scholarly journals Integrated analysis of potential pathways by which aloe-emodin induces the apoptosis of colon cancer cells

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Dongxiao Jiang ◽  
Shufei Ding ◽  
Zhujun Mao ◽  
Liyan You ◽  
Yeping Ruan
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Time Dependent ◽  
Integrated Analysis ◽  
Dependent Manner ◽  
Colon Cancer Cells ◽  
Dapi Staining ◽  
Aloe Emodin

Abstract Background Colon cancer is a malignant gastrointestinal tumour with high incidence, mortality and metastasis rates worldwide. Aloe-emodin is a monomer compound derived from hydroxyanthraquinone. Aloe-emodin produces a wide range of antitumour effects and is produced by rhubarb, aloe and other herbs. However, the mechanism by which aloe-emodin influences colon cancer is still unclear. We hope these findings will lead to the development of a new therapeutic strategy for the treatment of colon cancer in the clinic. Methods We identified the overlapping targets of aloe-emodin and colon cancer and performed protein–protein interaction (PPI), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. In addition, we selected apoptosis pathways for experimental verification with cell viability, cell proliferation, caspase-3 activity, DAPI staining, cell cycle and western blotting analyses to evaluate the apoptotic effect of aloe-emodin on colon cancer cells. Results The MTT assay and cell colony formation assay showed that aloe-emodin inhibited cell proliferation. DAPI staining confirmed that aloe-emodin induced apoptosis. Aloe-emodin upregulated the protein level of Bax and decreased the expression of Bcl-2, which activates caspase-3 and caspase-9. Furthermore, the protein expression level of cytochrome C increased in a time-dependent manner in the cytoplasm but decreased in a time-dependent manner in the mitochondria. Conclusion These results indicate that aloe-emodin may induce the apoptosis of human colon cancer cells through mitochondria-related pathways.

scholarly journals The Mechanism of Aloe-emodin in the Treatment of Colon Cancer based on Network Pharmacological Analysis

2020 ◽  
Author(s):  
Dongxiao Jiang ◽  
Shufei Ding ◽  
Zhujun Mao ◽  
Liyan You ◽  
yeping ruan
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Time Dependent ◽  
Dependent Manner ◽  
Colon Cancer Cells ◽  
Dapi Staining ◽  
Wide Range ◽  
Aloe Emodin

Abstract Background: Colon cancer is a malignant gastrointestinal tumor with a high incidence, high mortality and high metastasis in the world. Aloe-emodin is a monomer compound derived from hydroxyanthraquinone. It makes a wide range of anti-tumor effects and exists in Rhubarb, Aloe, and other plants. However, the mechanism of aloe-emodin against colon cancer still not clear. Here, we predict the potential targets and mechanisms of aloe-emodin based on network pharmacology analysis. Methods: First, determine the intersection target of aloe-emodin and colon cancer, analyze and construct PPI, Gene Ontology, and KEGG pathway analysis. In addition, we selected apoptosis pathways for experimental verification including cell viability determination, cell proliferation, caspase-3 activity determination, DAPI staining, cell cycle determination and western blot to evaluate the apoptosis effect of aloe-emodin on colon cancer cells.Results: The MTT assay and cell colony experiment showed that AE inhibited cell proliferation (P<0.01). DAPI staining confirmed that AE induced apoptosis. AE activates caspase-3, caspase-9 and Bax and down-regulates the expression of Bcl-2. Furthermore, the expression level of cytochrome C protein increased in a time-dependent manner in the cytoplasm but fell in a time-dependent manner in the mitochondria.Conclusion: These results indicate that aloe-emodin may induce apoptosis of human colon cancer cells through mitochondrial related pathways.

scholarly journals Tetrandrine inhibits colon carcinoma HT-29 cells growth via the Bcl-2/Caspase 3/PARP pathway and G1/S phase

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
JiaNan Li ◽  
QiuHong Wang ◽  
ZhiBin Wang ◽  
Na Cui ◽  
BingYou Yang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Molecular Docking ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Caspase 8 ◽  
Therapeutic Effects ◽  
Dependent Manner ◽  
Colon Cancer Cells ◽  
Ht 29 ◽  
Active Caspase

