Autophagy in combination therapy of temozolomide and IFN-γ in C6-induced glioblastoma: role of non-coding RNAs.
Hamideh BashiriMaryam Moazam-JaziMohammad Reza KarimzadehSaeideh Jafarinejad-FarsangiAmirhossein MoslemizadehMarziyeh LotfianZahra Miri KaramReza KheirandishMohammad Mojtaba FaraziPublished in: Immunotherapy (2023)
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.
Keyphrases
- endoplasmic reticulum stress
- oxidative stress
- combination therapy
- cell death
- diabetic rats
- dendritic cells
- immune response
- cell cycle arrest
- signaling pathway
- high glucose
- poor prognosis
- long non coding rna
- cell proliferation
- long noncoding rna
- stem cells
- high grade
- mesenchymal stem cells
- bone marrow
- smoking cessation