I like to know the possible markers of metabolism in cancer cells such as in monitoring glycolytic, extracellular acidification and oxygen consumption rates, effected by treatment with an extract.
It depends if you are fixing the cells for cellular markers or keeping them viable for live cell imaging markers. Also, whether you want to measure expression induction markers (mRNA expression), or on-going cellular processes (proteins, subcellular organelle activity like mitochondria and lysosomes).
Ferdinando Chiaradonna Prof. and Rabeah Al-Temaimi Prof., the question above specifically mentioned metabolism and clearly channelled towards glycolysis. Meanwhile, in literature, it has been repeatedly reported that in the course of tumour progression within its microenvironment there's potential tumour growth expansion thus increasing cellular demands and limit both nutrient and oxygen levels thereby prompting intermittent hypoglycemia, hypoxia and acidosis. These end results are drivers (stressor) for huge numbers of cancer stem cells (CSCs). We all know that CSCs now are the bane of drug resistance in cancer therapy, today. Of course, CSCs are dormant within the proliferative cancer cells and possess self-renewal ability post-therapeutically thus giving a chance of drug ineffectiveness and possible cancer growth back after a while.
Now, to my question above. I specified the metabolic event and even mentioned glycolysis and other driver-causing events but only wanted to know (bring about) in my proposed model of study (using CSCs) the possible parameters (of biochemical markers in this regard as above-explained) to study metabolic events for the genesis of hypoxia.