Affiliations 

  • 1 ER stress and Mucosal Immunology Laboratory, School of Health Sciences, University of Tasmania, Launceston, Tasmania, Australia
  • 2 Division of Hematologic Malignancies and Cellular Therapy, Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA
  • 3 Department of Medical, Oral and Biotechnological Sciences (DSMOB), Ageing Research Center and Translational medicine-CeSI-MeT, "G. d'Annunzio" University Chieti-Pescara, Chieti, Italy
  • 4 Respiratory Translational Research Group, Department of Laboratory Medicine, School of Health Sciences, University of Tasmania, Launceston, Tasmania, Australia
  • 5 Department of Biotechnology, School of engineering and Technology, Sharda University, Greater Noida, UP, Indonesia
  • 6 f Department of Biotechnology Engineering and Food Technology, Chandigarh University, Mohali, 140413, India
Biotechnol Genet Eng Rev, 2023 Apr;39(1):143-165.
PMID: 35904341 DOI: 10.1080/02648725.2022.2106002

Abstract

Glioblastoma (GBM) is presented with a poor prognosis. The endoplasmic reticulum stress (ERS) has been implicated as a major contributor to disease progression and chemoresistance in GBM. Triggering ERS by chemical agents or genetic modulations is identified as some of the reasons for regulating gene expression and the pathogenesis of GBM. ERS initiates unfolded protein response (UPR), an integrated system useful in restoring homeostasis or inducing apoptosis. Modulation of UPR might have positive outcomes in GBM treatment as UPR inducers have been shown to alter cell survival and migration. In the current review, we have utilized GSE7806, a publicly available dataset from Gene Expression Omnibus (GEO), to evaluate the genes expressed during 6.5 hr and 18 hr, which can be comparable to the early and late-onset of the disease. Subsequently, we have elucidated the prognosis and survival information whilst the expression of these genes in the GBM was noted in previous studies. This is the first of its kind review summarizing the most recent gene information correlating UPR and GBM.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.