scholarly journals Fucoidan and Alginate from the Brown Algae Colpomenia sinuosa and Their Combination with Vitamin C Trigger Apoptosis in Colon Cancer

Molecules ◽  
2022 ◽  
Vol 27 (2) ◽  
pp. 358
Author(s):  
Reem Al Monla ◽  
Zeina Dassouki ◽  
Nouha Sari-Chmayssem ◽  
Hiba Mawlawi ◽  
Hala Gali-Muhtasib
Keyword(s):  
Colon Cancer ◽  
Cell Death ◽  
Vitamin C ◽  
Cancer Cell ◽  
Brown Algae ◽  
Human Colon ◽  
Bioactive Molecules ◽  
Dapi Staining ◽  
Human Colon Cancer ◽  
Hct 116

Brown seaweeds are producers of bioactive molecules which are known to inhibit oncogenic growth. Here, we investigated the antioxidant, cytotoxic, and apoptotic effects of two polysaccharides from the brown algae Colpomenia sinuosa, namely fucoidan and alginate, in a panel of cancer cell lines and evaluated their effects when combined with vitamin C. Fucoidan and alginate were isolated from brown algae and characterized by HPLC, FTIR, and NMR spectroscopy. The results indicated that highly sulfated fucoidans had higher antioxidant and cytotoxic effects than alginate. Human colon cancer cells were the most sensitive to the algal treatments, with fucoidan having an IC50 value (618.9 µg/mL−1) lower than that of alginate (690 µg/mL−1). The production of reactive oxygen species was increased upon treatment of HCT-116 cells with fucoidan and alginate, which suggest that these compounds may trigger cell death via oxidative damage. The combination of fucoidan with vitamin C showed enhanced effects compared to treatment with fucoidan alone, as evidenced by the significant inhibitory effects on HCT-116 colon cancer cell viability. The combination of the algal polysaccharides with vitamin C caused enhanced degeneration in the nuclei of cells, as evidenced by DAPI staining and increased the subG1 population, suggesting the induction of cell death. Together, these results suggest that fucoidan and alginate from the brown algae C. sinuosa are promising anticancer compounds, particularly when used in combination with vitamin C.

scholarly journals Systemic Evaluation of Mechanism of Cytotoxicity in Human Colon Cancer HCT-116 Cells of Silver Nanoparticles Synthesized Using Marine Algae Ulva Lactuca Extract.

2021 ◽  
Author(s):  
Diptikanta Acharya ◽  
Sagarika Satapathy ◽  
Kanti Kusum Yadav ◽  
Prathap Somu ◽  
Gitanjali Mishra
Keyword(s):  
Colon Cancer ◽  
Silver Nanoparticles ◽  
Cell Death ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Human Colon ◽  
Ulva Lactuca ◽  
Bioactive Molecules ◽  
Human Colon Cancer ◽  
Hct 116

Abstract In the current study, biogenic silver nanoparticles (U-AgNPs) were synthesized using marine green macro-algal Ulva Lactuca extract, and evaluated mechanism behind the anticancer activity against the Human colon cancer (HCT-116). The novel biogenic U-AgNPs were characterized using various physiochemical techniques. The TEM micrographs confirmed the spherical morphology of synthesized U-AgNPs, with a mean size of 8–14 nm. FTIR Spectra analysis of U-AgNPs confirmed Ulva Lactuca extract bioactive molecules presence over U-AgNPs surface as a stabilizing agent, thereby improving biocompatibility. The cytotoxicity study revealed the dose dependent cell death in colon cancer cells with no loss of viability in normal human colon epithelial cells. Furthermore, the fluorescence micrographs of nucleus staining assay revealed the DNA fragmentation and nucleus condensation of cancer cells treated with U-AgNPs, indicating an apoptosis-mediated cell death. The western bolt and RT-PCR analysis of U-AgNPs treated cancer cells showed the rise in proapoptotic markers (P53, Bax, and P21) and decline in anti-apoptotic markers (Bcl-2), thus confirming the p53-dependent apoptosis mediated cell death in HCT-116. Overall, our study concluded that novel biogenic U-AgNPs nanoparticles, synthesized using marine green macro-algal Ulva Lactuca extract showed efficient anticancer activity against HCT-116 cell line and hence could work as potential therapeutic agent for targeted anti-cancer therapy.

scholarly journals p53 Is a Key Regulator for Osthole-Triggered Cancer Pathogenesis

