Over-expression and siRNA of a novel environmental lipopolysaccharide-responding gene on the cell cycle of the human hepatoma-derived cell line HepG2
- Resource Type
- Authors
- Nan-chun Chen; Wenhui Chang; Yaoming Chen; Jingyuan Chen; Suming Chen; Xiao-nan Zhang; Lichao Hou; Yubo Chai; Wenjing Luo; Tongjian Cai; Kejun Du
- Source
- Toxicology. 243:303-310
- Subject
- Lipopolysaccharides
Carcinoma, Hepatocellular
Blotting, Western
Gene Expression
Cell Cycle Proteins
Enzyme-Linked Immunosorbent Assay
Biology
Transfection
Toxicology
RNA interference
Cell Line, Tumor
Animals
Humans
Gene silencing
RNA, Small Interfering
Cell Cycle Protein
Cells, Cultured
Dental Pulp
Reverse Transcriptase Polymerase Chain Reaction
Immunochemistry
Cell Cycle
Liver Neoplasms
G1 Phase
Cell cycle
Flow Cytometry
Cell biology
Cytoplasm
Cell culture
Immunology
TLR4
Rabbits
- Language
- ISSN
- 0300-483X
Lipopolysaccharide (LPS) is the toxic determinant for Gram-negative bacterium infection. The individual response to LPS was related to its gene background. It is necessary to identify new molecules and signaling transduction pathways about LPS. The present study was undertaken to evaluate the effects of a novel environmental lipopolysaccharide-responding (Elrg) gene on the regulation of proliferation and cell cycle of the hepatoma-derived cell line, HepG2. By means of RT-PCR, the new molecule of Elrg was generated from a human dental pulp cell cDNA library. Expression level of Elrg in HepG2 cells was remarkably upgraded by the irritation of LPS. Localization of Elrg in HepG2 cells was positioned mainly in cytoplasm. HepG2 cells were markedly arrested in the G1 phase by over-expressing Elrg. The percentage of HepG2 cells in G1 phase partly decreased after Elrg-siRNA. In conclusion, Elrg is probably correlative with LPS responding. Elrg is probably a new protein in cytoplasm which plays an important role in regulating cell cycle. The results will deepen our understanding about the potential effects of Elrg on the human hepatoma-derived cell line HepG2.