Our results demonstrate that the LHX9 gene is frequently silenced in pediatric malignant astrocytomas by hypermethylation and that this epigenetic alteration is involved in glioma cell migration and invasiveness.
Exogenous expression of LHX9 in glioma cell lines did not directly affect cell proliferation and apoptosis but specifically inhibited glioma cell migration and invasion in vitro, suggesting a possible implication of LHX9 in the migratory phenotype of HGGs.
Bisulfite genomic sequencing and combined bisulfite restriction analysis showed that HGGs were frequently methylated at two CpG-rich LHX9 regions in comparison to benign, nondiffuse pilocytic astrocytomas and normal brain tissues.
Exogenous expression of LHX9 in glioma cell lines did not directly affect cell proliferation and apoptosis but specifically inhibited glioma cell migration and invasion in vitro, suggesting a possible implication of LHX9 in the migratory phenotype of HGGs.
We have investigated the possibility that mutations in the gene LHX9, whose murine ortholog causes isolated gonadal agenesis when inactivated, might be responsible for gonadal dysgenesis and agenesis in humans.
We have investigated the possibility that mutations in the gene LHX9, whose murine ortholog causes isolated gonadal agenesis when inactivated, might be responsible for gonadal dysgenesis and agenesis in humans.
We have investigated the possibility that mutations in the gene LHX9, whose murine ortholog causes isolated gonadal agenesis when inactivated, might be responsible for gonadal dysgenesis and agenesis in humans.