Targeting TRAF3IP2 disrupts cellular energetics through inhibition of NAMPT in triple negative breast cancer
Willingham K., Izadpanah A., Rashad Y., Reilich A., Daneshimehr F., Braun S.
Laboratory Study, published in Sci Rep (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Sci Rep (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41436543
- PMCID
- PMC12764808
- DOI
- 10.1038/s41598-025-29057-4
- Citations
- 1
Abstract (original English)
Triple-negative breast cancer (TNBC) is characterized by extensive metabolic alterations that enable its sustained growth therapeutic resistance. Nicotinamide phosphoribyltransferase (NAMPT) catalyzes the first and rate-limiting step in the nicotinamide dinucleotide (NAD) salvage pathway. Elevated NAMPT is associated with increased aggressiveness and poor prognosis in multiple cancers. Previously, we showed the role of TRAF3IP2 in TNBC tumorigenesis. Here, we aim to show that the anti-tumorigenic effects resulting from TRAF3IP2 inhibition are driven in part by decreases in cellular energetics in TNBC cells. Results show that inhibition of TRAF3IP2 leads to significant decrease in NAMPT expression, reduced NAD and ATP production, and disruption of TNBC bioenergetics through cell line-specific alterations in glycolysis and mitochondrial function. Notably, the established MDA-MB-231 line and the patient-derived 4IC model exhibited distinct OCR responses, underscoring metabolic heterogeneity across TNBC models. Additionally, this study showed that targeting TRAF3IP2 disrupts cellular energetics by affecting AMPK/LKB1 and mTOR signaling pathways and increasing reactive oxygen species (ROS) levels, ultimately leading to reduced cell viability and increased apoptosis. These findings suggest that TRAF3IP2 plays a critical role in maintaining TNBC bioenergetics and represents a potentia
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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