Background and Aims: Numerous cohort studies revealed that coffee consumption is inversely correlated
with the risk to develop cancer. Detailed in vitro studies are missing and up to now
there is no mechanism defined how coffee might achieve anti-cancer activity. We investigated
effects of regular and decaffeinated coffee or caffeine on viability of human breast-
pancreatic- and hepatic cancer cell lines. Additionally, effects on primary mouse
hepatocytes and mouse hepatoma cells were investigated.
Methods: Human breast cancer (MDA-MB; MCF7), pancreatic cancer (YAPC; PANC89) and hepatoma
(HepG2; Hep3B) cell lines were incubated with regular and decaffeinated coffee or
caffeine for 24 to 72 hours. Cell viability was measured by MTT assay. To quantify
apoptosis, activation of caspase 3 was measured using a colorimetric caspase 3 Assay
Kit. Activity of the wnt signaling pathway was measured using the beta-catenin-regulated
transcription (CRT) reporter assay. To investigate if coffee might support already
approved cancer therapies we incubated our hepatocellular carcinoma cell line with
coffee or Sorafenib and a combination of both.
Results: Regular as well as decaffeinated coffee dose- and time-dependently reduced tumor
cell viability, with regular coffee having slightly higher effects. Caffeine did not
significantly reduce tumor cell viability even at concentrations exceeding those present
in effective doses of regular coffee. For mouse hepatoma cells we could show that
both, regular and decaffeinated coffee, but not caffeine reduced cell viability at
concentrations not or significantly less toxic for primary hepatocytes. Coffee incubation
reduced tumor cell proliferation and induced apoptosis. Inhibitory effects on the
tumor relevant wnt-signaling pathway were observed in human hepatoma cell lines. A
combination of Sorafenib and coffee reduced hepatoma cell viability more efficiently
than each of the components alone.
Conclusions: Cohort studies indicated that coffee consumption is associated with a lower risk
to develop cancer. Our results indicate that coffee might even exert selective activity
against existing cancer at concentration achievable in patients. A mechanism behind
this observation might be interference with wnt signaling, which is increased in many
types of cancer. Our data additionally indicate that coffee might support therapy
of HCC.
