Variations journalières des glucosinolates dans les tissus et à la surface des feuilles de colza

*INRA Laboratoire des Médiateurs chimiques versailles (FRA) Diffusion du document : INRA Laboratoire des Médiateurs chimiques versailles (FRA) Diplôme : Maîtris

La sélection de la plante par l'insecte et la composition biochimique de la surface de la feuille

*INRA Laboratoire des Médiateurs chimiques Versailles (FRA) Diffusion du document : INRA Laboratoire des Médiateurs chimiques Versailles (FRA) Diplôme : Maîtris

Etude de l'implication de la molécule TRAIL et de ses récepteurs dans les cancers de la prostate

Dans les pays industrialisés, le cancer de la prostate est le cancer le plus diagnostiqué et la seconde cause de mort par cancer chez l'homme, après celui du poumon.Si les formes précoces de la maladie peuvent ^etre traitées avec succès (radiothérapie, curiethérapie, prostatectomie radicale), les formesles plus avancées, hormono-résistantes, demeurent incurables.Cette pathologie atteignant particulièrement l'homme âgé, l'augmentation de l'espérance de vie ainsi que l'arrivée de la génération du "baby-boom" dans l'^age à risque en font un problème de santé publique majeur. Il est par conséquent urgent de développer de nouvelles stratégies thérapeutiques permettant de lutter efficacement contre les cancers de la prostate. Dans ce contexte, nous avons étudié la molécule pro-apoptotique TRAIL et ses cinq récepteurs,"in vitro"et "in vivo", afin d'en évaluer les propriétés anti-tumorales.RENNES1-BU Sciences Philo (352382102) / SudocSudocFranceF

Sensitivity of prostate cells to TRAIL-induced apoptosis increases with tumor progression: DR5 and caspase 8 are key players.

International audienceBACKGROUND: As advanced prostate cancers are resistant to currently available chemotherapies, we evaluated the cytotoxic effect of TNF-related apoptosis-inducing ligand (TRAIL) and characterized the involvement of its five receptors DR4, DR5, DcR1, DcR2, and osteoprotegerin (OPG) and of the death-inducing signaling complex (DISC)-forming proteins caspase 8 and c-FLIP in prostate cell lines. METHODS: We used six prostate cell lines, each corresponding to a particular stage in prostate tumorigenesis, and analyzed TRAIL sensitivity in relation to TRAIL receptors' expression. RESULTS: TRAIL sensitivity was correlated with tumor progression and DR5 expression levels and apoptosis was exclusively mediated by DR5. DcR2 was significantly more abundant in tumor cells than in non-neoplastic ones and may contribute to partial resistance to TRAIL in some prostate tumor cells. Conversely, non-tumoral cells secreted high levels of OPG, which can protect them from apoptosis. Finally, caspase 8 expression levels were as DR5 directly correlated to TRAIL sensitivity in prostate tumor cells. CONCLUSION: TRAIL-induced apoptosis is closely related to the balanced expression of its different receptors in prostate cancer cells and their modulation could be of potential clinical value for advanced tumor treatment

Adaptation to statins restricts human tumour growth in Nude mice.

International audienceABSTRACT: BACKGROUND: Statins have long been used as anti-hypercholesterolemia drugs, but numerous lines of evidence suggest that they may also bear anti-tumour potential. We have recently demonstrated that it was possible to isolate cancer cells adapted to growth in the continuous presence of lovastatin. These cells grew more slowly than the statin-sensitive cells of origin. In the present study, we compared the ability of both statin-sensitive and statin-resistant cells to give rise to tumours in Nude mice. METHODS: HGT-1 human gastric cancer cells and L50 statin-resistant derivatives were injected subcutaneously into Nude mice and tumour growth was recorded. At the end of the experiment, tumours were recovered and marker proteins were analyzed by western blotting, RT-PCR and immunohistochemistry. RESULTS: L50 tumours grew more slowly, showed a strong decrease in cyclin B1, over-expressed collagen IV, and had reduced laminin 332, VEGF and CD34 levels, which, collectively, may have restricted cell division, cell adhesion and neoangiogenesis. CONCLUSIONS: Taken together, these results showed that statin-resistant cells developed into smaller tumours than statin-sensitive cells. This may be reflective of the cancer restricting activity of statins in humans, as suggested from several retrospective studies with subjects undergoing statin therapy for several years