Abstract Tetrandrine (Tet) bisbenzylisoquinoline alkaloids isolated from Stephania tetrandra and other related species of Menispermaceae. It has been demonstrated to have positive therapeutic effects on cardiovascular disease, hypertension, silicosis, autoimmune diseases. In recent years, some reports have shown that Tet has anticancer activity in human cancers. To explore the pharmacological activity and mechanism of Tet on colon cancer and its unique advantages as a natural product. In the present study, analyses of the cell cycle, apoptosis, targets prediction, molecular docking, and alterations in protein levels were performed to elucidate how Tet functions in colon cancer. We found that Tet robustly induced arrest at the G1 phase in colon cancer cell line HT-29. It induced HT-29 cell apoptosis in a dose-dependent manner. Similarly, analysis of protein expression levels in HT-29 cells showed down-regulation of Bcl-2, pro-caspase 3, pro-caspase 8, PARP, cyclin D1 (CCND1), cyclin-dependent kinase 4 (CDK 4), and up-regulation of Bax, active caspase 3, and active caspase 8. These results indicate that Tet induces apoptosis of colon cancer cells through the mitochondrial pathway and caspase family pathway. Molecular docking showed interaction effects and binding energy. Comparing with the CDK4 inhibitors ribociclib and palbociclib, the docking energy is similar to the docked amino acid residues. Therefore, we conclude that Tet and the CCND1/CDK4 compound could form hydrogen bonds and a stable compound structure, which can inhibit colon cancer cells proliferation by regulating CCND1/CDK4 compound and its downstream proteins phosphorylated Rb (p-Rb). In summary, Tet may be a potential drug for colon cancer therapy.

scholarly journals Growth Inhibition by Caffeic Acid, One of the Phenolic Constituents of Honey, in HCT 15 Colon Cancer Cells

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Saravana Kumar Jaganathan
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Caffeic Acid ◽  
Mtt Assay ◽  
Time Dependent ◽  
Ros Generation ◽  
Dependent Manner ◽  
Colon Cancer Cells ◽  
Phenolic Constituents ◽  
Induced Apoptosis

Previous work from our laboratory showed that the mechanism of crude-honey induced apoptosis in colon cancer cells. Since phenolic constituents of honey were attributed to its apoptosis-inducing ability, we studied caffeic acid, one of the phenolic constituents of honey, induced effect on colon cancer cells. Antiproliferative effect of caffeic acid was estimated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. MTT assay signified the antiproliferative nature of caffeic acid against the HCT 15 colon cancer cells. A time-dependent inhibition of colony formation was evident with caffeic acid treatment. Cell-cycle analysis of caffeic acid- (CA-) treated cells indicated increasing accumulation of cells at sub-G1phase. Photomicrograph images of treated cells showed membrane blebbing and cell shrinkage. Yo-pro-1 staining of caffeic-acid-treated cells confirmed apoptosis in dose- and time-dependent manner. Increasing ROS generation and reduction in the mitochondrial membrane potential were also accompanied in the caffeic acid-induced apoptosis. This work will promote caffeic acid as a likely candidate in the chemoprevention of colon cancer.

Lack of functional p53 renders DENSpm-induced autophagy and apoptosis in time dependent manner in colon cancer cells

Amino Acids ◽  
2014 ◽  
Vol 47 (1) ◽  
pp. 87-100 ◽  
Author(s):  
Ajda Çoker-Gürkan ◽  
Elif Damla Arisan ◽  
Pınar Obakan ◽  
Narçin Palavan-Unsal
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Time Dependent ◽  
Dependent Manner ◽  
Colon Cancer Cells

scholarly journals Synergistic Effects of Simvastatin and Irinotecan against Colon Cancer Cells with or without Irinotecan Resistance

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Hyun Joo Jang ◽  
Eun Mi Hong ◽  
Juah Jang ◽  
Jung Eun Choi ◽  
Se Woo Park ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Synergistic Effects ◽  
Combined Treatment ◽  
Molar Ratio ◽  
Colon Cancer Cells ◽  
Activity Assay ◽  
Ht 29

