Washington D.C [USA], October 21 : A new study revealed how obesity can contribute to promote breast cancer in women.
Obesity leads to the release of cytokines into the bloodstream, which impacts the metabolism of breast cancer cells, making them more aggressive as a result.
The research was conducted by scientists from Helmholtz Zentrum Munchen, Technische Universitat Munchen (TUM), and Heidelberg University Hospital reports on the 'Cell Metabolism'. The team has already been able to halt this mechanism with an antibody treatment.
There has been an immense rise in the number of obesities worldwide. The German Cancer Research Center (DKFZ) recently reported that, according to the WHO the number of children and adolescents with obesity increased tenfold between 1975 and 2016.
Various health impairments are caused due to severe overweight. Besides inducing cardiovascular diseases, obesity for example also promotes the development of cancer and metastases.
The study stated an as yet unknown mechanism making breast cancer more aggressive. The enzyme ACC1* plays a central role in this process," said Dr. Mauricio Berriel Diaz, deputy director of the Institute for Diabetes and Cancer (IDC) at Helmholtz Zentrum Munchen.
Diaz led the study together with Stephan Herzig, director of the IDC and professor for Molecular Metabolic Control at TUM and Heidelberg University Hospital.
"ACC1 is a key component of fatty acid synthesis," Diaz added. "However, its function is impaired by the cytokines leptin and TGF-ß." The levels of these cytokines are increased particularly in the blood of severely overweight subjects.
The scientists demonstrated that the described inhibition of ACC1 leads to the accumulation of the fatty acid precursor acetyl-CoA. This precursor is transferred to certain gene "switches" that in turn increase the metastatic capacity of cancer cells by activating a specific gene program.
The researchers want to substantiate the data on the newly discovered mechanism in further studies.They are also considering related intervention points that could possibly be exploited therapeutically.
"Blocking the signalling pathways and switching off the metastasis-related genes could be a therapeutic target," Herzig said. "As part of the so-called neoadjuvant therapy, the risk of metastases or the recurrence of tumours could be reduced prior to the surgical removal of the tumour."
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