Additional considerations in cancer cell radioresistance, integrin αvβ3 and thyroid hormones.
Gennadi V GlinskyAleck HercbergsShaker A MousaHung-Yun LinPaul J DavisPublished in: Endocrine research (2024)
In the current study, we report that genome-wide gene expression profiling analysis of human glioblastoma (GBM) and acute myelocytic leukemia (AML) cell lines exposed in vitro to noncytotoxic doses of CMT has identified decreased expression of discrete trios of genes each of which was previously linked to cancer cells' radioresistance. Following the CMT treatment in AML cells, expression of PARP9, PARP15 and STAT3 genes was significantly reduced, while in GBM cells, expression of PRKDC, EGFR and CCNDI was significantly decreased by the drug. Notably, a broader spectrum of genes implicated in cancer cells' radioresistance was observed in primary patient-derived GBM cells after the CMT treatment. Extensive additional experimental and clinical studies are indicated, including analyses of individual patient tumor genomics and of an array of different tumor types to define the sub-sets of tumors manifesting radioresistance in which tetrac-based agents may be expected to enhance therapeutic effects of radiation.
Keyphrases
- genome wide
- induced apoptosis
- cell cycle arrest
- poor prognosis
- genome wide identification
- acute myeloid leukemia
- dna methylation
- small cell lung cancer
- dna damage
- dna damage response
- endothelial cells
- oxidative stress
- copy number
- high resolution
- endoplasmic reticulum stress
- signaling pathway
- bone marrow
- emergency department
- transcription factor
- epidermal growth factor receptor
- bioinformatics analysis
- cancer stem cells
- long non coding rna
- combination therapy
- respiratory failure
- acute lymphoblastic leukemia
- hepatitis b virus
- drug induced
- electronic health record