This study investigates the effects of Flavokawain B (FKB) on the growth and development of metastatic hepatocellular carcinoma. HepG2 cells were used in this study and a neutral red assay was performed to determine the anti-proliferation effects of FKB at varying concentrations. Cell scratch and exclusion zone assays were performed to assess the inhibitory effects of FKB on the cell migration and invasion and relative mRNA levels were quantified using the RT-qPCR. FKB inhibited the proliferation of HepG2 cells at an IC50 value of 28 µM, which conforms to its apoptosis-inducing effects. Cell migration and invasion were significantly inhibited at 7, 14 and 28 µM of FBK. UCK2 expression was significantly downregulated after FKB treatments. Inhibition of STAT3 expression subsequently induced the downregulation of VEGF and HIF-1α expressions. Our data suggest that FKB inhibits HepG2 proliferation and suppresses its metastasis abilities, thus providing a potential alternative and viable strategy against HCC.

Hepatocellular carcinoma (HCC) is currently the third most common cancer-related death worldwide. HCC is associated with a high mortality rate due to early recurrence and its distant metastasis to the nearby organs. Current treatment options include surgical removal and transplantation as well as chemotherapy, which remains a major challenge to patient treatment. Flavokawain B (FKB) is a natural bioactive molecule capable of providing effective therapy against this life-threatening disease. This study investigates the effects of Flavokawain B (FKB) on the growth and development of metastatic hepatocellular carcinoma. HepG2 cells were used in this study and a neutral red assay was performed to determine the anti-proliferation effects of FKB at varying concentrations. Cell scratch and exclusion zone assays were performed to assess the inhibitory effects of FKB on cell migration and invasion and relative mRNA levels were quantified using the RT-qPCR. FKB inhibited the proliferation of HepG2 cells at an IC50 value of 28 µM, which conforms to its apoptosis-inducing effects. Cell migration and invasion were significantly inhibited at 7, 14, and 28 µM of FBK. UCK2 expression was significantly downregulated after FKB treatments. Inhibition of STAT3 expression subsequently induced the downregulation of VEGF and HIF-1α expressions. Our data suggest that FKB inhibits HepG2 proliferation and suppresses its metastasis abilities, thus providing a potential alternative and viable strategy against HCC.

Mitracarpus hirtus (L.) DC. is a weed plant commonly used for the treatment of eczema. The potential of the plant to treat cancer has not been emphasized, hence the need to explore its anticancer potential. M. hirtus was extracted and subjected to petition with solvents of increasing polarity. Its cytotoxic potential was evaluated against MCF-7, HepG2, and HeLa cells using the Neutral red assay and further verified through morphological assessment and DNA fragmentation assay. Crude chloroform fraction (CCF) displayed a cytotoxic effect on all the cell lines with low IC 50 concentrations ranging from 11 -17.87 µg/mL. Morphological assessment of MCF-7 exposed to CCF indicates apoptotic cell death and is further confirmed by its DNA fragmentation. Our data suggest that M. hirtus is a potential source for mining anticancer agents.