Comparative Analysis of HULC, NEAT1, FENDRR, and EMG3 Long Non-coding RNA Expression Profiles in K562 Chronic Myeloid Leukemia Cells Treated with Hydroxycarbamide, Cyclophosphamide, and Cytarabine Chemotherapy Agents Versus Thiosemicarbazone Complexe

Background: Chronic myeloid leukemia (CML) is a complex hematological malignancy characterized by abnormal myeloid cell proliferation. Long non-coding ribonucleic acids (lncRNAs) have gained attention for their role in cancer, including CML. This study investigated the expression patterns of lncRNAs NEAT1, EMG3, FENDRR, and HULC in K562 CML cells under various drug treatments. More precisely, the study evaluated the impact of chemotherapy agents hydroxycarbamide (HU), cyclophosphamide (CP), cytarabine (Arac), and thiosemicarbazone (TSC) complexes on lncRNA expression profiles. Methods: The K562 CML cell line was treated with chemotherapy drugs and TSC complexes at varying concentrations for different periods. Then, RNA extraction and complementary DNA synthesis were performed, and the expression levels of HULC, NEAT1, FENDRR, and EMG3 lncRNAs were examined by real-time polymerase chain reaction. The results were statistically analyzed using REST software. Results: CP treatment resulted in the significant upregulation of NEAT1, EMG3, and HULC, while HULC exhibited downregulation at lower concentrations and longer durations. HU treatment led to the consistent upregulation of FENDRR and HULC, indicating concentration-dependent responses. Moreover, combined CP and Arac treatment revealed concentration-dependent effects on lncRNAs, with NEAT1 and EMG3 displaying optimal responses at specific concentrations and durations. Complex drug treatments yielded diverse outcomes. NEAT1 responded positively to Complex 1 but negatively to Complex 3. In addition, EMG3 showed marked upregulation under Complex 3. FENDRR and HULC demonstrated variable expression changes under different concentrations and durations, emphasizing the intricate regulatory dynamics. TSC nickel and copper treatments had concentration-dependent effects on lncRNA expression. Finally, NEAT1, EMG3, and HULC displayed sensitivity to specific concentrations and durations, highlighting their potential responsiveness to these treatments. Conclusion: Overall, our findings provide insights into the dynamic expression of lncRNAs in response to drug treatments in CML. It is expected that understanding these regulatory mechanisms paves the way for targeted therapeutic interventions in CML, optimizing treatment strategies for improved patient outcomes.