scholarly journals The Combination of AHCC and ETAS Decreases Migration of Colorectal Cancer Cells, and Reduces the Expression of LGR5 and Notch1 Genes in Cancer Stem Cells: A Novel Potential Approach for Integrative Medicine

2021 ◽  
Vol 14 (12) ◽  
pp. 1325
Author(s):  
Francesca Paganelli ◽  
Francesca Chiarini ◽  
Annalisa Palmieri ◽  
Marcella Martinelli ◽  
Paola Sena ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Lentinula Edodes ◽  
Combined Treatment ◽  
Asparagus Officinalis ◽  
Therapeutic Effects ◽  
Cancer Cell Growth ◽  
Therapeutic Benefits ◽  
Healthy Donors ◽  
Colorectal Cancer Cells

The AHCC standardized extract of cultured Lentinula edodes mycelia, and the standardized extract of Asparagus officinalis stem, trademarked as ETAS, are well known supplements with immunomodulatory and anticancer potential. Several reports have described their therapeutic effects, including antioxidant and anticancer activity and improvement of immune response. In this study we aimed at investigating the effects of a combination of AHCC and ETAS on colorectal cancer cells and biopsies from healthy donors to assess the possible use in patients with colorectal cancer. Our results showed that the combination of AHCC and ETAS was synergistic in inducing a significant decrease in cancer cell growth, compared with single agents. Moreover, the combined treatment induced a significant increase in apoptosis, sparing colonocytes from healthy donors, and was able to induce a strong reduction in migration potential, accompanied by a significant modulation of proteins involved in invasiveness. Finally, combined treatment was able to significantly downregulate LGR5 and Notch1 in SW620 cancer stem cell (CSC) colonospheres. Overall, these findings support the potential therapeutic benefits of the AHCC and ETAS combinatorial treatment for patients with colorectal cancer.

Synergistic Effect of Combined Treatment with Longan Flower Extract and 5-Fluorouracil on Colorectal Cancer Cells

2019 ◽  
Vol 72 (2) ◽  
pp. 209-217
Author(s):  
Szu-Jung Chen ◽  
Yuan-Chiang Chung ◽  
Han-Lung Chang ◽  
Hsin-Ping Chang ◽  
Jui-Ling Chou ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Synergistic Effect ◽  
Cancer Cells ◽  
Combined Treatment ◽  
Flower Extract ◽  
Colorectal Cancer Cells

scholarly journals Iron Chelation Properties of Green Tea Epigallocatechin-3-Gallate (EGCG) in Colorectal Cancer Cells: Analysis on Tfr/Fth Regulations and Molecular Docking

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Zarith Nameyrra Md Nesran ◽  
Nurul Husna Shafie ◽  
Siti Farah Md Tohid ◽  
Mohd Esa Norhaizan ◽  
Amin Ismail
Keyword(s):  
Colorectal Cancer ◽  
Molecular Docking ◽  
Cancer Cells ◽  
Green Tea ◽  
Iron Chelation ◽  
Docking Study ◽  
Therapeutic Effects ◽  
Molecular Docking Study ◽  
Colorectal Cancer Cells

In many studies, green tea epigallocatechin-3-gallate (EGCG) has already shown its therapeutic effects in colorectal cancer cells (CRC). However, its mechanism of actions in CRC is poorly elucidated. Hence, this study attempts to elucidate the mechanism of actions of green tea ECGG via iron chelation activity in CRC. In order to investigate this property, HT-29 cell lines (CRC) were treated with EGCG for 24 h, 48 h, and 72 h. From western blot analysis, EGCG had upregulated transferrin receptor (TfR) protein and downregulated Ferritin-H (FtH) protein indicating that iron chelation activity has occurred in CRC. Meanwhile, the molecular docking study demonstrated that EGCG is able to strongly interact the ferritin protein with a high binding affinity (−7.3 kcal/mol) via strong hydrogen bindings to glutamic acid 64 and lysine 71; two moderate hydrogen bindings to asparagine 74 and a hydrophobic interaction to the hydrophobic pocket of lysine 71. The strong interaction predicted between EGCG to ferritin may lead to inhibition of ferritin by EGCG, thus supporting the downregulation of FtH observed in in vitro studies. Molecular docking study of TfR to EGCG cannot be modulated based on the in vitro results. In conclusion, EGCG possesses iron chelator property in CRC and this potential could be further exploited for CRC treatment.

scholarly journals Onion Peel Extract Inhibits Cancer Cell Growth and Progression through the Roles of L1CAM, NF-κB, and Angiogenesis in HT-29 Colorectal Cancer Cells

2021 ◽  
Vol 26 (3) ◽  
pp. 330-337
Author(s):  
Tamonwan Uttarawichien ◽  
Wilunplus Khumsri ◽  
Prasit Suwannalert ◽  
Nathawut Sibmooh ◽  
Witchuda Payuhakrit
Keyword(s):  
Colorectal Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Cell Growth ◽  
Onion Peel ◽  
Colorectal Cancer Cells ◽  
Onion Peel Extract ◽  
Ht 29 ◽  
Peel Extract

scholarly journals Astragaloside IV Enhances Cisplatin Chemosensitivity in Human Colorectal Cancer via Regulating NOTCH3

