title: Overexpression of phosphoserine aminotransferase PSAT1 stimulates cell growth and increases chemoresistance of colon cancer cells.
abstract: BACKGROUND
  Colorectal cancer (CRC) is one of the most common causes of cancer death throughout the world. In this work our aim was to study the role of the phosphoserine aminotransferase PSAT1 in colorectal cancer development.
  
  
  RESULTS
  We first observed that PSAT1 is overexpressed in colon tumors. In addition, we showed that after drug treatment, PSAT1 expression level in hepatic metastases increased in non responder and decreased in responder patients. In experiments using human cell lines, we showed that ectopic PSAT1 overexpression in colon carcinoma SW480 cell line resulted in an increase in its growth rate and survival. In addition, SW480-PSAT1 cells presented a higher tumorigenic potential than SW480 control cells in xenografted mice. Moreover, the SW480-PSAT1 cell line was more resistant to oxaliplatin treatment than the non-transfected SW480 cell line. This resistance resulted from a decrease in the apoptotic response and in the mitotic catastrophes induced by the drug treatment.
  
  
  CONCLUSIONS
  These results show that an enzyme playing a role in the L-serine biosynthesis could be implicated in colon cancer progression and chemoresistance and indicate that PSAT1 represents a new interesting target for CRC therapy.
authors.affiliation: CNRS, UMR 5160, CRLC, 15, av, Charles Flahault, BP14491, 34093, Montpellier Cedex 5, France. nadia.vie@aldorel.fnclcc.fr
authors.forename: Nadia
authors.initials: N
authors.lastname: Vié
authors.forename: Virginie
authors.initials: V
authors.lastname: Copois
authors.forename: Caroline
authors.initials: C
authors.lastname: Bascoul-Mollevi
authors.forename: Vincent
authors.initials: V
authors.lastname: Denis
authors.forename: Nicole
authors.initials: N
authors.lastname: Bec
authors.forename: Bruno
authors.initials: B
authors.lastname: Robert
authors.forename: Caroline
authors.initials: C
authors.lastname: Fraslon
authors.forename: Emmanuel
authors.initials: E
authors.lastname: Conseiller
authors.forename: Franck
authors.initials: F
authors.lastname: Molina
authors.forename: Christian
authors.initials: C
authors.lastname: Larroque
authors.forename: Pierre
authors.initials: P
authors.lastname: Martineau
authors.forename: Maguy
authors.initials: M
authors.lastname: Del Rio
authors.forename: Céline
authors.initials: C
authors.lastname: Gongora
mesh_terms: D000230:Adenocarcinoma / Q000188:drug therapy / Q000201:enzymology* / Q000556:secondary; D000368:Aged; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use; D002166:Camptothecin / Q000031:analogs & derivatives / Q000627:therapeutic use; D002470:Cell Survival; D015179:Colorectal Neoplasms / Q000188:drug therapy / Q000201:enzymology* / Q000473:pathology; D019008:Drug Resistance, Neoplasm; D005260:Female; D005472:Fluorouracil / Q000627:therapeutic use; D006801:Humans; D002955:Leucovorin / Q000627:therapeutic use; D008113:Liver Neoplasms / Q000188:drug therapy / Q000201:enzymology* / Q000556:secondary; D008297:Male; D008875:Middle Aged; D000637:Transaminases / Q000378:metabolism*; D014407:Tumor Cells, Cultured
chemical_list: D000637:Transaminases; C022393:phosphoserine aminotransferase; D002955:Leucovorin; D005472:Fluorouracil; D002166:Camptothecin