16-Hydroxycleroda-3,13-dien-15,16-olide deregulates PI3K and Aurora B activities that involve in cancer cell apoptosis

Clerodane Diterpene Ameliorates Inflammatory Bowel Disease and Potentiates Cell Apoptosis of Colorectal Cancer

“…Therefore, by observing the altered levels of cleavage caspase-8, caspase-9, and Bcl-2, the type of chemical-induced apoptosis could be putatively addressed. Previous studies of HCD-induced cancer cell death were focused on autophagic cell death and intrinsic apoptosis [15,16,33,34]. To the best of our knowledge, this study is the first to show the involvement of HCD-induced extrinsic apoptosis in colorectal cancer.…”

In vitro and in vivo characterization of a benzofuran derivative, a potential anticancer agent, as a novel Aurora B kinase inhibitor

“…Similarly, S6 suppressed the proliferation and colony formation of these three cell lines in a dose-dependent manner. In previous studies, higher expression levels of Aurora B were found in HepG2 cells, SW620 cells and HeLa cells [7,41], which may explain why these cell lines were more sensitive to S6 treatment. Similar to studies on VX680 and ZM447435 [6], significant down-regulation of phospho-H3 (Ser10) and elevation of the percentage of cells in the G2/M phase upon S6 treatment further confirmed the inhibition of the endogenous Aurora B kinase activity in these cells.…”

BCR-ABL Hits at Mitosis; Implications for Chromosomal Instability, Aneuploidy and Therapeutic Strategy

“…Another natural compound, 16-hydroxycleroda-3,13-dien-15,16-olide (PL3), one of the clerodane diterpenoid compounds isolated from Polyalthia longifolia, induced degradation of Aurora B, mitotic checkpoint dysfunctions and finally led to cell death of CML cells, including the T315I-mutated BCR-ABL+ BA/F3 cells (Lin et al, 2011). Additionally, it reversed the sensitivity to imatinib of T315I-mutated CML cells in comparizon to treatment only with imatinib.…”