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Ssu-Ming Huang ◽  
Cheng-Fang Tsai ◽  
Dar-Ren Chen ◽  
Min-Ying Wang ◽  
Wei-Lan Yeh
Keyword(s):  
Colon Cancer ◽  
Cell Death ◽  
Cell Lines ◽  
Cancer Cell ◽  
Human Colon ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Human Colon Cancer Cell ◽  
Human Colon Cancer ◽  
Colon Cancer Cell Lines

Osthole has been reported to have antitumor activities via the induction of apoptosis and inhibition of cancer cell growth and metastasis. However, the detailed molecular mechanisms underlying the anticancer effects of osthole in human colon cancer remain unclear. In the present study, we have assessed osthole-induced cell death in two different human colon cancer cell lines, HCT116 and SW480. Our results also showed that osthole activated proapoptotic signaling pathways in human colon cancer cells. By using cell culture insert system, osthole reduced cell motility in both human colon cancer cell lines. This study also provides evidence supporting the potential of osthole in p53 activation. Expression of p53, an apoptotic protein, was remarkably upregulated in cells treated with osthole. Importantly, the levels of phosphorylation of p53 on Ser15 (p-p53) and acetylation of p53 on Lys379(acetyl-p53) were increased under osthole treatment. Our results also demonstrated that p53 was activated followed by generation of reactive oxygen species (ROS) and activation of c-Jun N-terminal kinase (JNK). Our study provides novel insights of p53-mediated responses under osthole treatment. Taken together, we concluded that osthole induces cancer cell death and inhibits migratory activity in a controlled manner and is a promising candidate for antitumor drug development.

scholarly journals 6,7,4'-Trihydroxyisoflavone inhibits HCT-116 human colon cancer cell proliferation by targeting CDK1 and CDK2

2011 ◽  
Vol 32 (4) ◽  
pp. 629-635 ◽  
Author(s):  
D. E. Lee ◽  
K. W. Lee ◽  
S. K. Jung ◽  
E. J. Lee ◽  
J. A. Hwang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Human Colon ◽  
Colon Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Human Colon Cancer Cell ◽  
Human Colon Cancer ◽  
Hct 116

Anti-Tumor Mechanisms of Novel 3-(4-Substituted Benzyl)-5-Isopropil-5- Phenylhydantoin Derivatives in Human Colon Cancer Cell Line

2019 ◽  
Vol 19 (12) ◽  
pp. 1491-1502 ◽  
Author(s):  
Ana Obradović ◽  
Miloš Matić ◽  
Branka Ognjanović ◽  
Nenad Vuković ◽  
Milena Vukić ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cell ◽  
Cancer Cell Line ◽  
Human Colon ◽  
Colon Cancer Cell Line ◽  
Colon Cancer Cell ◽  
Human Colon Cancer Cell ◽  
Human Colon Cancer ◽  
Nitrite Production ◽  
Hct 116

Background: Hydantoin and its newly synthesized derivatives have recently become a focus of interest due to their numerous biological activities and newly emerging beneficial effects in different pathological conditions, including cancer. Objective: The aim of this study was to evaluate the possible anti-tumor mechanisms of a series of newly synthesized 3-(4-substituted benzyl)-5-isopropyl-5-phenylhydantoin derivatives in different aspects of cell physiology of human colon cancer cell line, HCT-116. Methods: The increasing concentrations of derivatives (0.01µM up to 100µM) were applied to cells during 24h, 48h, and 72h after which the evaluation of proliferation, apoptosis, oxidative/anti-oxidative status, nitrite production, and migration/invasion potential of treated cells was performed. Results: All tested compounds expressed the dose- and time-dependent anti-proliferative and pro-apoptotic activities against HCT-116 cells. The investigated derivatives induced a decrease in levels of oxidative stress parameters and an increase in levels of nitrite production by treated cells suggesting their significant antioxidative effects. The cell migration index and expression level of tumor invasion-promoting metalloproteinase- 9 (MMP-9) gene were significantly decreased after treatment with the tested hydantoin derivatives implicating their inhibitory role in colon cancer cell motility and invasion processes. The mRNA level of cyclooxygenase-2 (COX-2) gene as a pro-inflammatory gene related to colorectal carcinogenesis was reduced compared to values in the non-treated control cells indicating the significant anti-inflammatory/anti-tumor effects of these compounds. Conclusion: The obtained results show the significant anti-tumor potential of tested derivatives, especially 3- benzyl-5-isopropyl-5-phenylhydantoin and 3-(4-chlorobenzyl)-5-isopropyl-5-phenylhydantoin, suggesting their potential usage in the development of more effective chemotherapies.

