The tumour microenvironment can negatively modulate solid tumours through the hallmarks of cancer. Immuno-inflammatory, angiogenic and metabolic changes lead to a dysregulation of tumour cells to proliferate, survive, and induce invasion and metastasis. Mitochondrial function exerts an important role in energy production, cellular respiration, and cell death mechanisms. Deregulation of their structure or function caused by malignancies leads to impairment of metabolic pathways and mitochondrial regulatory mechanisms to produce faster energy for growth. Cytochrome C and Cleaved Caspase 3 are key surrogate markers of mitochondrial biology involved in metabolic processes and the intrinsic apoptotic pathway. There is no complete understanding of their different biological mechanisms in the tumour microenvironment of solid malignancies that govern a challenging inflammatory, immunosuppressive, or dysregulated metabolic environment. Solid tumours are resistant to cell death which affects the effectiveness of the treatment
response, resulting in poor prognosis for the patient. This study will investigate for the first time the ex-vivo intracellular and extracellular expression of Cytochrome C and Cleaved Caspase 3 in Colorectal, Upper Gastrointestinal, Ovarian, Lung, and Breast tumours using ELISA. This data will be correlated with extensive matched metabolism and inflammatory profile data. The outputs of this work will give us a better understanding of how these dysregulated processes in the complex tumour microenvironment maybe important is cancer treatment resistance.
