It exerts its effect via tumor protein p53 (mutation (Takayama et al
It exerts its effect via tumor protein p53 (mutation (Takayama et al., 2006). in HC-treated cells was observed from 12 h onwards. Higher apoptotic cell death in HC-treated cells compared to 5-FU-treated cells (leaves (PBLs) have been used for centuries throughout Asia, and by ayurvedic practitioners for the prevention and treatment of cancers (Garodia et al., 2007). While betel quid (BQ) chewing was found to be carcinogenic and BQ components were shown to induce inflammatory Mogroside IVe response in oral mucosal cells (Jeng et al., 2000, 2001; Trivedy et al., 2002). PBL was shown to have antioxidant, antimutagenic, anticarcinogenic, antiplatelet, and anti-inflammatory effects (Jeng et al., 2002; Chang et al., 2007; Kumar et al., 2010; Gundala and Aneja, 2014). In the past, various studies revealed the potential cytotoxic effect of PBL extracts on various cancer cells such as colon (Ng et al., Mogroside IVe 2014), cervical (Widowati et al., 2013), breast (Abrahim et al., 2012), and prostate (Abrahim et al., 2012). Among the many bioactive compounds of PBL, hydroxychavicol (HC) has been the most widely reported for its cytotoxic effect (Kumar et al., 2010; Gundala et al., 2014). Studies have shown its involvement in reactive oxygen species (ROS) generation (Gundala et al., 2014), DNA damage (Chen et al., 2000), cell cycle deregulation and apoptosis (Chang et al., 2002; Jeng et al., 2004; Chakraborty et al., 2012; Rahman et al., 2014). Abnormalities in cell Rabbit Polyclonal to PIAS4 proliferation and the evasion of programmed cell death (apoptosis) are the two prominent hallmarks of cancer (Hanahan and Weinberg, 2011). Disruptions in cell signaling pathways, such as the mitogen-activated protein kinase (MAPK) pathway, play an important role in cancer development and progression (Dhillon et al., 2007). Among the MAPK family proteins, the c-Jun N-terminal kinase (JNK) and P38 MAPK are associated with colon cancer, whereas the extracellular signal-regulated kinase (ERK) is linked with rectal cancer (Slattery et al., 2012). Various fundamental cellular processes involved in cancer progression, such as apoptosis, proliferation, differentiation, motility, stress response, and survival, are controlled by the JNK and P38 MAPK signaling pathways (Wagner and Nebreda, 2009). Many reports associated the disruption of cell cycle and induction of apoptosis in cancer cells by natural products with the signal transduction regulation (Sarkar et al., 2009; Chakraborty et al., 2012; Angulo et al., 2017). The first-choice chemotherapy drug for colon cancer has been 5-fluorouracil (5-FU); however, it has limited effectiveness due to its short biological half-life (Wigmore et al., 2010). It exerts its effect via tumor protein p53 (mutation (Takayama et al., 2006). Drug resistance has been a great challenge in the treatment of colon cancer. Any compounds that can exert an inhibitory effect on mutant cells could therefore serve as potential drugs for this purpose. The HT-29 Mogroside IVe cell line is a model of leaf; HC, hydroxychavicol; IC50, half maximal inhibitory concentration. Open in a separate window Open in a separate window Open in a separate window 3.3. HC induced G0/G1 cell cycle arrest in HT-29 cells The effects of 5-FU and HC on the cell cycle of HT-29 cells were established by cell cycle analysis using Mogroside IVe a flow cytometer. The 50 mol/L treatment of 5-FU induced cell cycle arrest at the G1/S phase from 12 to 30 h, which was deduced by the accumulation of cells at the S phase and the decreased population of cells in the G2/M phase (Fig. 2). Treatment with HC (30 g/mL) induced.