2016 ◽  
Vol 24 (6) ◽  
pp. 447-453 ◽  
Author(s):  
Tao Xie ◽  
Yao Li ◽  
Shi-Lei Li ◽  
Hai-Feng Luo
Keyword(s):  
Colorectal Cancer ◽  
Cell Growth ◽  
Protein Expression ◽  
Cancer Cells ◽  
Combined Therapy ◽  
Combined Treatment ◽  
Astragaloside Iv ◽  
Anticancer Properties ◽  
Colorectal Cancer Cells ◽  
Mrna And Protein Expression

Although astragaloside IV exhibits anti-inflammation, immunoregulatory, and anticancer properties, the chemosensitization effects of astragaloside IV in colorectal cancer have never been reported. Our study tested whether astragaloside could increase cisplatin sensitivity in colorectal cancer. CCK-8 assay was used to measure the cell viability of colorectal cancer cells. Quantitative real-time PCR and Western blot were performed to determine the mRNA and protein expression, respectively. Our data revealed that astragaloside IV administration significantly suppressed the cell growth of colorectal cancer cells, whereas no obvious cytotoxicity of astragaloside IV was observed in nonmalignant colonic cells. In addition, combined treatment with astragaloside IV dramatically elevated the chemosensitivity of colorectal cancer cells to cisplatin. Mechanical investigation revealed that the mRNA and protein expression of NOTCH3 was significantly lower in cisplatin and astragaloside IV-treated cells compared with cells treated with cisplatin alone. On the contrary, no obvious changes in tumor cell growth were shown after upregulation of NOTCH3 whether in the presence or absence of astragaloside IV. Thus, our data demonstrate that astragaloside IV increases the chemosensitivity of colorectal cancer cells to cisplatin, at least partly, through inhibition of NOTCH3. This study suggests that combined therapy with astragaloside IV might be a novel therapeutic approach for colorectal cancer.

scholarly journals Melatonin Sensitizes Human Colorectal Cancer Cells to γ-ray Ionizing Radiation In Vitro and In Vivo

2018 ◽  
Vol 19 (12) ◽  
pp. 3974 ◽  
Author(s):  
Qin Wang ◽  
Zhijuan Sun ◽  
Liqing Du ◽  
Chang Xu ◽  
Yan Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colorectal Carcinoma ◽  
Ionizing Radiation ◽  
Cancer Cells ◽  
Cellular Proliferation ◽  
Combined Treatment ◽  
Secretory Product ◽  
Colorectal Cancer Cells

Colorectal cancer is the most commonly reported gastrointestinal malignancy, with a recent, rapid increase of the annual incidence all over the world. Enhancing the radiosensitivity of cancer cells while preserving the health of normal cells is one of the most important tasks in clinical radiobiology. However, resistance to radiotherapy for colorectal cancer greatly decreases the therapeutic outcome. Melatonin (N-acetyl-5-methoxytryptamine), a natural secretory product that the pineal gland in the brain normally produces, has been reported to have anticancer properties. In the study, we investigated the combination of melatonin with radiotherapy as a treatment for colorectal cancer. We firstly explored the anti-tumor activity of melatonin combined with ionizing radiation (IR) against colorectal carcinoma in vitro. It was found that melatonin effectively inhibited human colorectal carcinoma cell line HCT 116 cellular proliferation, colony formation rate and cell migration counts following IR. Increasing the radiosensitivity of colorectal cancer cells by melatonin treatment was found to be associated with cell cycle arrest in the G2/M phase, downregulation of proteins involved in DNA double-strand break repair and activation of the caspase-dependent apoptotic pathway. Moreover, we also investigated the combined effect of IR and melatonin on colorectal tumor in vivo. Results from a tumor xenograft showed that melatonin plus IR treatment significantly suppressed tumor cell growth compared with melatonin or IR alone, resulting in a much higher tumor inhibition rate for the combined treatment. The data suggested that melatonin combined with IR could improve the radiosensitivity of colorectal cancer and thus enhance the therapeutic effect of the patients, implying melatonin could function as a potential sensitizer in tumor radiotherapy.

scholarly journals Combined Treatment of 5-Fluorouracil and Delta-Tocotrienol Induce of Apoptosis and Autophagy in Colorectal Cancer Cells

2018 ◽  
Vol 4 (Supplement 2) ◽  
pp. 203s-203s ◽  
Author(s):  
S.Y. Tham ◽  
C.W. Mai ◽  
J.Y. Fu ◽  
H.-S. Loh
Keyword(s):  
Colorectal Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Treatment Approach ◽  
Expression Profiles ◽  
Combined Treatment ◽  
High Dose ◽  
First Choice ◽  
Colorectal Cancer Cells ◽  
The Individual

