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].