ArticleCancer biology & medicine2023
Acetylated-PPARγ expression is regulated by different
Article in Cancer biology & medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Clinicopathological characteristics of primary malignant cutaneous perivascular epithelioid cell tumor: case report and literature review.Journal of pathology and translational medicine · 2026Article
- Clinical Implications of Polyploid Giant Cancer Cells in Solid Tumors: Biology, Diagnosis, and Therapeutic Considerations.Cancers · 2026Review
- Etiology of polyploid giant cancer cells: a new frontier in cancer biology.Cancer cell international · 2026Review
- The influence of cell-cell fusion on cancer heterogeneity and its promise for targeted treatments.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- miR-1246 enhances chemo-resistance of polyploid giant cancer cells in H1299 cells by targeting GSK3β/β-catenin.Discover oncology · 2025Article
- The role of ubiquitination and deubiquitination in cancer lipid metabolism.Frontiers in oncology · 2025Review
- Polyploid giant cancer cells and tumor budding: translation from basic research to clinical application.Frontiers in oncology · 2025Review
- Role of the CTCF/p300 axis in osteochondrogenic-like differentiation of polyploid giant cancer cells with daughter cells.Cell communication and signaling : CCS · 2024Article
- Article
- Hypolipidemic Effect of Rice Bran Oil Extract Tocotrienol in High-Fat Diet-Induced Hyperlipidemia Zebrafish (Danio Rerio) Induced by High-Fat Diet.International journal of molecular sciences · 2024Article
- Dormant cancer cells and polyploid giant cancer cells: The roots of cancer recurrence and metastasis.Clinical and translational medicine · 2024Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivePolyploid giant cancer cells (PGCCs) with daughter cells express epithelial-mesenchymal transition (EMT)-associated proteins. Highly malignant tumor cells with EMT properties can transdifferentiate into mature tumor cells. In this study, we elucidated the potential for, and underlying mechanism of, adipogenic differentiation of PGCCs with daughter cells (PDCs).
methodsCobalt chloride was used to induce PGCC formation in HEY (wild-type
resultsPDCs transdifferentiated into functional adipocytes. Two different cell cycle distributions were observed in PDCs after adipogenic differentiation. The expression levels of PPARγ, Ace-PPARγ, and Ace-P53 were higher in PDCs after adipogenic differentiation than in cells before adipogenic differentiation. Ace-PPARγ and FABP4 expression increased in HEY cells and decreased in MDA-MB-231 PDCs after
conclusionsAcetylation of P53 and PPARγ plays an important role in the adipogenic differentiation of PDCs.
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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.