Asperuloside regulates the proliferation, apoptosis, and differentiation of chronic myeloid leukemia cell line K562 through the RAS/MEK/ERK pathway

Context: Chronic myeloid leukemia (CML) is a malignant hematopoietic stem cell disease caused by excessive proliferation and abnormal differentiation of hematopoietic stem cells. Asperuloside (ASP) is considered to have good biological activity and may be a good anti-CML drug.

Objective: This study aimed to explore the effects and possible mechanisms of ASP on the biological behavior of K562 cells based on RNA-seq.

Materials and methods: The IC₅₀ of ASP in K562 cells was calculated by the concentration-effect curve. Cell viability, Apoptosis, and differentiation were detected by CCK8, flow cytometry, benzidine staining, and WB analysis, respectively. Further, RNA-seq was used to analyze the possible mechanism of ASP regulating K562 cells.

Results: ASP significantly inhibited the proliferation, and promoted Apoptosis and differentiation of K562 cells. A total of 117 differentially expressed genes were screened by RNA-seq, mainly involved in the Ras/MEK/ERK pathway. PD98059 was used to inhibit the Ras/MEK/ERK pathway in K562 cells, and results confirmed that PD98059 could not only inhibit the Ras/MEK/ERK pathway, but also inhibit the regulation of ASP on the proliferation and differentiation of K562 cells.

Conclusion: ASP inhibited the proliferation, promoted Apoptosis and differentiation of K562 cells by regulating the Ras/MEK/ERK pathway, and played a good anti-CML role.

Anti-cancer; Iridoid; Pharmacological research; RNA-seq.