CMK

The PI3K Inhibitor, LY294002, Reduces the Cell Viability of CMK and MOLM-13 AML Cell Lines

Acute myeloid leukemia (AML), accounting for 80% of blood cancer cases, has a poor prognosis. Despite existing treatments, the disease's heterogeneity necessitates novel therapies. Şansaçar et al. explored the anticancer effects of PI3K and HDAC inhibition on CMK and MOLM-13 AML cell lines.

LY294002, a specific PI3K inhibitor, blocks AKT phosphorylation by binding to the kinase's ATP site, suppressing the PI3K/AKT pathway crucial for cancer cell proliferation. We treated CMK and MOLM-13 cells with 1–20 µM LY294002 (Fig. 1). Both cell lines showed significant viability reduction at low micromolar doses, with similar sensitivity (IC20: CMK = 1 µM, MOLM-13 = 2.8 µM). Additional HDAC inhibitors (SAHA, Tubastatin A, PCI-34051) were tested (Fig. 1a, b). Our findings suggest LY294002 effectively inhibits leukemia cell proliferation via PI3K/AKT pathway suppression.

Anticancer Activity of AuNPs and Ultrasound Against Pediatric Acute Leukemia Cell Lines

Pediatric acute leukemia remains a challenging disease with limited therapeutic options. Green-synthesized gold nanoparticles (AuNPs) and ultrasound (US) therapy have emerged as potential anticancer strategies due to their biocompatibility and targeted effects. Guo's team explored the synergistic anticancer effect of Memecylon edule-mediated AuNPs combined with US therapy against pediatric acute leukemia cell lines (Kasumi-1), while minimizing damage to normal cells (CMK).

Flow cytometry is being used to investigate AuNPs and US treatment in both Kasumi-1 and CMK cell lines by determining the number of viable cells (Fig. 2). Figure 3 presented the Kasumi-1 and CMK cell median counts from five repeated tests. These outcomes revealed a modest reduction in the ratio from 67.1 ± 3.2 to 55 ± 6.2% of the viable cells after application of the synthesized AuNPs to normal CMK cell lines treated with US. In contrast, the total number of viable Kasumi-1 cancer cells decreased dramatically after combined AuNPs and US treatment, from 60.4 ± 4.5 to 27.7 ± 5.9%. Therefore, these findings suggest that Kasumi-1 cancer cells are more susceptible to US-induced cell damage than CMK cells. The findings, on the other hand, show that combining AuNPs with cell cultures resulted in a significant increase in cancer cell death, thus demonstrating the synergistic effect of AuNPs and US disruption. In addition, normal CMK cells appear to be highly resistant to the synergistic impact. As a result of the study, the current findings provide promise in the destruction of cancer cells, especially when compared to some of the standard approaches for cancer cell destruction.