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Mitochondrial fitness and cancer risk
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Journal Article
Mitochondrial fitness and cancer risk
2022
Overview
Changes in metabolism are a hallmark of cancer, but molecular signatures of altered bioenergetics to aid in clinical decision-making do not currently exist. We recently identified a group of human tumors with constitutively reduced expression of the mitochondrial structural protein, Mic60, also called mitofilin or inner membrane mitochondrial protein (IMMT). These Mic60-low tumors exhibit severe loss of mitochondrial fitness, paradoxically accompanied by increased metastatic propensity and upregulation of a unique transcriptome of Interferon (IFN) signaling and Senescence-Associated Secretory Phenotype (SASP). Here, we show that an optimized, 11-gene signature of Mic60-low tumors is differentially expressed in multiple malignancies, compared to normal tissues, and correlates with poor patient outcome. When analyzed in three independent patient cohorts of pancreatic ductal adenocarcinoma (PDAC), the Mic60-low gene signature was associated with aggressive disease variants, local inflammation, FOLFIRINOX failure and shortened survival, independently of age, gender, or stage. Therefore, the 11-gene Mic60-low signature may provide an easily accessible molecular tool to stratify patient risk in PDAC and potentially other malignancies.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
/ Antineoplastic Combined Chemotherapy Protocols
/ Cancer
/ Carcinoma, Pancreatic Ductal - pathology
/ Consent
/ Datasets
/ Fitness
/ Humans
/ Medicine and Health Sciences
/ Mitochondrial Proteins - metabolism
/ Pancreatic Neoplasms - pathology
/ Patients
/ Proteins
/ Research and Analysis Methods
/ Tumors
/ Values