scholarly journals Cytotoxicity of aporphines in human colon cancer cell lines HCT-116 and Caco-2: An SAR study

2011 ◽  
Vol 21 (15) ◽  
pp. 4462-4464 ◽  
Author(s):  
Shashikanth Ponnala ◽  
Sandeep Chaudhary ◽  
Antonio González-Sarrias ◽  
Navindra P. Seeram ◽  
Wayne W. Harding
Keyword(s):  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Human Colon ◽  
Colon Cancer Cell ◽  
Human Colon Cancer Cell ◽  
Human Colon Cancer ◽  
Colon Cancer Cell Lines ◽  
Hct 116 ◽  
Sar Study

Sulforaphane Induces Cell Death Through G2/M Phase Arrest and Triggers Apoptosis in HCT 116 Human Colon Cancer Cells

2016 ◽  
Vol 44 (06) ◽  
pp. 1289-1310 ◽  
Author(s):  
Kuo-Ching Liu ◽  
Ting-Ying Shih ◽  
Chao-Lin Kuo ◽  
Yi-Shih Ma ◽  
Jiun-Long Yang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Death ◽  
Western Blotting ◽  
Human Colon ◽  
Human Colon Cancer ◽  
Flow Cytometric ◽  
Phase Arrest ◽  
M Phase ◽  
Hct 116 ◽  
Hct 116 Cells

Sulforaphane (SFN), an isothiocyanate, exists exclusively in cruciferous vegetables, and has been shown to possess potent antitumor and chemopreventive activity. However, there is no available information that shows SFN affecting human colon cancer HCT 116 cells. In the present study, we found that SFN induced cell morphological changes, which were photographed by contrast-phase microscopy, and decreased viability. SFN also induced G2/M phase arrest and cell apoptosis in HCT 116 cells, which were measured with flow cytometric assays. Western blotting indicated that SFN increased Cyclin A, cdk 2, Cyclin B and WEE1, but decreased Cdc 25C, cdk1 protein expressions that led to G2/M phase arrest. Apoptotic cell death was also confirmed by Annexin V/PI and DAPI staining and DNA gel electrophoresis in HCT 116 cells after exposure to SFN. The flow cytometric assay also showed that SFN induced the generation of reactive oxygen species (ROS) and Ca[Formula: see text] and decreased mitochondria membrane potential and increased caspase-8, -9 and -3 activities in HCT 116 cell. Western blotting also showed that SFN induced the release of cytochrome c, and AIF, which was confirmed by confocal microscopy examination. SFN induced ER stress-associated protein expression. Based on those observations, we suggest that SFN may be used as a novel anticancer agent for the treatment of human colon cancer in the future.

scholarly journals Sturgeon (Acipenser)-Derived Chondroitin Sulfate Suppresses Human Colon Cancer HCT-116 Both In Vitro and In Vivo by Inhibiting Proliferation and Inducing Apoptosis

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1130 ◽  
Author(s):  
Ruiyun Wu ◽  
Nan Shang ◽  
Meng Gui ◽  
Jian Yin ◽  
Pinglan Li
Keyword(s):  
Colon Cancer ◽  
Chondroitin Sulfate ◽  
Cancer Cell ◽  
Human Colon ◽  
Colon Cancer Cell ◽  
Apoptosis Induction ◽  
Human Colon Cancer ◽  
Hct 116

Chondroitin sulfate (CS), mainly present in the cartilage and bone of animals, is known as a potential food-derived bioactive that has several biological functions, such as anti-arthritic and anti-inflammatory activity. Sturgeon (Acipenser), an important fishery resource in China, contains an abundance of CS in their cartilage. In our previous study, we have extracted and purified CS from sturgeon cartilage. Herein, we further investigate the health benefits of sturgeon-derived chondroitin sulfate (SCS), especially for colorectal cancer treatment. The in vitro study indicated that SCS could inhibit the proliferation of the human colon cancer cell line HCT-116 in a dose-dependent manner, which was associated with cell cycle arrest. In addition, SCS also led to extensive cellular apoptosis in colon cancer cell HCT-116 cells. Meanwhile, an in vivo study showed that SCS treatment significantly inhibited the tumor development of xenograft HCT-116 in mice via proliferation suppression and apoptosis induction. Further, a mechanistic study demonstrated that the apoptosis induction was mainly due to the activation of the Bcl-2 family-associated mitochondrial pathway. Overall, our results provided a basis for SCS as a promising agent against colon cancer.

Sign in / Sign up

Export Citation Format

Share Document