Abstract
Clausenidin is a pyranocoumarin majorly found in medicinal herbs of the Rutaceae family used to treat cancer patients locally in Asia. The compound is presumed to have anti-cancer cell effect but its exact mechanism of action is still unknown. The study aimed to evaluate the effect of pure clausenidin on p53-mediated apoptosis as well as other cell death pathways in colon cancer (HT-29) cell lines. The anti-proliferative effect of clausenidin by cell cycle and annexin V assay using flow cytometry was evaluated. Morphological analysis of the treated cells was performed using scanning and transmission electron microscopy. Furthermore, the effect of p53 mRNA on cell cycle and apoptosis-related genes and proteins in clausenidin-treated HT-29 cells was investigated using qPCR and Western blot assays, respectively. Clausenidin induced a p53 dependent G0/G1 cell cycle arrest in HT-29 cells. It was also observed that the anti-cancer cell effect of clausenidin occurred via p53 mediated activation of p21, bax and transrepression of survivin and bcl 2 that culminated in the apoptosis of colon cancer cells. The transmission electron microscopy (TEM) micrographs confirmed the occurrence of apoptosis in clausenidin-treated HT-29 cells. Clausenidin is a potent anti-HT-29 cell agent that can be used to treat colon tumors. Key words: Clausenidin, p53, p21, apoptosis, cell cycle.
Highlights
The protein, Tumor suppressor protein 53 (P53) (TP53) was first identified in 1979 and named after its molecular weight, which is 53 kDa (Levine et al, 1991)
It was observed that the anti-cancer cell effect of clausenidin occurred via p53 mediated activation of p21, bax and transrepression of survivin and bcl 2 that culminated in the apoptosis of colon cancer cells
Human colorectal adenocarcinoma cell line (HT-29) cell line was purchased from American Type Culture Collection (ATCC) and maintained in Dulbecco’s Modified Eagle’s Medium (DMEM) medium supplemented with 10% fetal bovine serum (FBS)
Summary
The protein, P53 (TP53) was first identified in 1979 and named after its molecular weight, which is 53 kDa (Levine et al, 1991). Deletion of the p53 gene in cells leads to the decrease in rate of apoptosis (Slatter et al, 2011; Vikhanskaya et al, 2007). Because this protein play a profound role in the maintenance of cell integrity, it is often referred to as ‘guardian of the genome’ (Lane, 1992). Previous study reported that clausenidin (Figure 1) isolated from C. excavata induces caspase-dependent cell death in colon cancer cell line (Waziri et al, 2016). The study aims to unravel the effect of clausenidin on p53-dependent-cell cycle arrest and apoptosis in colon cancer cell line
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