Clinical and epidemiological studies have indicated
that the consumption of green tea has a number of beneficial
effects on health. Epigallocatechin-3-gallate (EGCg),
the major polyphenolic compound present in green tea, has
received much attention as an active ingredient. Among the
numerous promising profiles of EGCg, the present study
focused on the anticancer effects. Apoptosis induced by
EGCg and subsequent cell growth suppression have been
demonstrated in a number of cell culture studies. However,
the underlying mechanism of apoptotic cell death remains
unclear. Thus, the aim of the present study was to identify
the major molecule that mediates proapoptotic cell death
by EGCg. The effect of EGCg on cell proliferation and the
induction of mRNA that modulates apoptotic cell death was
evaluated in the A549 human non-small-cell lung cancer cell
line. In addition, morphological changes were assessed by
microscopy in A549 cells that had been treated with 100 µM
EGCg for 24 h. The MTT assay revealed that cell proliferation
was significantly reduced by EGCg in a dose‑dependent
manner (3-100 µM). The mRNA expression level of B-cell
lymphoma-extra large (Bcl-xL) was decreased in A549 cells
following 24 h incubation with 100 µM EGCg. Therefore, the
results indicated that the inhibition of cell proliferation by
EGCg may be achieved via suppressing the expression of the
cell death-inhibiting gene, Bcl-xL.
Clinical and epidemiological studies have indicatedthat the consumption of green tea has a number of beneficialeffects on health. Epigallocatechin-3-gallate (EGCg),the major polyphenolic compound present in green tea, hasreceived much attention as an active ingredient. Among thenumerous promising profiles of EGCg, the present studyfocused on the anticancer effects. Apoptosis induced byEGCg and subsequent cell growth suppression have beendemonstrated in a number of cell culture studies. However,the underlying mechanism of apoptotic cell death remainsunclear. Thus, the aim of the present study was to identifythe major molecule that mediates proapoptotic cell deathby EGCg. The effect of EGCg on cell proliferation and theinduction of mRNA that modulates apoptotic cell death wasevaluated in the A549 human non-small-cell lung cancer cellline. In addition, morphological changes were assessed bymicroscopy in A549 cells that had been treated with 100 µMEGCg for 24 h. The MTT assay revealed that cell proliferationwas significantly reduced by EGCg in a dose‑dependentmanner (3-100 µM). The mRNA expression level of B-celllymphoma-extra large (Bcl-xL) was decreased in A549 cellsfollowing 24 h incubation with 100 µM EGCg. Therefore, theresults indicated that the inhibition of cell proliferation byEGCg may be achieved via suppressing the expression of thecell death-inhibiting gene, Bcl-xL.
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