Aims. We here investigated whether the combination of simvastatin and irinotecan could induce the synergistic effect on colon cancer cells with or without resistance to irinotecan.Methods. We investigated cell proliferation assay and assessed cell death detection ELISA and caspase-3 activity assay of various concentrations of simvastatin and irinotecan to evaluate the efficacy of drug combination on colon cancer cells with or without irinotecan resistance.Results. The IC50values of simvastatin alone and irinotecan alone were115.4±0.14 μM (r=0.98) and62.5±0.18 μM (r=0.98) in HT-29 cells without resistance to irinotecan. The IC50values of these two drugs were221.9±0.22 μM (r=0.98) and195.9±0.16 μM (r=0.99), respectively, in HT-29 cell with resistance to irinotecan. The results of combinations of the various concentrations of two drugs showed that combined treatment with irinotecan and simvastatin more efficiently suppressed cell proliferation of HT-29 cells even with resistance to irinotecan as well as without resistance. Furthermore, the combination of simvastatin and irinotecan at2:1molar ratio showed the best synergistic interaction.Conclusion. Simvastatin could act synergistically with irinotecan to overcome irinotecan resistance of colon cancer.

scholarly journals Purvalanol induces endoplasmic reticulum stress-mediated apoptosis and autophagy in a time-dependent manner in HCT116 colon cancer cells

2015 ◽  
Vol 33 (6) ◽  
pp. 2761-2770 ◽  
Author(s):  
AJDA COKER-GÜRKAN ◽  
ELIF DAMLA ARISAN ◽  
PINAR OBAKAN ◽  
KÜBRA AKALIN ◽  
UTKU ÖZBEY ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cancer Cells ◽  
Time Dependent ◽  
Dependent Manner ◽  
Colon Cancer Cells

scholarly journals Epibrassinolide Treatment Caused Autophagy or Apoptosis Decision in a Time-Dependent Manner through ER Stress in Colon Cancer Cells

Proceedings ◽  
2017 ◽  
Vol 1 (10) ◽  
pp. 986 ◽  
Author(s):  
Pınar Obakan-Yerlikaya ◽  
Kaan Adacan ◽  
Elif Damla Arısan ◽  
Ajda Çoker-Gürkan ◽  
Narçın Palavan-Ünsal
Keyword(s):  
Colon Cancer ◽  
Er Stress ◽  
Cancer Cells ◽  
Time Dependent ◽  
Dependent Manner ◽  
Colon Cancer Cells

scholarly journals Colorectal Cancer Apoptosis Induced by Dietary δ-Valerobetaine Involves PINK1/Parkin Dependent-Mitophagy and SIRT3

2021 ◽  
Vol 22 (15) ◽  
pp. 8117
Author(s):  
Nunzia D’Onofrio ◽  
Elisa Martino ◽  
Luigi Mele ◽  
Antonino Colloca ◽  
Martina Maione ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Mitochondrial Dysfunction ◽  
Cancer Cells ◽  
Current Knowledge ◽  
Apoptotic Cell ◽  
Critical Role ◽  
Dependent Manner ◽  
Colon Cancer Cells ◽  
Protein Levels

Understanding the mechanisms of colorectal cancer progression is crucial in the setting of strategies for its prevention. δ-Valerobetaine (δVB) is an emerging dietary metabolite showing cytotoxic activity in colon cancer cells via autophagy and apoptosis. Here, we aimed to deepen current knowledge on the mechanism of δVB-induced colon cancer cell death by investigating the apoptotic cascade in colorectal adenocarcinoma SW480 and SW620 cells and evaluating the molecular players of mitochondrial dysfunction. Results indicated that δVB reduced cell viability in a time-dependent manner, reaching IC50 after 72 h of incubation with δVB 1.5 mM, and caused a G2/M cell cycle arrest with upregulation of cyclin A and cyclin B protein levels. The increased apoptotic cell rate occurred via caspase-3 activation with a concomitant loss in mitochondrial membrane potential and SIRT3 downregulation. Functional studies indicated that δVB activated mitochondrial apoptosis through PINK1/Parkin pathways, as upregulation of PINK1, Parkin, and LC3B protein levels was observed (p < 0.0001). Together, these findings support a critical role of PINK1/Parkin-mediated mitophagy in mitochondrial dysfunction and apoptosis induced by δVB in SW480 and SW620 colon cancer cells.

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