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Updated: Apr 24, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
CBX7 gene expression plays a negative role in adipocyte cell growth and differentiation
Floriana Forzati1, Antonella Federico1, Pierlorenzo Pallante1
1Istituto di Endocrinologia ed Oncologia Sperimentale del CNR e/o Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università degli Studi di Napoli "Federico II", 80131 Naples, Italy.
Abstract:
We have recently generated knockout mice for the Cbx7 gene, coding for a polycomb group protein that is downregulated in human malignant neoplasias. These mice develop liver and lung adenomas and carcinomas, which confirms a tumour suppressor role for CBX7. The CBX7 ability to downregulate CCNE1 expression likely accounts for the phenotype of the Cbx7-null mice. Unexpectedly, Cbx7-knockout mice had a higher fat tissue mass than wild-type, suggesting a role of CBX7 in adipogenesis. Consistently, we demonstrate that Cbx7-null mouse embryonic fibroblasts go towards adipocyte differentiation more efficiently than their wild-type counterparts, and this effect is Cbx7 dose-dependent. Similar results were obtained when Cbx7-null embryonic stem cells were induced to differentiate into adipocytes. Conversely, mouse embryonic fibroblasts and human adipose-derived stem cells overexpressing CBX7 show an opposite behaviour. These findings support a negative role of CBX7 in the control of adipocyte cell growth and differentiation.
Insights
The polycomb group protein CBX7 acts as a tumor suppressor and negatively regulates adipogenesis. CBX7 deficiency in mice leads to increased tumor development and enhanced fat tissue accumulation, impacting cell growth and differentiation.
Area of Science:
- Cell Biology
- Molecular Biology
- Oncology
Background:
- Polycomb group (PcG) proteins regulate gene expression and are implicated in development and cancer.
- CBX7, a PcG protein, is downregulated in human malignant neoplasias.
- The precise biological functions of CBX7, particularly in tumorigenesis and metabolic processes, require further elucidation.
Purpose of the Study:
- To investigate the in vivo role of the Cbx7 gene in tumor development.
- To explore the potential involvement of CBX7 in adipogenesis and adipose tissue regulation.
- To elucidate the molecular mechanisms underlying CBX7's function in cell growth and differentiation.
Main Methods:
- Generation and analysis of Cbx7-knockout mice.
- Assessment of tumor development (adenomas, carcinomas) in liver and lung.
- Analysis of adipocyte differentiation in Cbx7-null mouse embryonic fibroblasts and embryonic stem cells.
- Evaluation of gene expression, specifically CCNE1, in relation to CBX7 function.
- Experiments involving overexpression of CBX7 in mouse embryonic fibroblasts and human adipose-derived stem cells.
Main Results:
- Cbx7-knockout mice developed liver and lung adenomas and carcinomas, confirming a tumor suppressor role for CBX7.
- CBX7 deficiency led to increased fat tissue mass in mice.
- Cbx7-null mouse embryonic fibroblasts and stem cells exhibited enhanced adipocyte differentiation in a dose-dependent manner.
- Overexpression of CBX7 inhibited adipocyte differentiation.
- CBX7's downregulation of CCNE1 expression is implicated in the observed phenotypes.
Conclusions:
- CBX7 functions as a tumor suppressor, inhibiting the development of liver and lung cancers.
- CBX7 plays a critical negative regulatory role in adipogenesis and adipose tissue development.
- CBX7 influences adipocyte cell growth and differentiation, with its absence promoting these processes.
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