Limitations
There are some limitations to this scoping review. Most studies used the
same knockdown approach and technology, which was the RNAi silencing
technique. As a consequence, there may be some bias and a lack of
variability in the study samples. In line with the advancement in
biotechnology, the researcher might apply the deep sequencing technique,
such as next generation sequencing (NGS) platform to explore novel RNA
targets that interact with ZFAS1 in gliomagenesis
[54]. Besides, CRISPR-CAS9 is also a
good technology for genome editing as it is faster, cheaper, more
accurate, and more efficient than other genome editing methods to study
functional regulatory actions by ZFAS1 . The study included in
this review used small sample sizes, for example just 15 patients were
included to characterize ZFAS1 expression in glioma grade III and
IV, while only 10 patients for grade I and II glioma. Furthermore, the
study did not analyze the other potential miRNA, like miR-124-3p,
miR-186 and miR-146b-5p, and ZFAS1 related target genes in
gliomagenesis, as example p53. Finally, there were very few original
articles on ZFAS1 and glioma compared to other cancer types
indicating that further studies using different cell lines such as
U343-MG and LN18 for molecular analysis and uncovering novel cancer
pathways including Phosphatase and tensin homolog (PTEN )
sinceĀ PTEN mutations are strongly associated with shorter
survival in glioma patients, implying that PTEN status strongly
correlates with patient prognosis and PTEN is a prominent tumor
suppressor [55] or Receptor Tyrosine
Kinase (RTK) as RTK is well-known in glioma initiation and progression
as it serve as docking sites for cytoplasmic signaling effectors once
phosphorylated. However, in cancer, RTKs are abnormally activated and
thus contribute to the oncogenic phenotype by (1) encouraging cancer
cell overproduction of growth factors; (2) overexpression and/or
amplification of the RTK itself, enabling hypersensitivity to low ligand
concentrations; (3) acquiring mutations in their ligand-binding or
kinase domains; (4) fusion of kinase domains with motifs of other,
unrelated proteins; or (5) chromosomal translocation, giving rise to a
chimeric product with enhanced kinase activity
[56].