Investigating the Association between the Autophagy Markers LC3B, ISQSTM1/p62/I, and DRAM and Autophagy-Related Genes in Glioma

High-grade gliomas are extremely fatal tumors, marked by severe hypoxia and therapeutic resistance. Autophagy is a cellular degradative process that can be activated by hypoxia, ultimately resulting in tumor advancement and chemo-resistance. Our study aimed to examine the link between autophagy mark...

Full description

Saved in:
Bibliographic Details
Published inInternational journal of molecular sciences Vol. 25; no. 1
Main Authors Danish, Farheen, Qureshi, Muhammad Asif, Mirza, Talat, Amin, Wajiha, Sufiyan, Sufiyan, Naeem, Sana, Arshad, Fatima, Mughal, Nouman
Format Journal Article
LanguageEnglish
Published MDPI AG 01.01.2024
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:High-grade gliomas are extremely fatal tumors, marked by severe hypoxia and therapeutic resistance. Autophagy is a cellular degradative process that can be activated by hypoxia, ultimately resulting in tumor advancement and chemo-resistance. Our study aimed to examine the link between autophagy markers’ expression in low-grade gliomas (LGGs) and high-grade gliomas (HGGs). In 39 glioma cases, we assessed the protein expression of autophagy markers LC3B, SQSTM1/p62, and DRAM by immunohistochemistry (IHC) and the mRNA expression of the autophagy genes PTEN, PI3K, AKT, mTOR, ULK1, ULK2, UVRAG, Beclin 1, and VPS34 using RT-qPCR. LC3B, SQSTM1/p62, and DRAM expression were positive in 64.1%, 51.3%, and 28.2% of glioma cases, respectively. The expression of LC3B and SQSTM1/p62 was notably higher in HGGs compared to LGGs. VPS34 exhibited a significant differential expression, displaying increased fold change in HGGs compared to LGGs. Additionally, it exhibited robust positive associations with Beclin1 (rs = 0.768), UVRAG (rs = 0.802), and ULK2 (rs = 0.786) in HGGs. This underscores a potential association between autophagy and the progression of gliomas. We provide preliminary data for the functional analysis of autophagy using a cell culture model and to identify potential targets for therapeutic interventions.
ISSN:1422-0067
1422-0067
DOI:10.3390/ijms25010572