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Elevated Levels of CTRP1 in Obesity Contribute to Tumor Progression in a p53-Dependent Manner
SIMPLE SUMMARY: Obesity is regarded as a risk factor for various cancers. However, the molecular mechanisms linking obesity with cancer remain primarily uncharacterized. In this study, we demonstrate that CTRP1, an adiponectin paralogue, promotes tumor growth in a p53-dependent manner. Obese mice on...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8306638/ https://www.ncbi.nlm.nih.gov/pubmed/34298831 http://dx.doi.org/10.3390/cancers13143619 |
Sumario: | SIMPLE SUMMARY: Obesity is regarded as a risk factor for various cancers. However, the molecular mechanisms linking obesity with cancer remain primarily uncharacterized. In this study, we demonstrate that CTRP1, an adiponectin paralogue, promotes tumor growth in a p53-dependent manner. Obese mice on a high-fat diet showed a higher level of CTRP1 protein in serum. It is also known that CTRP1 treatment contributes to tumor growth and cell migration. These results indicate that an elevated level of CTRP1 in obesity promotes tumor progression. ABSTRACT: Mounting evidence supports the relationship between obesity and cancer. However, the molecular mechanisms linking obesity with cancer remain largely uninvestigated. In this study, we demonstrate that the expression of C1q/TNF-related protein 1 (CTRP1), an adiponectin paralogue, contributes to tumor growth by regulating the tumor suppressor p53. In our study, obese mice on a high-fat diet showed higher serum CTRP1 levels. Through in vitro experiments, we showed that the secreted form of CTRP1 in the culture medium decreased p53 expression and p53-dependent transcription in the cells. Moreover, CTRP1 treatment enhanced colony formation and cell migration. These results collectively suggest that elevated levels of CTRP1 in obesity significantly contribute to tumor progression. |
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