Version 1
: Received: 26 October 2023 / Approved: 27 October 2023 / Online: 27 October 2023 (13:22:38 CEST)
How to cite:
Swati, K.; Quazi, S.; Arfin, S.; Panda, S.P.; Prakash, A.; Kumar, D. Deciphering the Role of SEC61G in Glioblastoma Multiforme Progression. Preprints2023, 2023101809. https://doi.org/10.20944/preprints202310.1809.v1
Swati, K.; Quazi, S.; Arfin, S.; Panda, S.P.; Prakash, A.; Kumar, D. Deciphering the Role of SEC61G in Glioblastoma Multiforme Progression. Preprints 2023, 2023101809. https://doi.org/10.20944/preprints202310.1809.v1
Swati, K.; Quazi, S.; Arfin, S.; Panda, S.P.; Prakash, A.; Kumar, D. Deciphering the Role of SEC61G in Glioblastoma Multiforme Progression. Preprints2023, 2023101809. https://doi.org/10.20944/preprints202310.1809.v1
APA Style
Swati, K., Quazi, S., Arfin, S., Panda, S.P., Prakash, A., & Kumar, D. (2023). Deciphering the Role of SEC61G in Glioblastoma Multiforme Progression. Preprints. https://doi.org/10.20944/preprints202310.1809.v1
Chicago/Turabian Style
Swati, K., Anand Prakash and Dhruv Kumar. 2023 "Deciphering the Role of SEC61G in Glioblastoma Multiforme Progression" Preprints. https://doi.org/10.20944/preprints202310.1809.v1
Abstract
Aim: Glioblastoma multiform (GBM) is a prevalent brain cancer which accounts for 80% of cases globally with a noticeably short life expectancy subsequent diagnosis. There are several factors associated with GBM including alterations and over expressions of oncoproteins. Analysis of SEC61G expression in GBM patient’s favor tumour progression, which promotes an environment of oxidative stress, while preventing apoptosis.
Methods: In this article using in silico tools including GEPIA2, ULCAN, LinkedOmics, Gene MANIA and mirTEd, we observed the role of SEC61G gene in GBM progression by analyzing the expression, positive correlation associated with metabolic, mitochondrial gene, immune cell infiltration level, gene interaction networks, miRNA association as well as survival analysis.
Results: The expression of the mitochondrial, metabolic genes PGLS, PGK1, EIF6, and EIF3K which are involved in redox metabolism and CD63 immunoregulation, as well as other genes that promote tumour progression and invasion, including EGFR, LANCL2, BCL2L12, SEC61G-DT, KDELR1, CDKN2A, IFNA16, IFNA10, and BCL7C were positively correlated with the increased/high expression of SEC61G.We also found hsa-mir-380-5p to be unregulated in glioblastoma phenotypes.
Conclusion: Our findings suggest that SEC61G associated redox metabolism, complement system and immunoregulation, as well as miRNA expression can be targeted to develop a potential therapeutic approach for GBM patients.
Biology and Life Sciences, Biology and Biotechnology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
