The decline in skeletal muscle mass and function (atrophy) represents one of the most dramatic changes during the progression of cancer. For patients with metastatic cancer, 50-80% develop the muscle atrophy condition cancer cachexia (CC), which is directly associated to reduced quality of life, treatment toxicity, and low survival. Despite its high prevalence and the devastating prognosis for patients with CC, little is known about its molecular triggers. Mitochondrial dysfunction and inflammation are emerging hallmarks of CC. We and others have previously shown that mitochondrial dysfunction leads to muscle and systemic inflammation, resulting in muscle atrophy. Intriguingly, systemic inflammation promotes muscle atrophy and can cause mitochondrial dysfunction, creating a vicious, yet poorly described cycle in CC.
What you will do
In this project, the mitochondrial dysfunction and inflammatory signals observed in different models of CC (in cultured cells and muscle tissue from mice) will be characterized and we will aim at elucidating their molecular linkers. To achieve this, we will perform molecular biology techniques, including RNA extraction and quantitative PCR (gene expression analyses), protein extraction and western blotting (protein expression analyses), immunofluorescence and super-resolution confocal imaging, mitochondrial respiration analyses and ELISAs (cytokine detection).
Who do we look for
To undertake this project, we are looking for a highly motivated and skilled MSc student in the field of life sciences (biology, biochemistry, biotechnology, molecular biomedicine, immunology&inflammation). The student should be curiosity-driven, organized and willing to learn how to work both independently and in collaboration with other researchers. The student will receive direct full supervision by Dr. Andrea Irazoki from Dr. Lykke Sylow's group, located at BMI at KU. The project is expected to start in February 2023 and finish by the end of the academic year.