| General information | Literature | Expression | Regulation | Mutation | Homolog | Interaction |
Basic Information | |
|---|---|
Gene ID | 3480 |
Name | IGF1R |
Synonymous | insulin-like growth factor 1 receptor;IGF1R;insulin-like growth factor 1 receptor |
Definition | IGF-I receptor|insulin-like growth factor I receptor|soluble IGF1R variant 1|soluble IGF1R variant 2 |
Position | 15q26.3 |
Gene type | protein-coding |
Title | Abstract |
| Clinical significance of proliferation, apoptosis and senescence of nasopharyngeal cells by the simultaneously blocking EGF, IGF-1 receptors and Bcl-xl genes. | BACKGROUND: In previous work, we constructed short hairpin RNA (shRNA) expression plasmids that targeted human EGF and IGF-1 receptors messenger RNA, respectively, and demonstrated that these vectors could induce apoptosis of human nasopharyngeal cell lines (CNE2) and inhibit ligand-induced pAkt and pErk activation. METHOD: We have constructed multiple shRNA expression vectors of targeting EGFR, IGF1R and Bcl-xl, which were transfected to the CNE2 cells. The mRNA expression was assessed by RT-PCR. The growth of the cells, cell cycle progression, apoptosis of the cells, senescent tumor cells and the proteins of EGFR, IGF1R and Bcl-xl were analyzed by MTT, flow cytometry, cytochemical therapy or Western blot. RESULTS: In group of simultaneously blocking EGFR, IGF1R and Bcl-xl genes, the mRNA of EGFR, IGF1R and Bcl-xl expression was decreased by (66.66+/-3.42)%, (73.97+/-2.83)% and (64.79+/-2.83)%, and the protein expressions was diminished to (67.69+/-4.02)%, (74.32+/-2.30)%, and (60.00+/-3.34)%, respectively. Meanwhile, the cell apoptosis increased by 65.32+/-0.18%, 65.16+/-0.25% and 55.47+/-0.45%, and senescent cells increased by 1.42+/-0.15%, 2.26+/-0.15% and 3.22+/-0.15% in the second, third and fourth day cultures, respectively. CONCLUSIONS: Simultaneously blocking EGFR, IGF1R and Bcl-xl genes is capable of altering the balance between proliferating versus apoptotic and senescent cells in the favor of both of apoptosis and senescence and, therefore, the tumor cells regression. |