Related Experiment Video

Updated: May 22, 2025

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

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

Published on: October 27, 2020

12.7K

Investigating the Mechanism of IFN-γ-Inducible Lysosomal Thiol Reductase-Mediated Inhibition of Breast Cancer Cell

Qin Liu1, Xiaoning Yuan1, Youcheng Shao1

  • 1Department of Pathology and Pathophysiology Hubei Provincial Key Laboratory of Developmentally Originated Disease, TaiKang Medical School (School of Basic Medical Sciences), Wuhan University Wuhan Hubei China.

Cancer Innovation
|March 17, 2025
PubMed
Abstract

Insights

Gamma-interferon-inducible lysosomal thiol reductase (GILT) is underexpressed in breast cancer. Restoring GILT inhibits tumor growth by targeting the MYC/WDR5 complex, offering new therapeutic strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Breast cancer poses a significant global health challenge.
  • Identifying novel therapeutic targets and effective drugs is crucial for breast cancer treatment.

Purpose of the Study:

  • To investigate the role and mechanism of gamma-interferon-inducible lysosomal thiol reductase (GILT) in breast cancer.
  • To explore the potential of GILT as a therapeutic target for breast cancer.

Main Methods:

  • Utilized molecular biology techniques including western blot, co-immunoprecipitation, and immunofluorescence assays.
  • Employed a nude mouse xenograft tumor model to assess GILT's impact on tumor growth.
  • Analyzed GILT expression levels in breast cancer cells versus normal cells.

Main Results:

  • GILT protein expression was significantly lower in breast cancer cells compared to normal cells.
  • Overexpression of GILT suppressed breast cancer cell proliferation, migration, and tumor growth.
  • GILT was found to inhibit the MYC/WDR5 transcription complex, indicating a tumor-suppressive function.
  • The inhibitor OICR-9429 demonstrated synergistic effects with GILT in inhibiting cancer cell proliferation.

Conclusions:

  • GILT plays a tumor-suppressive role in breast cancer by inhibiting the MYC/WDR5 complex.
  • GILT restoration presents a potential therapeutic strategy for breast cancer.
  • The small molecule inhibitor OICR-9429 shows promise for synergistic therapy with GILT.
Keywords:
IFN‐γ‐inducible lysosomal thiol reductaseMYCOICR‐9429WDR5breast cancer

More Related Videos

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice00:07

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

7.2K
Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells13:38

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells

Published on: January 18, 2017

12.2K

Related Concept Videos

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
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...
7.2K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
5.9K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.6K
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
7.2K