Related Experiment Video
Updated: Jan 12, 2026
08:53
In Vivo Immunofluorescence Localization for Assessment of Therapeutic and Diagnostic Antibody Biodistribution in Cancer Research
Published on: September 16, 2019
9.5K
Isoliquiritigenin Inhibits Triple-Negative Breast Cancer Progression via Targeting the IRF5/SLC7A5/IDO1-Mediated
Sihai Duan1,2, Xiaoyan Li3, Cailu Song3
1Department of Breast and Thyroid Surgery, The Central Hospital of Yongzhou, Yongzhou, 425007, China.
Oncology Research
|November 3, 2025
Summary
Isoliquiritigenin (ISL) suppresses triple-negative breast cancer (TNBC) by targeting interferon regulatory factor 5 (IRF5). This natural compound disrupts tryptophan metabolism, offering a potential new therapeutic strategy for TNBC.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Triple-negative breast cancer (TNBC) presents a poor prognosis.
- Isoliquiritigenin (ISL), a chalcone from licorice, is investigated for its therapeutic potential.
- Interferon regulatory factor 5 (IRF5) is a key factor in TNBC.
Purpose of the Study:
- To elucidate the molecular mechanisms of ISL targeting IRF5 in TNBC.
- To determine the role of IRF5 in TNBC cell proliferation and metabolism.
- To evaluate ISL's impact on tryptophan metabolism pathways in TNBC.
Main Methods:
- IRF5 knockdown in TNBC cell lines using short hairpin RNA.
- Cell proliferation assessed via CCK-8 and colony formation assays.
- Expression analysis of IRF5, SLC7A5, and IDO1 using Western blotting and RT-PCR.
- Quantification of intracellular tryptophan and metabolites via HPLC.
Main Results:
- IRF5 is highly expressed in TNBC cell lines and its silencing inhibits proliferation.
- IRF5 knockdown reduces SLC7A5 and IDO1 expression, decreasing intracellular tryptophan.
- ISL treatment suppressed TNBC cell proliferation and disrupted tryptophan metabolism.
Conclusions:
- ISL inhibits TNBC progression by downregulating IRF5.
- ISL interferes with SLC7A5/IDO1-mediated tryptophan metabolic reprogramming.
- ISL represents a potential therapeutic agent for TNBC.
Keywords:
Interferon regulatory factor 5 (IRF5)indoleamine 2,3-dioxygenase 1 (IDO1)isoliquiritigeninsolute carrier family 7 member 5 (SLC7A5)triple-negative breast cancertryptophan metabolismMore Related Videos
Related Concept Videos
01:22PI3K/mTOR/AKT Signaling Pathway
5.3K
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...
5.3K
02:57Targeted Cancer Therapies
8.6K
The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
There are several types of targeted therapies against...
8.6K
03:03mTOR Signaling and Cancer Progression
4.6K
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...
The mTOR pathway or the...
4.6K
02:34Inhibition of Cdk Activity
5.5K
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...
5.5K
01:31The Intrinsic Apoptotic Pathway
8.2K
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...
8.2K