Autophagy in combination therapy of temozolomide and IFN-γ in C6-induced glioblastoma: role of non-coding RNAs

Author:

Bashiri Hamideh1ORCID,Moazam-Jazi Maryam2,Karimzadeh Mohammad Reza3,Jafarinejad-Farsangi Saeideh4ORCID,Moslemizadeh Amirhossein5,Lotfian Marziyeh6,Karam Zahra Miri7,Kheirandish Reza8,Farazi Mohammad Mojtaba1

Affiliation:

1. Physiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, 76198-13159, Iran

2. Cellular & Molecular Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, 19857-17413, Iran

3. Department of Medical Genetics, School of Medicine, Bam University of Medical Sciences, Bam, 76198-13159, Iran

4. Student Research Committee, Kerman University of Medical Sciences, Kerman, 76198-13159, Iran

5. Department of Immunology, Tehran University of Medical Sciences, Tehran, Iran

6. Endocrinology & Metabolism Research Center, Institute of Basic & Clinical Physiology Sciences, Kerman University of Medical Sciences Kerman, 76198-13159, Iran

7. Cardiovascular Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, 76198-13159, Iran

8. Department of Pathobiology, Faculty of Veterinary Medicine, Shahid Bahonar University of Kerman, Kerman, 76198-13159, Iran

Abstract

Aim: We predicted the modulation of autophagy and apoptosis in response to temozolomide (TMZ) and IFN-γ based on changes in the expression of non-coding RNAs in C6-induced glioblastoma (GBM). Materials & methods: Each rat received an intraperitoneal injection of TMZ (7.5 mg/kg) and/or IFN-γ (50,000 IU). Results: The reduced expression of H19 and colorectal neoplasia differentially expressed ( CRNDE) was associated with a reduction in autophagy in response to TMZ, IFN-γ and TMZ + IFN-γ therapy, whereas the decreased level of miR-29a (proapoptotic miRNA) was associated with an increase in apoptosis. Conclusion: It appears that H19 promotes switching from autophagy to apoptosis in response to combination therapy of TMZ and IFN-γ through the miR-29a/autophagy-related protein 9A (ATG9A) pathway in C6-induced GBM.

Funder

Kerman University of Medical Sciences

Publisher

Future Medicine Ltd

Subject

Oncology,Immunology,Immunology and Allergy

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