Glioblastoma (GBM) is the most common primary brain malignancy in adults and one of the most aggressive of all cancers in humans. It is very repetitive and treatment-resistant, largely because the infiltrative nature and inter- and intratumoral heterogeneity. This heterogeneity requires different landscape genomics and cell types within and between the tumor and the tumor microenvironment (TME). In the GBM, is the driving resistance heterogeneity of treatment, recurrence, and prognosis is poor, represent a major obstacle to personalized medicine.

Over the past decade, the sequencing technology has facilitated a deeper understanding of GBM heterogeneity by “zooming in” more progressive on tumor genomics and transcriptomics. initial efforts to use mass ribonucleic acid (RNA) sequencing, which examined the combined gene expression of tumor specimens as a whole. While innovative at the time, this bulk RNAseq mask important contribution of sub-populations of different tumor’s gene expression as a whole.

This work evolved into mass use RNA sequencing on tumor subsections anatomically and spatially distinct, previously unappreciated complexity exhibited genome of GBM. The revolutionary next step forward has been the emergence of a single cell RNA sequencing (scRNAseq), which examined the gene expression at the single cell level. scRNAseq has enabled us to understand in detail the heterogeneity GBM unprecedented.

We review studies of seminal in the development of our understanding of GBM heterogeneity, with a focus on scRNAseq and insight that have been provided in the understanding of GBM tumor mass, peritumoral space, and TME. We highlight the preclinical and clinical implications of this work and consider the potential impact of neuro-oncology, and to improve patient outcomes through personalized medicine.

[Knockdown of Fez family of zinc finger protein 1 antisense ribonucleic acid 1 (FEZF1-AS1) inhibits invasion and migration of esophageal squamous cell carcinoma cells by blocking the JAK2 / STAT3 pathway]

Objective To investigate the relationship between the long chain of non-coding RNA Fez family of zinc protein finger 1 antisense ribonucleic acid 1 (FEZF1-AS1) and invasion, migration and Janus kinase 2 / signal transducer and activator of transcription 3 (JAK2 / STAT3) signaling pathway in carcinoma squamous cell (ESCC) cells of the esophagus. Methods The expression ‘of FEZF1-AS1 in cancer tissues and cell lines ESCC ESCC was detected by real-time quantitative PCR.

After knocking out FEZF1-AS1 of KYSE150 and KYSE510 cells with expression vectors lentiviral built, changes in cell cycle were detected by flow cytometry, the ability of cell proliferation by colony test formations, the ability of cell invasion by TranswellTM invasion assay, the ability of cell migration by TranswellTM migration and early test, and the level of phosphorylated proteins JAK2 and STAT3 (p-STAT3) by Western blotting.

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Results FEZF1-AS1 are highly expressed in cancer tissues ESCC and FEZF1-AS1 expression in cells KYSE510 KYSE150 and higher than that in normal esophageal squamous epithelial cells. Upon knockdown FEZF1-AS1 expression, cell cycle and proliferation of cancer cells ESCC did not change obviously, but cell invasion and migration was significantly inhibited, and the protein levels decreased JAK2 and p-STAT3 protein increases. Conclusion FEZF1-AS1 knockdown blocks JAK2 / STAT3 pathway and inhibits cell invasion and migration of ESCC.