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  • br Fucoidan act as anticancer drug by arresting cell cycle

    2020-08-02


    4.2. Fucoidan act as anticancer drug by arresting Pyocyanin of HepG2 cancer cells
    It is well established that the cancer cells have ability to go for continuous proliferation which is essentially associated with the de-regulation of the cell cycle progress and promotion of invasion [31]. Fucoidan constituted HepG2 cancer cells that were showed significant (p ≤ 0.05) accumulation of proliferative cells in the G0/G1 phase of the cell cycle in a concentration dependent manner. The observed cell ac-cumulation in the G0/G1 phase of cell cycle was about 65–85% (50–200 μg/ml) over the untreated control cells (50%) and comparable to the quercetin standard (87%) (Fig. 4). Moreover, fucoidan sig-nificantly arrested the EJ cell in G1 phase of the cell cycle with 
    concentration dependent manner and stated that growth inhibitory effect of fucoidan in EJ cells was reflected in terms of arresting the G1 phase of the cell cycle [28]. In previous study depicted that the ethyl acetate fraction of brown seaweed, T. conoides arrested the G0/G1 phase of cell cycle about 1.3–1.7 fold higher than the untreated control cells [7]. Most of reports also highlighted the similar sort of results that were depicted the functional role of fucoidan in cell cycle arrest at G1 phase. It was consistently defined due to the down regulation of cyclin (D1, D2, CDK2 & CDK4) and up regulation of p21/WAF1/CIP1 in various cancer cells. In addition, increased level of CDK inhibitors like p21 and phosphorylation inhibition played an imperative role in G1 arrest however the cell cycle arrested by fucoidan differ from some extent based on the type of cancer cells [18,24].
    4.3. Understanding the anti-cancer effect of fucoidan through apoptosis induction, genetic damage and other associated characters in HepG2 cancer cells
    One or other way of the cancer cell initiation and continuous pro-gression are due to alteration in apoptotic pathway and predominantly in hepatocarcinogenesis through dysregulation of apoptosis [35]. Therefore, it is essential to inhibit/restrain cancer cells development by adapting naturally occurring dietary plants which have enormous po-tential to induce apoptosis in cancer cells [36]. In the present pragmatic study with respect to fucoidan induced genetic damage and apoptosis in HepG2 cancer cells were analyzed with comet assay and annexin V-FITC assay kit, respectively. Genetic damage was scoured in terms of various factor such as head, tail and tail moment by comet assay soft-ware whereas apoptosis analyzed in four groups of cells by flowcyt-ometer (Figs. 5 and 6&A). The fucoidan induced genetic damage and apoptosis in HepG2 cancer cells were regarded to be 45–50% when compared to the untreated control cells (Table 2 & Fig. 6). The degree of genetics damage enhanced by fucoidan was reflected in terms of tail moment that were revealed about 12.8, 7.1 & 3.8 folds higher than that of untreated control cells (Table 2). On other hand, fucoidan enhanced total apoptotic cells were statistically (p ≤ 0.05) significant and effec-tively boosted than the standard of quercetin at their maximum con-centration (44%). These results concluded that the inhibition of HepG2 cancer cell proliferation and cell arrest by the effect of fucoidan can be significantly well correlated with their genetic damage and apoptosis. Eventually, genetic damage played major role on cell death/senescence that can either be dependent or independent of the immune system [37]. However, the natural link between early tumorigenic events and the induction of the p53-mediated checkpoints that were constituted a r> Fig. 4. Cell cycle phase distribution of exponentially proliferative HepG2 cancer cells and G1 phase of the cell cycle arrest induced by fucoidan constituted with nuance of concentration for 48 h. Histogram image regarded after cells stained with PI by flowcytometer.
    barrier to tumour progression [38]. In the recent study was stated about 14–42% of apoptosis by altering nuclear condensation and also by mitochondrial membrane potential (ΔΨm) in HepG2 cancer cells con-stituted with fucoidan of T.conoides [7]. Other reports on different cancers such as hematopoietic, lung, breast and colon have clearly exhibited that fucoidan induced the apoptosis through cytoplasmic shrinkage and chromatin condensation [18]. Another report also proved regarding fucoidan induced apoptosis through activation of caspase-cascade path and regulation of signaling molecules such as c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), p38 signaling, Bcl-2 protein expression and Akt signaling. Fur-ther, fucoidan provoked apoptosis by shifting mitochondrial functions and accumulated dead cells/apoptotic cells in the G0/G1 phase of the