Aim: We aimed to identify the antitumoral mechanism of lycopene on human cancer cells of common solid cancers. Methods: The effect of lycopene was assessed by MTT (Methylthiazoltetrazolium) assay at various times and concentrations on human cancer cells of lung (AGS), breast (MCF-7 and MDA-MB-231), colon (WiDR), prostate (PC-3 and LNCaP) and stomach (AGS).  Mechanisms of action were assessed by apoptosis (DNA ladder formulation, DAPI strain, TUNEL assay and western analysis of p53, bcl-2 and bax) and cell cycle study (flow cytometry, BrdU assay and western analysis of cyclinD1, p21 and p27). Results: The results confirmed statistically significant (p&lt;0.05), dose-dependent <i>in vitro </i>inhibitory effect of lycopene on all the cancer cells studied (maximum 54% inhibition on WiDR colon cancer cells). Although a small late apoptosis was noted (10-17% at 96 h), the results were not significant.  Cell cycle arrest in Gl phase was observed (up to 142%, most well seen at 48 h), reciprocated by a decrease in the cell population in S phase.  A decrease of cyclin D1 and an increase of p27 were also noted.  No changes were noted in the expressions of bcl-2 and bax.  Although p523 was slightly decreased, there was no change in the level of its downstream protein p21. Conclusions: Lycopene inhibited growth of common human solid cancer cells <i>in vitro.  </i>Maximum inhibition was noted on WiDR colon cancer cells, mediated through G1 cell cycle arrest and altered expressions of proteins cyclin D1 and p27.  The mechanism was independent of p53 pathway and not mediated by apoptosis.

Thesis (M..D.)--Aberdeen University, 2009. / Title from web page (viewed on Aug. 26, 2009). Includes bibliographical references.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2002. / Härtill 5 uppsatser.