A research team, led by CHEN Yan at the Institute for Nutritional Sciences (INS), Shanghai Institutes for Biological Sciences, CAS, recently found that one member of PAQR family RKTG can cooperate with tumor suppressor gene p53 in tumorigenesis and epithelial-mesenchymal transition (EMT). The finding has demonstrated a critical role of RKTG in suppressing tumorigenesis and also uncovered functional cooperation of RKTG with p53 in EMT, a critical process in cancer invasion and metastasis.

RKTG is a potential tumor suppressor gene due to its negative roles in regulating Ras/Raf/MEK/ERK pathway and Gβγ-mediated signaling. Interestingly, RKTG-deficient mice are free of tumors, although they are prone to form skin cancer upon carcinogen administration. On the other hand, p53 is a well-characterized tumor suppressor gene and p53-heterozygous mice develop sarcoma and other tumors starting from 12 months of age. JIANG Yuhui, a graduate student at CHEN Yan’s lab detected spontaneous skin cancer-like tumors in ~25% of RKTG-nullizygous and p53-heterozygous mice within 7 months of age. Hyperplasia and EMTwere observed in the tumor-overlaying epidermis. After a series of in vitro and in vivo experiments, they demonstrated critical roles of RKTG and p53 in regulating EMT.

This study entitled "Functional cooperation of RKTG with p53 in tumorigenesis and epithelial-mesenchymal transition " was recently published in Cancer Research. (INS)

AUTHOR CONTACT:
CHEN Yan, Ph.D., Professor
Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences,
Shanghai, China.
Phone: 86.21.5492.0916; Fax: 86.21.5492.0291; E-mail: ychen3@sibs.ac.cn