Related Experiment Video

Updated: Mar 27, 2026

Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome
07:23

Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome

Published on: June 15, 2016

9.0K

RUNX1 restrains STAT1-GITRL signaling to shape an immunosuppressive CRC microenvironment

Wenting He1,2, Lisheng Zheng2, Weiye Huang2

  • 1Guangdong Cardiovascular Institute, Guangzhou, China.

Cell Death Discovery
|March 26, 2026
PubMed

Insights

RUNX1 promotes colorectal cancer immune evasion by suppressing GITRL expression, increasing Treg cells, and reducing CD8+ T cell activity. This RUNX1/STAT1/GITRL pathway is a potential target for immunotherapy.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • The role of RUNX1 in epithelial tumors is recognized, but its function in the colorectal cancer (CRC) tumor immune microenvironment (TME) is unclear.
  • Understanding RUNX1's impact on TME is crucial for developing effective CRC therapies.

Purpose of the Study:

  • To investigate RUNX1's contribution to TME remodeling in colorectal cancer.
  • To elucidate the molecular mechanisms by which RUNX1 influences immune cell infiltration and function in CRC.

Main Methods:

  • Analysis of clinical CRC tissues to correlate RUNX1 expression with immune cell infiltration and GITRL levels.
  • In vitro and in vivo functional studies using mouse models to assess the impact of RUNX1 on immune responses and therapeutic sensitivity.
  • Mechanistic studies involving protein-protein interactions and transcriptional regulation.

Main Results:

  • RUNX1 expression negatively correlates with GITRL levels and is associated with increased Treg cell infiltration in CRC.
  • RUNX1 impairs GITRL-GITR signaling, promoting Treg infiltration and suppressing CD8+ T cell activation.
  • Elevated RUNX1 enhances CRC tumor sensitivity to GITR agonistic antibody therapy.
  • RUNX1 interacts with STAT1 to inhibit GITRL transcription.

Conclusions:

  • The RUNX1/STAT1/GITRL axis plays a significant role in CRC immune evasion.
  • Targeting this axis offers a potential therapeutic strategy for enhancing GITR-based immunotherapy in colorectal cancer.

More Related Videos

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin10:21

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin

Published on: September 12, 2019

7.8K
Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells09:16

Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells

Published on: September 1, 2019

8.1K

Related Concept Videos

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...
13.8K
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...
5.1K
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...
5.4K
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...
6.3K
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
2.6K
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...
10.9K