We found that FGFR signaling represses GLI1 expression downstream of activated SMO in the SHH MB line DAOY and induces <i>MKI67</i>, <i>HES1</i>, and <i>BMI1</i> in DAOY and in the group 3 MB line HD-MBO3.
Previous studies have shown that P73 antisense RNA 1T (non-protein coding), also known as TP73-AS1, is a long non-coding RNA (lncRNA) and involved in the development of medulloblastoma.
The knockdown of TP73-AS1 inhibited cell proliferation, invasion, migration, and promoted apoptosis of medulloblastoma cells, while the miR-494-3p inhibitor abolished the effects of TP73-AS1 knockdown on medulloblastoma cells.
Previous studies have shown that P73 antisense RNA 1T (non-protein coding), also known as TP73-AS1, is a long non-coding RNA (lncRNA) and involved in the development of medulloblastoma.
The knockdown of TP73-AS1 inhibited cell proliferation, invasion, migration, and promoted apoptosis of medulloblastoma cells, while the miR-494-3p inhibitor abolished the effects of TP73-AS1 knockdown on medulloblastoma cells.
About 30% of patients experience relapse after treatment, possibly because of our inability to identify and eliminate the cancer stem cells.Zhang et al. recently investigated these cells in the SHH subgroup of medulloblastoma and identified drugs that may target them.
Here we generate humanized models for Sonic Hedgehog (SHH)-subgroup MB via MYCN overexpression in primary human hindbrain-derived neuroepithelial stem (hbNES) cells or iPSC-derived NES cells, which display a range of aggressive phenotypes upon xenografting. iPSC-derived NES tumors develop quickly with leptomeningeal dissemination, whereas hbNES-derived cells exhibit delayed tumor formation with less dissemination.
The in vivo role of CRNDE knockdown or miR-29c-3p overexpression on tumor growth and apoptosis was evaluated in a xenograft mouse model of human medulloblastoma.
RNA pull-down and RNA binding protein immunoprecipitation (RIP) were performed to confirm the molecular interactions between CRNDE and miR-29c-3p involved in medulloblastoma cells.
TAA, as the essential components of disseminated tumor, produced high level of CCL2 to shape inflammation microenvironment, which stimulated the enrichment of MBSCs in disseminated MB.
To compare results from a third (1995-2010) cohort of children with medulloblastoma with two previous series (J Neurosurg 86:13-21, 1997; Arch Dis Child 54:200-203, 1979) to analyse the effects of management changes aimed at improving both overall and event-free survivals (OS and EFS) and functional outcomes.
Here we report the identification of KCTD15 as a novel player in the complex network of regulatory proteins, which modulate Hh pathway, this could be a promising new target for therapeutic approach against MB.
Phosphorylated CHK1 serine 345 (pCHK1 S345), phosphorylated Histone 2A variant (γ-H2AX), and cleaved caspase-3 were quantified in mouse G3MB tumor tissues by immunohistochemistry at different time points up to 24 h post-dose.
Phosphorylated CHK1 serine 345 (pCHK1 S345), phosphorylated Histone 2A variant (γ-H2AX), and cleaved caspase-3 were quantified in mouse G3MB tumor tissues by immunohistochemistry at different time points up to 24 h post-dose.