ArticleApoptosis : an international journal on programmed cell death2026
LncRNA PVT1 drives macrophage polarization and triple-negative breast cancer progression via PPARγ-mediated transcriptional activation.
Article in Apoptosis : an international journal on programmed cell death, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Global pattern and evolution of PPARγ in breast cancer: a 25-Year bibliometric and visualized knowledge map analysis.Frontiers in oncology · 2026Pooled it
- Bergamottin demonstrates preclinical effectiveness against pancreatic cancer by modulating PPAR-γ to induce apoptosis.Translational cancer research · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC) is a clinically aggressive subtype with limited therapeutic strategies. Although long non-coding RNAs (lncRNAs) are increasingly linked to tumor progression, their regulatory role in macrophage polarization during TNBC remains unclear. This study investigates the molecular interplay between lncRNA PVT1 and PPARγ in driving macrophage reprogramming during TNBC progression. Utilizing an orthotopic TNBC mouse model, single-cell RNA sequencing (scRNA-seq) identified nine distinct cell types, with pseudotime trajectory analysis revealing macrophage accumulation in advanced tumor stages. Reannotation of macrophages highlighted M2-like polarization dominance during TNBC development. Bulk sequencing of TNBC macrophages and integrated GEO/TCGA analyses identified PPARγ as a key regulator and PVT1 as a differentially expressed lncRNA in TNBC versus normal tissues. In vitro experiments with THP-1/U937 macrophages demonstrated that PVT1 knockdown or PPARγ modulation altered macrophage polarization, subsequently affecting MDA-MB-231 and MCF-7 breast cancer cell proliferation and invasion. Mechanistically, RNA/DNA pulldown and luciferase assays confirmed that PVT1 recruits NOP56 and E2F1 to form a transcriptional complex, enhancing E2F1-driven PPARγ expression. In vivo, orthotopic tumors generated from PVT1-silenced THP-1/MDA-MB-231 cell mixtures exhibited suppressed growth, increased M1-like macrophages, and elevated apoptosis (TUNEL assay), whereas PPARγ overexpression accelerated tumor progression with M2-dominant infiltration (flow cytometry). These findings establish lncRNA PVT1 as a critical epigenetic scaffold coordinating NOP56-E2F1-PPARγ signaling to polarize macrophages toward a pro-tumorigenic M2 phenotype, thereby fueling TNBC aggressiveness. This study unveils novel therapeutic targets for TNBC by disrupting the PVT1-PPARγ axis to rebalance macrophage dynamics and induce tumor-suppressive immunity.
Indexed as
Identifiers
41518478What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.