Iranian biomedical journal · 2026
Effect of HIF-1α and LDHA Blockade on Gene Expression of Tumor Immune Evasion in Myeloid Leukemia Cell Lines.
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Eskandari Tamana, Shams Mehrshad, Khanari Ali, Kahrizi Amir, Asgarian-Omran Hossein, Valadan Reza, Tehrani Mohsen, Taghiloo Saeid
Аннотация
BACKGROUND: Tumor cells utilize metabolic reprogramming to obtain the energy required for rapid proliferation. In this study, we blocked two key factors, hypoxia-inducible factor 1-alpha (HIF-1α) and lactate dehydrogenase (LDHA), in the metabolic pathway in acute myeloid leukemia (AML) cell lines to evaluate their effect on the expression of genes involved in tumor evasion.
METHODS: Silibinin and sodium oxamate, as HIF-1α and LDHA blockers, respectively, were used to treat K-562 and HL-60 cells. The MTT assay was used to assess cell viability, and quantitative reverse transcription PCR was used to measure the mRNA expression levels of PD-L1, CD47, and CD155.
RESULTS: Both K-562 and HL-60 cells showed a significant decrease in CD47 expression. Additionally, HL-60 cells indicated a significant suppression of CD155 expression. In contrast, PD-L1 expression remained unchanged after treatment.
CONCLUSION: Our findings suggest that blocking signaling pathways involved in metabolic reprogramming of cancer cells could be a promising approach for modulating the expression of certain immune checkpoint ligands, warranting further investigation.
METHODS: Silibinin and sodium oxamate, as HIF-1α and LDHA blockers, respectively, were used to treat K-562 and HL-60 cells. The MTT assay was used to assess cell viability, and quantitative reverse transcription PCR was used to measure the mRNA expression levels of PD-L1, CD47, and CD155.
RESULTS: Both K-562 and HL-60 cells showed a significant decrease in CD47 expression. Additionally, HL-60 cells indicated a significant suppression of CD155 expression. In contrast, PD-L1 expression remained unchanged after treatment.
CONCLUSION: Our findings suggest that blocking signaling pathways involved in metabolic reprogramming of cancer cells could be a promising approach for modulating the expression of certain immune checkpoint ligands, warranting further investigation.