Cell Death Differ: Single-cell imaging studies have shown that BCL(X) L and BCL2 increase the metabolic adaptability of breast cancer cells

Previous studies have shown that members of the BCL2 family can regulate the apoptosis pathway within cells by controlling mitochondrial outer membrane permeability (MOMP).
addition to this function, the BCL2 protein regulates mitochondrial fusion and division, affecting mitochondrial structure and bioenearity.
BCL2 and BAX regulate the activity of mitochondrial adenine nucleotide transport proteins.
, however, there is very little research on the effects of BCL2 and BCL(X) L on mitochondrial bioenear energy and their relationship to MOMP processes at the single-cell level.
because cancer cells are under metabolic pressure and often accumulate ultra-high levels of BCL2 and BCL(X)L, the effects of BCL2 family proteins on biological energy are particularly important in cancer cells.
BCL2 and BCL(X) L cells maintained high mitochondrial ATP levels in this study, the researchers aimed to report genetic experimental analysis using time-lapse single-cell imaging and mitochondrial/cytostylin ATP FRET reporting revealed? Effects of BCL2 and BCL(X)L on cellular energy in breast cancer cells.
over-expression of BCL2 and BCL(X)L increased cell proliferation and migration under glucose-restricted conditions Researchers found that BCL2 and BCL(X) L increased the metabolic robustness of MCF7 breast cancer cells and were associated with increased levels of mitochondrial NAD(P) H and ATP.
results using F1F0 enzyme inhibitor oligonomycin show that BCL2, especially BCL(X)L, can more effectively bind the proton dynamics of mitochondrial protons to the production of ATP without affecting the activity of ATP hexase.
this metabolic advantage is associated with increased resistance to nutritional deprivation and increased response to metabolic stress, and has no far-reaching effect on cell death.
all, the results showed that over-expression of BCL(X) L and BCL2 in tumor cells increased the resistance of tumor cells to metabolic stress in tumor micro-environments, but was independent of cell death signals.
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