Glioblastoma Therapy in the Age of Molecular Medicine

Geraldo, Luiz Henrique Medeiros; García, Celina; Fonseca, Anna Carolina Carvalho da; Dubois, Luiz Gustavo; Spohr, Tânia Cristina Leite de Sampaio e; Matias, Diana; Magalhães, Eduardo Sabino de Camargo; Amaral, Rackele Ferreira do; Rosa, Bárbara Gomes da; Grimaldi, Izabella; Leser, Felipe Saceanu; Janeiro, José Marcos; Macharia, Lucy Wanjiku; Wanjiru, Caroline M.; Pereira, Cláudia Maria; Moura‐Neto, Vivaldo; Freitas, Catarina; Lima, Flávia Regina Souza

doi:10.1016/j.trecan.2018.11.002

Cited by 79 publications

(62 citation statements)

References 231 publications

(186 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The results demonstrated that silencing HMGN5 decreased the migratory and invasive capacity of U87 and U251 cells. Moreover, MMP-2 and MMP-9, the members of the metalloproteases family, which were frequently involved in glioblastoma invasiveness [19], were downregulated along with the reduction of HMGN5 in glioblastoma cells.…”

Section: Discussionmentioning

confidence: 99%

HMGN5 Silencing Suppresses Cell Biological Progression via AKT/MAPK Pathway in Human Glioblastoma Cells

Wang

et al. 2020

BioMed Research International

View full text Add to dashboard Cite

HMGN5 regulates biological function and molecular transcription via combining with a nucleosome. There has been growing evidence that aberrant expression of HMGN5 is associated with malignant neoplasm development and progression. In the present study, we found that the expression of HMGN5 is significantly higher in high-grade glioblastoma tissues than in low-grade samples. To clarify the function of HMGN5 in glioblastoma, we knocked down HMGN5 in U87 and U251 glioblastoma cells via siRNA. The results demonstrated that HMGN5 was involved in the regulation of proliferation and apoptosis, migration, and invasion of glioblastoma cells. These outcomes also indicated that silencing HMGN5 possibly suppressed the expression of p-AKT and p-ERK1/2. Taken together, our research reveals that HMGN5 might be an efficient target for glioblastoma-targeted therapy.

show abstract

Section: Discussionmentioning

confidence: 99%

HMGN5 Silencing Suppresses Cell Biological Progression via AKT/MAPK Pathway in Human Glioblastoma Cells

Wang

et al. 2020

BioMed Research International

View full text Add to dashboard Cite

show abstract

“…GLIOBLASTOMA MULTIFORME (GBM) GBM, a WHO grade IV astrocytoma is an extremely aggressive, invasive, and destructive primary brain tumor in the adult population (Geraldo et al, 2019). Lee and co-workers demonstrated a strong negative correlation between the expression of Astrocyte Elevated Gene-1 (AEG-1), an oncogene, and EAAT2 by immunofluorescence analyses in human glioma tissue arrays .…”

Section: Neurological Disorders and Eaat2 Expressionmentioning

confidence: 99%

Epigenetic Regulation of Excitatory Amino Acid Transporter 2 in Neurological Disorders

Alam

Datta

2019

Front. Pharmacol.

View full text Add to dashboard Cite

Excitatory amino acid transporter 2 (EAAT2) is the predominant astrocyte glutamate transporter involved in the reuptake of the majority of the synaptic glutamate in the mammalian central nervous system (CNS). Gene expression can be altered without changing DNA sequences through epigenetic mechanisms. Mechanisms of epigenetic regulation, include DNA methylation, post-translational modifications of histones, chromatin remodeling, and small non-coding RNAs. This review is focused on neurological disorders, such as glioblastoma multiforme (GBM), Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), bipolar disorder (BD), and neuroHIV where there is evidence that epigenetics plays a role in the reduction of EAAT2 expression. The emerging field of pharmaco-epigenetics provides a novel avenue for epigenetics-based drug therapy. This review highlights findings on the role of epigenetics in the regulation of EAAT2 in different neurological disorders and discusses the current pharmacological approaches used and the potential use of novel therapeutic approaches to induce EAAT2 expression in neurological disorders using CRISPR/Cas9 technology.

show abstract

“…Scheme outlining the differences between DNA (left) and PNA (right) monomers be insulin-like growth factors, fibroblast growth factor and their receptors [74,75] . Excellent review articles describing current therapeutic approaches and novel trends in GBM management are available [69,[76][77][78][79][80][81][82] .…”

Section: Glioblastomamentioning

confidence: 99%

Peptide nucleic acid-based targeting of microRNAs: possible therapeutic applications for glioblastoma

Gambari¹,

Gasparello²,

Finotti³

2019

JCMT

View full text Add to dashboard Cite

A large and incremental number of non-coding RNAs, including microRNAs (miRNAs) have been recently demonstrated to play a very important role in human pathologies, including cancer. Therefore, microRNAs have been proposed as therapeutic targets and molecules exhibiting anti-miRNA activity or mimicking functional miRNAs have been developed. Among biomolecules proposed in anti-miRNA therapy, peptide nucleic acids (PNAs) are appealing, in consideration of their stability and efficacy in recognizing RNA targets. PNAs against tumor associated miRNAs have proven to be efficient in inducing anti-tumor effects both in vitro and in vivo. For instance, PNAs targeting miR-155-5p are able to induce apoptosis in glioma cell lines and to enhance the sensitivity to temozolomide (TMZ) in TMZ resistant glioma cells. In vivo, PNAs anti-miR-21 were found to exhibit anti-tumor effects associated with improved survival when administered to animals with intracranial gliomas.

show abstract

Glioblastoma Therapy in the Age of Molecular Medicine

Cited by 79 publications

References 231 publications

HMGN5 Silencing Suppresses Cell Biological Progression via AKT/MAPK Pathway in Human Glioblastoma Cells

HMGN5 Silencing Suppresses Cell Biological Progression via AKT/MAPK Pathway in Human Glioblastoma Cells

Epigenetic Regulation of Excitatory Amino Acid Transporter 2 in Neurological Disorders

Peptide nucleic acid-based targeting of microRNAs: possible therapeutic applications for glioblastoma

Contact Info

Product

Resources

About