Parkinson's Disease Gene Called Parkin Found as Key to Effective Tumor Suppression and Metastasis Prevention

The Wistar Institute recently directed an investigation about Parkin and confirmed that it causes both acute metabolic and oxidative stress. Parkin is a protein regulator and a tumor suppressor that declines in most cases of cancer. According to the study, Parkin is able to discontinue mitochondrial trafficking and hinders tumor cell activities. Because of this, Parkin was considered an effective suppressor of both primary and metastatic tumor development.

The tumor suppression study showed that the metabolic and mitochondrial activities are responsible activators of disease. Both metabolic and mitochondrial reprogramming are known in the neuroscience community as the foundation of tumor development.

The Wister Institute Cancer Center expert and author of the study Dario Altieri said that changes in metabolism push the development of small and premalignant lesion transition into a hostile type of tumor, which is the frequent beginning of a metastatic progression. When metabolic reprogramming takes place, cancer cells require a lot of energy supplication in order for it to thrive and grow in an unusual environment.

Whats is Parkin?

To understand how a tumor is suppressed, the experts examined a gene correlated to Parkinson's Disease called Parkin. Parkin has the capability to ensure the security of the human brain cells through its own selective method. This method, also called mitophagy, removes damaged mitochondria. According to NewsMedical, some of the past research credits Parkin as one of the properties responsible for the metabolism of cancer cells and hinders tumor growth. However, the lack of evidence regarding the theory remains the role of Parkin unconfirmed.

Parkin was examined by the experts along with its presence on numerous types of cancer cells, including specimens from prostate cancer, that did not exhibit the protein. It was found that the Parking deletion from the normal cells has resulted in an increased motility rate. Prostate cancer cells active with Parkins examined in vivo were observed to smaller tumors, which is considered as low metastatic compared to the aggressive tumors.

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Parkin in Tumor Suppression and Metastasis Prevention

Throughout the series of tests, the experts determined that the Parkin expression scales from low to undetectable in both the tissue samples and cancer cell lines collected from subjects. In addition, Parkin expression was also low in the tumor collection from The Cancer Genome Atlas database. In conclusion, the wide-scale proteomic study of the Parkin expression and cancer cells resulted in the definitive alteration of protein networks responsible for metastasis, as well as the decreased potential of oncogenic signals.

To further establish the potential of Parkin, the team utilized its tumor suppression properties for controlling the metabolism of an enzyme known as the transketolase or TKT. The specified enzyme is correlated with the pathway that cancer cells get their energy from called glycolysis. TKT is also considered an active countermeasure against the cells' oxidative stress.

Parkins were proven in the study to have a key role in suppressing the pathway of tumor growth and reduces the chances of malignant cells developing into an aggressive and metastatic tumor through metabolism programming. The whole coverage of the study was published in the journal Science Advances Cancer, titled "A Cancer Ubiquitome Landscape Identifies Metabolic Reprogramming As Target Of Parkin Tumor Suppression."