Data on tumor progression of c-mos deficiency in murine models of KrasG12D lung and ApcMin colorectal cancer
Zhengxi Chen,
Ju Qiao,
Qirui Wang,
Qian Xiao
Affiliations
Zhengxi Chen
Department of Pharmacology, School of Medicine, Yale University, 10 Amistad St, New Haven, CT, USA; Department of Orthodontics, Shanghai Ninth People׳s Hospital, School of Stomatology, Shanghai key Laboratory of Stomatology, Shanghai Jiao Tong University, Shanghai, China
Ju Qiao
Department of Mechanical and Industrial Engineering, Northeastern University, Boston, MA, USA
Qirui Wang
Department of Molecular Biology, State Administration of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, China
Qian Xiao
Department of Pharmacology, School of Medicine, Yale University, 10 Amistad St, New Haven, CT, USA; Corresponding author.
The c-mos proto-oncogene was one of the first proto-oncogenes to be cloned. Apart from its role in meiosis, many efforts have been made to illuminate the mechanisms by which c-mos might acts as an oncogene. Increased Mos expression was found in most human tumor tissues. However, a detailed role of c-mos in tumor progression remains unknown.In this study, we analyzed online databases to find out the correlation between Mos expression and poor survival rates in human cancer patients. Then, we crossed c-mos knockout mice with ApcMin or KrasG12D mice to generate intestinal cancer model and lung cancer model, respectively. Tumor progression was monitored, and the influence of c-mos deficiency on cancer formation was investigated.
