miR 21 inhibitor enhances anti proliferation influence of taxol to glioblastoma cells independent of PTEN standing Past examine proved that miR 21 could direct regulate PTEN tumor suppressor gene mRNA translation at submit transcriptional degree in hepatocellular carcinoma and GBM cells. Various genetic alterations of PTEN, like TGF-beta mutation, deletion, and translation suppression, could lead to aberrant EGFR pathway activation in GBM. Maier et al also analyzed the purpose of PTEN in invasion working with the two extremely infiltrative glioma cell lines U87MG and LN229. We deduced that knocking down miR 21 sensitized GBM to taxol by PTEN mRNA translation blockage. Still, it is worth noting that cytotoxicity information algorithm benefits indicated the miR 21 inhibitor additively interacted with taxol on U251cells and synergistically on LN229 cells for MTT assay and additively for Annexin V/PI apoptosis assay in each GBM cell lines.
Curiously, the data of miR 21 inhibitor suppressed U251 GBM growth indicated there was an independent PTEN pathway whilst the PARP specific mechanism wasn't distinct. The above information proposed that the two within the PTEN mutant and in the wild variety GBM cells, miR 21 blockage could maximize the chemo sensitivity to taxol. Chan et al reported that knocking down miR 21 could boost caspase3/7 activity similarly although in LN229 and U87 GBM cell that had various PTEN background. Our earlier exploration indicated that antisense miR 21 ODN could induce U251 and LN229 GBM cell apoptosis via attenuating EGFR signaling pathway.
In addition to, numerous cancer cell apoptosis or metastasis associated genes together with PDCD4, P53 signaling network, RECK, S TRAIL and so forth had been validated to become miR 21s function targets in the two brain tumors along with other epithelium authentic human cancers. Presumably, miR 21 inhibitor mediated human GBM cell apoptosis influence Survivin in a one hit numerous target mechanism rather than straight inhibition of PTEN mRNA translation. Mild apoptosis induction big difference of miR 21 inhibition in U251 and LN229 GBM cell proposed, compared to miR 21 blockage, PTEN broad style or induction was a fine tune during the oncogenesis of GBM. And miR 21 suppression had clinical potential to improve chemo drug impact of chemotherapy in GBM patient with different PTEN genetic background. EGFR has become a central emphasis of examine in glioma as a result of its proposed role in the transformation and development of glial tumors, and the fact that EGFR may be the most commonly amplified gene in GBM.
Activation of EGFR signaling plays a central role in GBM. AKT will be the direct effector of EGFR downstream signaling, Topoisomerase the expression of phosphorylated AKT could be the important aspect representing the actions of EGFR pathways. Both in U251 and in LN229 GBM cells, the miR 21 inhibitor could suppress the EGFR signaling pathway activity. In the data incorporated in the manuscript, its hard to elucidate the exact mechanism that miR 21 inhibitor triggered EGFR suppression in both PTEN mutant and wild sort GBM.
Curiously, the data of miR 21 inhibitor suppressed U251 GBM growth indicated there was an independent PTEN pathway whilst the PARP specific mechanism wasn't distinct. The above information proposed that the two within the PTEN mutant and in the wild variety GBM cells, miR 21 blockage could maximize the chemo sensitivity to taxol. Chan et al reported that knocking down miR 21 could boost caspase3/7 activity similarly although in LN229 and U87 GBM cell that had various PTEN background. Our earlier exploration indicated that antisense miR 21 ODN could induce U251 and LN229 GBM cell apoptosis via attenuating EGFR signaling pathway.
In addition to, numerous cancer cell apoptosis or metastasis associated genes together with PDCD4, P53 signaling network, RECK, S TRAIL and so forth had been validated to become miR 21s function targets in the two brain tumors along with other epithelium authentic human cancers. Presumably, miR 21 inhibitor mediated human GBM cell apoptosis influence Survivin in a one hit numerous target mechanism rather than straight inhibition of PTEN mRNA translation. Mild apoptosis induction big difference of miR 21 inhibition in U251 and LN229 GBM cell proposed, compared to miR 21 blockage, PTEN broad style or induction was a fine tune during the oncogenesis of GBM. And miR 21 suppression had clinical potential to improve chemo drug impact of chemotherapy in GBM patient with different PTEN genetic background. EGFR has become a central emphasis of examine in glioma as a result of its proposed role in the transformation and development of glial tumors, and the fact that EGFR may be the most commonly amplified gene in GBM.
Activation of EGFR signaling plays a central role in GBM. AKT will be the direct effector of EGFR downstream signaling, Topoisomerase the expression of phosphorylated AKT could be the important aspect representing the actions of EGFR pathways. Both in U251 and in LN229 GBM cells, the miR 21 inhibitor could suppress the EGFR signaling pathway activity. In the data incorporated in the manuscript, its hard to elucidate the exact mechanism that miR 21 inhibitor triggered EGFR suppression in both PTEN mutant and wild sort GBM.
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