Targeting Features of Curaxin CBL0137 on Hematological Malignancies In Vitro and In Vivo.
Timur I FetisovAnna A BorunovaAlina S AntipovaElena E AntoshinaLubov S TrukhanovaTatyana G GorkovaSvetlana N ZuevskayaAlexei MaslovKaterina GurovaAndrei GudkovEkaterina A LesovayaGennady A BelitskyMarianna G YakubovskayaKirill I KirsanovPublished in: Biomedicines (2023)
The anticancer activity of Curaxin CBL0137, a DNA-binding small molecule with chromatin remodulating effect, has been demonstrated in different cancers. Herein, a comparative evaluation of CBL0137 activity was performed in respect to acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), chronic myeloid leukemia and multiple myeloma (MM) cultured in vitro. MTT assay showed AML and MM higher sensitivity to CBL0137's cytostatic effect comparatively to other hematological malignancy cells. Flow cytometry cell cycle analysis revealed an increase in subG1 and G2/M populations after CBL0137 cell treatment, but the prevalent type of arrest varied. Apoptosis activation by CBL0137 measured by Annexin-V/PI dual staining was more active in AML and MM cells. RT2 PCR array showed that changes caused by CBL0137 in signaling pathways involved in cancer pathogenesis were more intensive in AML and MM cells. On the murine model of AML WEHI-3, CBL0137 showed significant anticancer effects in vivo, which were evaluated by corresponding changes in spleen and liver. Thus, more pronounced anticancer effects of CBL0137 in vitro were observed in respect to AML and MM. Experiments in vivo also indicated the perspective of CBL0137 use for AML treatment. This in accordance with the frontline treatment approach in AML using epigenetic drugs.
Keyphrases
- acute myeloid leukemia
- allogeneic hematopoietic stem cell transplantation
- induced apoptosis
- cell cycle arrest
- cell cycle
- acute lymphoblastic leukemia
- small molecule
- endoplasmic reticulum stress
- dna binding
- flow cytometry
- signaling pathway
- cell death
- oxidative stress
- cell proliferation
- multiple myeloma
- transcription factor
- chronic myeloid leukemia
- stem cells
- dna methylation
- cell therapy
- squamous cell carcinoma
- dna damage
- genome wide
- high throughput
- endothelial cells
- epithelial mesenchymal transition
- replacement therapy
- cancer therapy
- combination therapy
- young adults
- genetic diversity
- mesenchymal stem cells