ABSTRACT
ECRG-1 (esophageal cancer-related gene 1) has been previously found to be down-regulated in human esophagus cancer. Transient expression of green fluorescent protein (GFP)-tagged ECRG1 showed plasma membrane localization. Treatment of esophagus cancer cell line (NEC) with ECRG-1 fusion protein and over-expression of ECRG-1 in NEC cells can significantly reduce the in vitro proliferation rate of NEC cells. Treatment of established NEC tumors in the nude mice with ECRG-1 fusion protein leads to decreased tumor weight and volume. Over-expression of ECRG-1 in NEC cells can also inhibit tumor formation in nude mice. Cell-cycle analysis showed that over-expression of ECRG-1 in NEC cells results in G(2)/M phase arrest. Our findings indicate that ECRG1 may be a candidate tumor suppressor gene for esophageal cancer (EC) involved in cell-cycle control. Since ECRG-1 gene significantly suppresses the growth of NEC cells both in vitro and in vivo, its loss may contribute to the causation and progression of the EC in Lin-xian county, which is a high incidence area of EC in China.
Subject(s)
Esophageal Neoplasms/prevention & control , Esophagus/metabolism , Recombinant Fusion Proteins/genetics , Animals , Cell Cycle , Cell Line, Tumor , Cloning, Molecular , Esophageal Neoplasms/genetics , Esophageal Neoplasms/pathology , Humans , Membrane Proteins , Mice , Mice, Nude , Serine ProteasesABSTRACT
OBJECTIVE：To study the effcet of Nitric oxide (No) on transcriptional expression of c-fos and c-jun oncogene of cultured rabbit arterial smooth muscle cells (ASMC),and its mechanism.METHODS:(1)To culture rabbit ASMC from explants;(2) To determine if NO,FeSO4,and methylene blue have toxic effect on ASMC by cell counting;(3)RNA isolation from ASMC by Guanidinium Thiocyanate-phenol-chloroform method;(4)RNA-DNA blot hybridization.RESULTS:Under the condition of no toxic effects,NO inhibited the expression of c-fos and c-jun oncogene of ASMC apparently,FeSO4 and methylene blue antagonized the inhibition effcet.CONCLUSION:NO inhibited the expression of c-fos and c-jun oncogene of ASMC through cGMP.This may be related to the important mechanism that NO inhibits the proliferation of ASMC.
