Related Experiment Video

Updated: Nov 21, 2025

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes
10:00

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes

Published on: March 24, 2015

13.6K

Type I Interferons as Joint Regulators of Tumor Growth and Obesity

Sandra Gessani1, Filippo Belardelli2

  • 1Center for Gender-Specific Medicine, Istituto Superiore di Sanità, 00161 Rome, Italy.

Cancers
|January 12, 2021
PubMed

Insights

Type I interferons (IFN-I) have a dual role in cancer, acting as antitumor agents but also potentially promoting tumor persistence with prolonged signaling. Their complex effects on obesity also warrant further investigation.

Area of Science:

  • Immunology
  • Oncology
  • Metabolic Diseases

Background:

  • Type I interferons (IFN-I) are crucial antiviral cytokines with significant roles in cancer immunity and treatment response.
  • IFN-I signatures in tumors can predict therapeutic outcomes, but sustained signaling may impair immune function.
  • The impact of IFN-I on obesity, a condition linked to cancer, is complex and context-dependent.

Purpose of the Study:

  • To explore the multifaceted roles of Type I interferons (IFN-I) in cancer development, treatment response, and obesity.
  • To elucidate the "Janus face" of IFN-I, highlighting their dual functions in different biological contexts.
  • To understand the regulatory mechanisms of IFN-I in both tumor growth and metabolic health.

Main Methods:

  • Analysis of studies involving mouse models and human cancer patients.
  • Investigation of IFN-I signatures within the tumor microenvironment.
  • Examination of IFN-I expression in adipose tissue and its effects on obesity models.

Main Results:

  • Endogenous IFN-I are vital for controlling tumor growth and response to therapies like chemotherapy and radiotherapy.
  • While IFN-I can be beneficial, prolonged signaling can lead to immune dysfunction and tumor persistence.
  • IFN-I exhibit opposing effects on obesity; localized expression can inhibit it, whereas excessive production can promote it.

Conclusions:

  • Type I interferons play a complex, context-dependent role in cancer and obesity, acting as both beneficial and detrimental factors.
  • Further research is needed to understand the precise mechanisms governing IFN-I's dual actions and the influence of factors like genetics, diet, and the microbiome.
Keywords:
cancerimmunoregulationinflammationobesitytumor microenvironmenttype I interferons

More Related Videos

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo08:19

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo

Published on: July 20, 2019

6.2K
A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF311:44

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3

Published on: January 24, 2016

12.2K

Related Concept Videos

Psychoneuroimmunology: Diabetes and Cancer01:19

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...
143
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
1.8K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
9.2K
Tumor Immunotherapy01:27

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.
871
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
10.4K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
4.7K