Related Experiment Video

Updated: May 7, 2026

Initiation of Metastatic Breast Carcinoma by Targeting of the Ductal Epithelium with Adenovirus-Cre: A Novel Transgenic Mouse Model of Breast Cancer
07:13

Initiation of Metastatic Breast Carcinoma by Targeting of the Ductal Epithelium with Adenovirus-Cre: A Novel Transgenic Mouse Model of Breast Cancer

Published on: March 26, 2014

22.8K

NCOR2 represses MHC class I molecule expression to drive metastatic progression of breast cancer

Pavla Ticha1,2, Jason J Northey1,3, Radhika Narain1

  • 1Department of Surgery and Center for Bioengineering and Tissue Regeneration, University of California, San Francisco, San Francisco, CA, USA.

Nature Communications
|May 5, 2026
PubMed

Insights

Nuclear corepressor 2 (NCOR2) epigenetically regulates Major Histocompatibility Complex (MHC) class I presentation in breast cancer. Reducing NCOR2 enhances immune surveillance, preventing metastasis and improving survival in triple-negative breast cancer (TNBC) patients.

Area of Science:

  • Oncology
  • Immunology
  • Epigenetics

Background:

  • Metastasis relies on tumor cells evading immune surveillance.
  • Major Histocompatibility Complex (MHC) presentation is crucial for T cell-mediated tumor cell eradication.
  • Triple-negative breast cancer (TNBC) often exhibits aggressive metastatic behavior.

Purpose of the Study:

  • To investigate the role of nuclear corepressor 2 (NCOR2) in regulating MHC class I presentation on breast tumor cells.
  • To determine the correlation between NCOR2 expression, MHC class I levels, and patient survival in TNBC.
  • To explore therapeutic strategies targeting NCOR2 to enhance anti-tumor immunity and prevent metastasis.

Main Methods:

  • Analysis of NCOR2 expression in relation to MHC class I levels and metastasis-free survival in TNBC patients.
  • Investigating the effect of reducing NCOR2 expression or its interaction with Histone Deacetylase (HDAC3) on immune cell activity and MHC class I expression.
  • Assessing the impact of NCOR2 modulation on CD8+ T cell activity and apoptosis induction in disseminated cancer cells.

Main Results:

  • High NCOR2 expression in TNBC patients correlates with reduced metastasis-free survival and decreased MHC class I expression.
  • Metastatic lesions in TNBC patients show high nuclear NCOR2 and reduced CD8+ T cell infiltration.
  • Reducing NCOR2 enhances innate immune cell recruitment and activity, increasing MHC class I levels on cancer cells.
  • Targeting NCOR2 potentiates CD8+ T cell activity, induces apoptosis, and prevents metastatic progression.

Conclusions:

  • NCOR2 is a critical epigenetic regulator of MHC class I presentation in breast cancer.
  • NCOR2 inhibition represents a promising therapeutic strategy to overcome immune evasion in metastatic breast cancer.
  • Targeting NCOR2 could enhance anti-tumor immunity and reduce mortality in TNBC patients.

More Related Videos

A Portal Vein Injection Model to Study Liver Metastasis of Breast Cancer07:35

A Portal Vein Injection Model to Study Liver Metastasis of Breast Cancer

Published on: December 26, 2016

43.7K

Related Concept Videos

MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
3.1K
MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...
21.2K
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
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
2.0K
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