Related Experiment Video

Updated: Apr 27, 2026

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity
09:32

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity

Published on: October 17, 2025

659

Galanin receptor 2 utilizes distinct signaling pathways to suppress cell proliferation and induce apoptosis in HNSCC

Takeharu Kanazawa1, Kiyoshi Misawa2, Yuki Misawa2

  • 1Department of Otolaryngology‑Head and Neck Surgery, Jichi Medical University School of Medicine, Shimotsuke, Tochigi 329‑0498, Japan.

Molecular Medicine Reports
|July 15, 2014
PubMed

Insights

Galanin receptors GALR1 and GALR2 suppress head and neck squamous cell carcinoma (HNSCC) growth. Reactivating these pathways, particularly GALR2, offers therapeutic potential by halting cell cycle progression and inducing apoptosis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Galanin and its receptors, GALR1 and GALR2, function as tumor suppressors.
  • These receptors are potential therapeutic targets in head and neck squamous cell carcinoma (HNSCC).

Purpose of the Study:

  • To investigate the antitumor effects of GALR1 and GALR2 re-expression in HNSCC.
  • To elucidate the molecular mechanisms underlying galanin-mediated tumor suppression.

Main Methods:

  • Re-expression of GALR1 and GALR2 in HNSCC cell lines.
  • Assessment of cell proliferation, cell cycle regulators (CKI, cyclin D1), and apoptosis (caspase-3).
  • Pharmacological inhibition of ERK1/2 signaling pathway (U0126) and G-protein coupled receptors (pertussis toxin).

Main Results:

  • GALR1 re-expression suppressed HNSCC cell proliferation via ERK1/2-dependent regulation of CKI and cyclin D1.
  • GALR2 re-expression, in combination with galanin, increased CKI, decreased cyclin D1, and induced apoptosis.
  • Galanin stimulation in GALR2-expressing cells activated ERK1/2, suppressed proliferation, decreased cyclin D1, and induced DNA ladder formation.
  • ERK1/2 inhibition blocked cyclin D1 suppression but not apoptosis induction by galanin in GALR2-expressing cells.

Conclusions:

  • GALR2, in the presence of galanin, exerts antitumor effects through cell cycle arrest and apoptosis in HNSCC.
  • Reactivation of GALR1 and GALR2 signaling pathways holds therapeutic promise for HNSCC treatment.

More Related Videos

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

2.3K
Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

13.1K

Related Concept Videos

Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
4.6K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.6K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

1.5K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.0K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
7.8K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

2.6K