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  • br cell cycle Apart anticancer

    2020-08-12

    
    cell cycle [24,18]. Apart, anticancer potential of fucoidan was explored by the increase of immune response signaling molecules like inter-leukins (IL-2, IL-12) and interferon gamma (IFN-γ) [12]. Thus, immune-therapy potential of fucoidan was proven through intruding 23986-74-5 pro-liferation by increasing anti-inflammatory (IL-2, IL-4, and IL-10) and reducing pro-inflammatory (IL-6 and TNF-α) cytokines in gastric and mammary cancers [39,40]. In addition, fucoidan exhibited immune therapy was takes place through the programmed cell death activated by 1/PDL1 signaling pathway [41]. In the present study explored that the apoptotic cell morphology altered by fucoidan in terms of nuclear condensation was further confirmed by Hoechst 33,342 staining (Fig.6. B). It was clearly illustrated the differences in HepG2 cancer cells constituted with fucoidan (bright chromatin condensation and nuclear
    Fig. 5. Genetic damage induction by fucoidan in HepG2 cancer cells detected by comet assay.
    Table 2
    Percentage of genetic damage induced by fucoidan in HepG2 cancer cells.
    Concentration (μg/ml) Genetic damage (%)
    Head Tail Tail moment
    The values are presented as mean ± SD in triplicate and significance
    Fig. 6. Fucoidan induced apoptosis in HepG2 cancer cells (constituted with different con-centration of fucoidan for 48 h and staining with annexin-V FITC/PI. The values are pre-sented as mean ± SD in triplicate and sig-nificance (p ≤0.05) determined by student t-test between fucoidan treated vs untreated control. A. Each quadrant indicates the per-centage of normal cells (annexin V-/PI-), early apoptosis (annexin V+/PI-) and late apoptosis (annexin V+/PI+). B & C. Fucoidan (200 μg/ mL) altered nuclear morphology by Hoechst 33,342 stains and mitochondrial membrane potential (ΔΨm) by JC-1stains were observed under fluorescence microscopy (original mag-nification, 400x). Red fluorescence indicates mitochondria with intact membrane potential and green fluorescence indicates de-energized mitochondria).
    fragmentation) than that of untreated one (weak homogeneous blue). Similarly, altered mitochondrial membrane potential as result of fu-coidan treatment was examined with JC-1 staining and it was also evidenced further for the fucoidan induced apoptosis in HepG2 cancer cells (Fig. 6C). Hence, the alteration in terms of significant increase in the green fluorescence intensity occurred due to oxidative stress and subsequent mitochondrial damage [42,43]
    5. Conclusion
    In the present study clearly shows ∼50% of HepG2 cancer cell proliferation was inhibited by the fucoidan and the effect was accord-ingly regarded by way of concentration. Based on the previous and present studies, the fucoidan apparently promoted cells accumulation in the G1 phase of the cell cycle. In addition, fucoidan inhibited cell proliferation, colony formation and cell migration were significantly well associated with G1 phase of the cell cycle arrest and apoptosis
    induction. On other hand, the quantified genetic damage induced by fucoidan was significantly correlated with apoptosis as well. The fluorescence microscopy study was eventually proved further that fu-coidan promoted the apoptotic cell formation in HepG2 cancer cells in terms of change in the nuclear content and mitochondrial membrane potential. The recent systematic and typical reports clearly supported for the present study that the effect of combinatory mycotoxin (Aflatoxin and Sterigmatocystin) on HepG2 cells were regard as like as fucoidan in terms of cytotoxicity and apoptosis associated endpoints, cell cycle arrest, mitochondria integrity, and apoptosis related proteins such as caspase-3 and p53 [44]. In the present pragmatic study con-cluded that the fucoidan contain brown seaweeds consumed as dietary supplement not predispose to liver cancer however further in-vivo in-vestigation would certainly strengthen this results.
    Transparency document
    The Transparency document associated with this article can be found in the online version.
    Declaration of Competing Interest
    There was no competing interest.
    Acknowledgment
    This contributed research work was supported by University Grant Commission (UGC), Government of India, New Delhi (Ref. No. TAM-8496).
    References
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