Propolis is a natural protector and a vital, complementary ingredient for all medicinal disciplines. This study confirms it increases cell death in colon cancer. Once again, Propolis to the rescue! Eat your fiber and take your propolis...
Future in vivo studies should evaluate the
CC-preventive potential of a dietary supplement that produces high levels of
colonic butyrate, propolis, and diet-derived JAK/STAT inhibitors.
Propolis
Augments Apoptosis Induced by Butyrate via Targeting Cell Survival Pathways
PLoS One,
2013 Sept
Diet is one
of the major lifestyle factors affecting incidence of colorectal cancer (CC),
and despite accumulating evidence that numerous diet-derived compounds modulate
CC incidence, definitive dietary recommendations are not available.
We propose
a strategy that could facilitate the design of dietary supplements with
CC-preventive properties. Thus, nutrient combinations that are a source of
apoptosis-inducers and inhibitors of compensatory cell proliferation pathways
(e.g., AKT signaling) may produce high levels of programmed death in CC cells.
Here we
report the combined effect of butyrate, an apoptosis inducer that is produced
through fermentation of fiber in the colon, and propolis, a honeybee product,
on CC cells. We established that propolis increases the apoptosis of CC cells
exposed to butyrate through suppression of cell survival pathways such as the
AKT signaling. The programmed death of CC cells by combined exposure to
butyrate and propolis is further augmented by inhibition of the JNK signaling
pathway. Analyses on the contribution of the downstream targets of JNK
signaling, c-JUN and JAK/STAT, to the apoptosis of butyrate/propolis-treated CC
cells ascertained that JAK/STAT signaling has an anti-apoptotic role; whereas,
the role of cJUN might be dependent upon regulatory cell factors.
Thus, our
studies ascertained that propolis augments apoptosis of butyrate-sensitive CC
cells and re-sensitizes butyrate-resistant CC cells to apoptosis by suppressing
AKT signaling and downregulating the JAK/STAT pathway.
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