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    2020-08-02


    Table 1
    Percentage of Diphenylterazine (DTZ) arrest induced by fucoidan in HepG2 cancer cells.
    Concentration (μg/ml) Cell cycle arrest (%)
    The values are presented as mean ± SD in triplicate and significance (p ≤ 0.05) determined by student t-test between fucoidan treated vs. untreated control. 
    was well correlated with their DNA damage and apoptosis induction. In addition, fucoidan induced DNA damage and apoptosis was further confirmed in terms of change in the morphology of HepG2 cancer cell by the effect of fucoidan on nuclear condensation and shift of mi-tochondrial membrane potential (ΔΨm) that were detected with Hoechst and JC-1 stains, respectively by fluorescence microscopy (Fig. 6B & C).
    4. Discussion
    4.1. Anti-cancer effect of fucoidan against HepG2 cancer cell line
    In general, mutated gene causes cancer by promoting uncontrolled cell growth and cell division through violating normal cellular function, mainly cell cycle arrest and programmed cell death as well. If not in-hibited/restrain the cancer cell growth, the cell has got accelerated the angiogenesis as well as stimulates the metastasis. In fact, dietary plants are encompassed in terms of medical values that can serve as invaluable source for anticancer drug development. Moreover, the anti-cancer drugs available in the dietary supplement are quite safe and effective regulation of normal cell metabolism and also accelerating the pro-grammed cell death by interrupting the uncontrolled cell proliferation [28]. It is well-know that the brown seaweeds are being used as med-icinal dietary supplements in most of the Asian countries. All the dietary brown seaweeds have fucoidan, a sulphated polysaccharide which is substantially prevalent in various biological properties such as antioxidant, anticancer, anticoagulant, immunomodulatory, immune-response and anti-inflammatory [29,12]. Such as other brown seaweed, Turbinaria conoides has broadly used as an edible seaweed and also included with fucoidan displaying in different sorts of biological ac-tivities that were massively demonstrated under in-vitro/in-vivo [30,7]. In the present pragmatic investigation was carried out in terms of an-ticancer effect of fucoidan in HepG2 cancer cell line by analyzing cell proliferation, colony formation, cell migration, cell cycle progression, genetic damage and apoptotic cell death. Fucoidan induced genetic damage and apoptosis was further confirmed by visualizing the cell morphological changes by Hoechst staining and alteration of mi-tochondrial membrane potential by JC-1 staining. The results of cell viability clearly demonstrated that only ≤ 50% cells were found to be viable when HepG2 cells constituted with fucoidan and the effect was merely relay on concentration dependent. As a result, the fucoidan was significantly (p ≤ 0.05) reduced the proliferation of the HepG2 cancer cells and the reduction potential was as comparable as quercetin stan-dard. Similarly, in the recent in-vitro studies demonstrated that fucoidan
    Fig. 3. Fucoidan inhibited HepG2 cancer cell migration was analyzed by wound healing assay. (A) Wound healing image was captured under inverted light microscope. (B) Wound healing calculated and expressed as the per-centages of means ± standard deviation of three independent experiments. *p ≤ 0.05, vs. the untreated control (0 μg/ml).
    from T. conoides explored dose-dependent anti-proliferation in EJ and HepG2 cancer cells [29,7]. Essentially, colony formation assay was conducted further to ac-quire the anti-cancer effect of fucoidan based on the proliferative po-tential and prolong viability of HepG2 cancer cells. It was observed that fucoidan caused a concentration-dependent decline in the colony forming ability of HepG2 cancer cells and found more effective than Diphenylterazine (DTZ) that of quercetin standard. Decline of colony formation ability by var-ious concentration of fucoidan was exactly about 1.3, 1.8 and 2.7 fold higher than that of untreated control (100%; Fig. 2). This result clearly divulged that fucoidan possess significant (p ≤ 0.05) anti-proliferative effect against HepG2 cancer cells. Indeed, cell migration is one the essential processes during the cancer cell development and metastatic spread [31]. In this study, percentage of cell migration was suppressed in response to an increase in fucoidan concentration (50, 100, 200 μg/ ml) and the suppressive effect was about 1.2, 1.5 and 1.9 fold over the untreated control (90%), respectively (Fig. 3). The wound healing effect of fucoidan was also exhibited in a concentration-dependent manner and significantly (p ≤ 0.05) higher than that of quercetin standard (57%) (Fig. 3). In-vitro anticancer effect of fucoidan on the colorectal carcinoma cells, DLD-1 and HCT-116 was reported to be inhibited the colony formation of cancer cells at the concentration of 200 μg/ml and found no cytotoxicity up to 400 μg/ml [32]. Recent studies revealed that most of the marine plant derived anticancer drugs including fu-coidan acted in dose-dependent decline of colony formation ability and cell migration in HepG2 cancer cells. In the present study was totally obsessed with similar result, regarding the effect of fucoidan on colony formation and cell migration assays as reported elsewhere [33,28,31]. This dietary brown seaweed was eventually proven and encompassed with active compounds against tumor cells [34].