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New regulator of mitochondrial cell death will become a new target for cancer therapy

20 September 2019 14:33

Researchers at The Wistar Institute have described the role of mitochondria in the management of survival of cancer cells. They also found that the mitochondrial expression is regulated by Myc, a mediator of cell proliferation which promotes the development of many types of cancer. The results were published in the journal EBioMedicine.

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Mitochondria - organelles that supply energy to the cells and control the multiple mechanisms of cell death. They play a complex role in cancer, which is an area of ​​intensive research. In particular, the dynamics of mitochondria, a process that controls the size, shape and position of the mitochondria in a cell involved in tumor progression, but until now the mechanisms are not clear.

"We know that the reprogramming of mitochondrial function plays a role in cancer development and metastasis, - says the study's senior author, Dario C. Altiero, MD, president and chief executive officer of Vistar -. Our results indicate the new players and the way in this process of opening the specific therapeutic potential to eliminate tumor cells in patients. "

Laboratory Altieri and international team of staff showed that the MFF gene is amplified in patients with prostate cancer, Affecting recurrence and reduced survival. They also observed an increase in protein expression MFF compared to normal tissues in the mouse model of prostate cancer and in tissue samples of patients with other types of cancer, including lung cancer and multiple myeloma.

Importantly, the researchers used the Myc oncoprotein, which is usually amplified in various types of cancer and controls reprogramming mitochondria during tumor progression.

Researchers have shown that cancer MFF interacts with VDAC1, mitochondrial cell death regulator, disabling its function in order to maintain the viability of the tumor cells. The researchers found that the destruction of the complex MFF-VDAC1 activate multiple mechanisms of mitochondrial cell death, reducing tumor growth in preclinical models.

"In our situation, targeting MFF provided preclinical anti-cancer activity, - says Ekta Agarwal, PhD, Researcher, Laboratory of Altieri and one of the first authors of the study -. Our data shows that the violation of MFF-VDAC1 complex could become a new therapeutic strategy that has the potential to be effective in a number of cancers. "



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