast cancer.

Scientific reports·2026

Same author

Immunoregulatory kinases and T-cell pathways in DNA-damage response and autoimmune inflammation: Emerging roles of BUB1 and IGFL2.

International immunopharmacology·2026

Search research articles

Related Experiment Video

Updated: Jun 16, 2026

Systemic Injection of Neural Stem/Progenitor Cells in Mice with Chronic EAE

Systemic Injection of Neural Stem/Progenitor Cells in Mice with Chronic EAE

Published on: April 15, 2014

Neuropeptide Y as a Neuro-Immune Checkpoint in Cancer.

Zohre Eftekhari¹, Seyed Amir Sadeghi², Fatemeh Kazemi-Lomedasht³

¹Venom and Biotherapeutics Molecules Laboratory, Biotechnology Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran.

Journal of Neuroimmune Pharmacology : the Official Journal of the Society on Neuroimmune Pharmacology

|June 13, 2026

Summary

Neuropeptide Y (NPY) is a key regulator in the tumor microenvironment, influencing both cancer progression and immune suppression. Targeting NPY signaling may enhance cancer immunotherapy by reprogramming the neuro-immune axis.

Keywords:

Angiogenesis Cancer progression Immunosuppression Neuro-immune crosstalk Neuropeptide Y Tumor microenvironment

More Related Videos

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Published on: March 7, 2025

Related Experiment Videos

Last Updated: Jun 16, 2026

Systemic Injection of Neural Stem/Progenitor Cells in Mice with Chronic EAE

Systemic Injection of Neural Stem/Progenitor Cells in Mice with Chronic EAE

Published on: April 15, 2014

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Published on: March 7, 2025

Area of Science:

Oncology
Neuroimmunology
Molecular Biology

Background:

Neuropeptide Y (NPY) is a neuropeptide involved in appetite, stress, and circadian rhythms.
NPY is increasingly recognized as a mediator at the intersection of neural and immune signaling within the tumor microenvironment (TME).
NPY can be released by tumor-innervating sympathetic fibers and tumor cells, creating autocrine and paracrine signaling loops that promote tumor progression.

Purpose of the Study:

To review the dual role of NPY as a neuromodulator and immunoregulator in cancer.
To highlight NPY signaling as a neuro-immune checkpoint integrating stress signals with tumor immune suppression.
To explore the potential of targeting the NPY-receptor axis for novel cancer therapies.

Main Methods:

Review of existing literature on NPY's role in cancer.
Analysis of NPY's effects on malignant and immune cells via its receptors (Y1R, Y2R, Y4R, Y5R, Y6R).
Examination of NPY's impact on immune cell populations including macrophages, NK cells, and T cells.

Main Results:

NPY activation of Y1R and Y2R is linked to enhanced tumor proliferation, angiogenesis, and vascular remodeling.
Y5R activation connects stress signaling to accelerated tumor growth.
NPY promotes M2-like immunosuppressive macrophages, reduces NK cell cytotoxicity, and dampens T cell activation, fostering an immune-evasive TME.

Conclusions:

NPY acts as a critical neuro-immune regulator in the TME, promoting tumor progression and immune evasion.
NPY signaling represents an underappreciated neuro-immune checkpoint.
Targeting the NPY-receptor axis offers potential therapeutic strategies to enhance cancer immunotherapy, especially in stress-related cancers.