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摘要

A?loss?of?cell?polarity?is?thought?to?play?a?critical?role?in?thedevelopment?of?epithelial?neoplasias.?As?the?small?GTPaseRab25?regulates?polarized?trafficking?to?the?cell?membrane?andis?expressed?throughout?the?gastrointestinal?mucosa,?Nam?andcolleagues?set?out?to?investigate?whether?it?has?a?role?in?neoplas-tic?transformation?of?intestinal?epithelial?cells?(840–849).?Initialanalysis?indicated?that?expression?of?Rab25?was?substantiallydecreased?in?human?colon?adenocarcinomas?compared?withnormal?colon,?independent?of?stage,?and?that?lower?Rab25expression?predicted?shorter?patient?survival?times.?To?followup?on?these?data,?which?suggested?that?Rab25?functions?as?atumor?suppressor?in?intestinal?epithelial?cells,?the?authors?ana-lyzed?Rab25-deficient?mice.?Although?these?animals?showed?nogross?abnormalities,?when?they?were?crossed?with?Apc Min/+ ?mice(a?model?of?a?hereditary?syndrome?that?predisposes?to?coloncancer),?the?Rab25-deficient?Apc Min/+ ?mice?developed?increasednumbers?of?intestinal?polyps?and?colonic?tumors?compared?withparental?Apc Min/+ ?mice.?The?demonstration?that?Rab25-deficientSmad3 +/– ?mice?developed?more?colonic?tumors?than?did?controlSmad3 +/– ?mice?provided?further?confirmation?of?the?probabletumor-suppressive?role?of?Rab25?in?intestinal?epithelial?cells.