Anti-HOXB9 (full length) polyclonal antibody

Aim: To explore the role of miR-196a on the regulatory mechanism in hepatocelluar carcinoma. Methods: The antisense RNA of microRNA-196a was synthesized and cloned into the vector. HepG2 cells were infected by inhibiting miR196a vector. The HepG2 cells were divided into miR196a lower expression group, NC group and N group in vitro. The expression of the targets of miR-196a was detected by qPCR. Cell growth was analyzed by cck8 assay. The invasion was detected by transwell method. Apoptosis was detected by annexinV/PI. The P53, caspase-3, HOXB9, HOXB8 mRNA and their protein was detected by qPCR and Western-blot. Results: (1) The expression level of miR-196a was less than normal (41%). (2) The proliferation of HepG2 was also markedly suppressed in inhibiting miR196a at the 24 h point than normal about 72.29 +/- 2.51% (P < 0.01). (3) The number of cells that migrated through the chamber of miR196a inhibiting group is less than normal and NC (P < 0.01). (4) The cell apoptosis in miR196a inhibiting group is more than NC and normal group (P < 0.05). HOXB8 mRNA and protein expression, in HepG2 cell line miR196a inhibiting group is significantly less than normal, NC (P < 0.05). Caspase-3 mRNA and protein expression is maximum in three groups (P < 0.05). In three groups there was no significant difference in the expression of P53 mRNA and protein and HOXB9mRNA. Conclusions: Our results demonstrate that miR-196a can effect the proliferation, the apoptosis and migration of HepG2 cell lines by gene HOXB8, caspase-3 regulation. However, there is no correlation between miRNA196a and P53 and HOXB9. (C) 2015 Elsevier Masson SAS. All rights reserved.

BTG/tob family proteins are thought to be a potential tumor suppressor due to their anti-proliferative activity. We cloned zebrafish btg-b, a member of the BTG1/2 subfamily, using in situ hybridization screening. The tissue-specific expression of brg-b is first observed in the organizer region at the early gastrula stage. Later in development, the forebrain, the hindbrain, the polster and the paraxial mesoderm transiently express btg-b. Recently, mouse Btg1 and Btg2 have been shown to be a cofactor for Hoxb9. Double in situ hybridization with zebrafish btg-b and hoxb9a indicates that the expression domains of these two genes overlap in the posterior paraxial mesoderm. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.