Background: 5-fluorouracil (5-FU) has been a first choice chemotherapeutic drug used to treat colorectal cancer. However, its therapeutic outcome often be limited by high-dose toxicities and drug resistance development. Hence, the current research advocates combined application of delta-tocotrienol (δ-T3), as a natural chemosensitizer, with 5-FU as a novel treatment approach for colorectal cancer. Aim: To investigate the combinatorial anticancer effects of δ-T3 and 5-FU on colorectal cancer cell lines. Methods: Cell viability assay was performed to investigate the individual and combined effects of δ-T3 (0.1-100 µM) and 5-FU (0.1-100 µM) on HCT116, HCC2998, Caco-2 and SW48 colorectal cancer cells at 72 h. Subsequently, the synergistic combination were evaluated for the effects on clonogenicity, apoptosis and autophagy. Morphologic assessment was conducted by bright-field and fluorescence microscopy. The protein expression profiles of programmed cell death and survival markers were determined by Western blotting. Results: Combined treatment of subeffective dose of δ-T3 significantly lowered the IC50 of 5-FU in Caco-2 and SW48 colorectal adenocarcinomas for 16-fold and fourfold respectively, signifying a chemosensitising effect. Clonogenic survival assay showed that the combined treatment profoundly hampered the cell survival as compared with the individual single treatments. Apoptosis was induced by the combined treatment as confirmed by flow cytometry. Interestingly, both apoptotic and autophagic morphologies were observed, including nuclear condensation, cell shrinkage, cytoplasmic vacuolation and extension. The presence of autophagy was further confirmed by increase LC3A/B ratio and high volume of acidic vesicular organelles. The combined treatment were found to upregulate prodeath proteins such as Bax, caspase-8, caspase-3, PARP and downregulate prosurvival proteins such as cIAP, XIAP and survivin. Conclusion: The enhanced cell death induced by 5-FU and δ-T3 combined treatment involved both apoptosis and autophagy, suggesting a novel and effective treatment approach for colorectal cancer.

scholarly journals Anti-tumor effects of the ethanolic extract of Trichosanthes kirilowii seeds in colorectal cancer

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Su Mi Park ◽  
Sang Kyu Jeon ◽  
Ok Hyeon Kim ◽  
Jung Yun Ahn ◽  
Chang-Hyun Kim ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Ethanolic Extract ◽  
Migration And Invasion ◽  
Therapeutic Effects ◽  
Growth Factor Signaling ◽  
Compound C ◽  
Colorectal Cancer Cells ◽  
Trichosanthes Kirilowii ◽  
Ht 29

Abstract Background Trichosanthis semen, the seeds of Trichosanthes kirilowii Maxim. or Trichosanthes rosthornii Harms, has long been used in Korean medicine to loosen bowels and relieve chronic constipation. Although the fruits and radixes of this medicinal herb and their constituents have been reported to exhibit therapeutic effects in various cancers, the anti-cancer effects of its seeds have been relatively less studied. In this study, we investigated the effects of an ethanolic extract of T. kirilowii seeds (TKSE) against colorectal cancer and its mechanism. Methods The anti-tumor effects of the TKSE were evaluated in HT-29 and CT-26 colorectal cancer cells and in a CT-26 tumor-bearing mouse model. Results TKSE suppressed the growth of HT-29 and CT-26 cells (both colorectal cancer cell lines) and the cytotoxic effect of TKSE was greater than that of 5-fluorouracil (5-Fu) in HT-29 cells. TKSE significantly induced mitochondrial membrane potential loss in HT-29 and CT-26 cells and dose-dependently inhibited Bcl-2 expression and induced the cleavages of caspase-3 and PARP. In particular, TKSE at 300 µg/mL induced nuclear condensation and fragmentation in HT-29 cells. Furthermore, TKSE dose-dependently inhibited activations of the Akt/mTOR and ERK pathways, and markedly induced the phosphorylation of AMPK. An AMPKα inhibitor (compound C) effectively blocked the TKSE-induced mitochondrial dysfunction. In addition, TKSE attenuated the hypoxia-inducible factor-1α/vascular endothelial growth factor signaling pathway in HT-29 cells under hypoxic-mimic conditions and inhibited migration and invasion. Oral administration of TKSE (100 or 300 mg/kg) inhibited tumor growth in a mouse CT-26 allograft model but was not as effective as 5-Fu (the positive control), which was administered intraperitoneally. In the same model, 5-Fu caused significant body weight loss, but no such loss was observed in TKSE-treated mice. Conclusion Taken together, these results suggest TKSE has potent anti-tumor effects which might be partly due to the activation of AMPK, and the induction mitochondrial-mediated apoptosis in colorectal cancer cells. These findings provide scientific evidence supporting the potential use of TKSE as a complementary and alternative medicine for the treatment of colorectal cancer.

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