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.

scholarly journals Emodin Induces Apoptosis of Colon Cancer Cells via Induction of Autophagy in a ROS-Dependent Manner

2018 ◽  
Vol 26 (6) ◽  
pp. 889-899 ◽  
Author(s):  
Yuanyuan Wang ◽  
Qin Luo ◽  
Xianlu He ◽  
He Wei ◽  
Ting Wang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Chinese Herbs ◽  
Ros Generation ◽  
Dependent Manner ◽  
Colon Cancer Cells ◽  
Ros Accumulation ◽  
Cancer Types ◽  
Induced Apoptosis ◽  
Cancer Suppression

Recent studies revealed that emodin extracted from Chinese herbs exhibits an anticancer effect on different cancer types, including colon cancer. However, the mechanism is not well understood. In our study, we confirmed that emodin treatment inhibited cell viability and induced apoptosis in colon cancer cells. Further experiments found that emodin was also able to induce autophagy, which is indispensible for apoptosis induced by emodin. More interestingly, emodin treatment also results in mitochondrial dysfunction and ROS accumulation in colon cancer cells. Finally, we stressed that ROS accumulation is essential for autophagy and apoptosis induced by emodin. In conclusion, emodin induces apoptosis in colon cancer cells through induction of autophagy, during which ROS generation is of the essence. Our findings improve understanding of emodin’s effect on colon cancer suppression and provide a new theoretical basis for colon cancer therapy.

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.

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

Requirement for store-operated calcium entry in sodium butyrate-induced apoptosis in human colon cancer cells

2011 ◽  
Vol 32 (1) ◽  
pp. 83-90 ◽  
Author(s):  
Suxia Sun ◽  
Wenjun Li ◽  
He Zhang ◽  
Longying Zha ◽  
Yong Xue ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Butyric Acid ◽  
Sodium Butyrate ◽  
Dependent Manner ◽  
Colon Cancer Cells ◽  
Acetoxymethyl Ester ◽  
Hct 116 ◽  
Hct 116 Cells ◽  
Induced Apoptosis

The SOCE (store-operated Ca2+ entry) pathway plays a key role in both normal cells and cancerous cells. However, its molecular mechanism remains a long-lasting puzzle of Ca2+ signalling. In this paper, we provide evidence that butyric acid, a dietary fibre-derived short-chain fatty acid, induces apoptosis of colon cancer cells via SOCE signalling networks. We found that sodium butyrate (NaB) induces Ca2+ release from endoplasmic reticulum, which in turn causes extracellular Ca2+ influx in HCT-116 cells. The Ca2+ release and influx are important, because the addition of chelators, EGTA or BAPTA/AM [1,2-bis-(o-aminophenoxy)ethane-N,N,N′,N′-tetra-acetic acid tetrakis(acetoxymethyl ester)] respectively blocked NaB-induced apoptosis. Furthermore, down-regulation of STIM1 (stromal interaction molecule 1) by RNA interference or pharmacological blockade of the SOCC (store-operated Ca2+ channel) by 2-APB (2-aminoethoxydiphenyl borate) or SKF-96365 inhibited NaB-induced extracellular Ca2+ influx and apoptosis in HCT-116 cells. Thus we conclude that NaB triggers colon cancer cell apoptosis in an SOCE-dependent manner. This finding provides new insights into how butyric acid suppresses colon carcinogenesis.

scholarly journals The Indolic Diet-Derivative, 3,3′-Diindolylmethane, Induced Apoptosis in Human Colon Cancer Cells through Upregulation of NDRG1

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
A. Lerner ◽  
M. Grafi-Cohen ◽  
T. Napso ◽  
N. Azzam ◽  
F. Fares
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Colonic Cancer ◽  
P53 Gene ◽  
Dependent Manner ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Hct 116 ◽  
Poorly Differentiated ◽  
Induced Apoptosis

N-myc downstream regulated gene-1 participates in carcinogenesis, angiogenesis, metastases, and anticancer drug resistance. In the present study, we analyzed the expression pattern of N-myc downstream regulated gene-1 following treatment of human colonic cancer cell lines; HCT-116 (well differentiated with wild-type p53 gene) and Colo-320 (poorly differentiated with mutant p53 gene), with 3,3′-diindolylmethane, a well-established proapoptotic agent product derived from indole-3-carbinol. Treatment of Colo-320 and HCT-116 with 3,3′-diindolylmethane disclosed inhibition of cell viability in a dose-dependent manner, mediated through apoptosis induction. The increased expression of N-myc downstream regulated gene-1 was detected only in poorly differentiated colon cancer cells, Colo-320 cell line. Our results suggest that N-myc downstream regulated gene-1 expression is enhanced by 3,3′-diindolylmethane in poorly differentiated cells and followed by induction of apoptosis. 3,3′-diindolylmethane induced apoptosis may represent a new regulator of N-myc downstream regulated gene-1 in poorly differentiated colonic cancer cells.

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
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