Transcriptional and Proliferative Heterogeneity Among Leukemia Cell Lines: A Baseline Characterization of Epigenetic and DNA-Repair Pathways
<span style="color: rgb(17, 17, 17); font-family: Poppins; font-size: 14px;">Leukemia comprises biologically diverse hematologic malignancies with subtype-specific molecular characteristics that influence disease behavior and therapeutic response. To establish baseline transcriptional and proliferative profiles across representative leukemia models, we quantified the expression of TRDMT1 (DNMT2), RAD51, TET2, and XPA in six leukemia cell lines (ARH-77, CCRF-SB, HL-60, K-562, Kasumi-1, SUP-T1) and assessed their growth dynamics over a 96-hour period. qPCR analysis revealed significant differences in the baseline expression of all four genes among cell lines. ARH-77 showed the highest expression levels for each gene, while HL-60 and K-562 generally displayed lower expression. Growth assays demonstrated variable proliferation rates, with SUP-T1 and CCRF-SB exhibiting the greatest increases in cell number. To contextualize these findings within clinical disease patterns, expression of the same genes was examined in hematologic malignancies using the BloodSpot dataset (GSE13159). Public transcriptomic data demonstrated heterogeneous subtype-dependent expression ranges for TRDMT1, RAD51, TET2, and XPA, and these patterns aligned with the variability observed across the leukemia cell lines. Together, these results provide a comparative molecular and phenotypic baseline for commonly used leukemia models and establish a reference framework for subsequent functional and therapeutic studies.</span>
Authors
- Venhar Çınar (ORCID: https://orcid.org/0000-0003-1544-8994)
- Mai R. S. Abusalim (ORCID: https://orcid.org/0000-0002-2778-0380)
- Ayşe Uz
- Serpil Taheri
- Sevim Ecmel Mehmetbeyoğlu Duman
- Amine Sudenur Sancak
Publication Details
- Journal
- Erciyes University - AVESIS
- Published
- 2025-12-01
- Primary Topic
- Acute Myeloid Leukemia Research
- Type
- article
- Field-Weighted Citation Impact
- 0.00