scholarly journals Stromal Cell and Colonocyte EGFR Are Required for Efficient Tumor Xenograft Growth of Colon Cancer Cells

2011 ◽  
Vol 140 (5) ◽  
pp. S-825
Author(s):  
Urszula Dougherty ◽  
Reba Mustafi ◽  
Jiang Wu ◽  
Hongyan Zhu ◽  
Loren J. Joseph ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Stromal Cell ◽  
Tumor Xenograft ◽  
Colon Cancer Cells ◽  
Xenograft Growth ◽  
Tumor Xenograft Growth

scholarly journals A novel epigenetic regulation of circFoxp1 on Foxp1 in colon cancer cells

2020 ◽  
Vol 11 (9) ◽  
Author(s):  
Yanwei Luo ◽  
Fengxia Liu ◽  
Jinqi Ma ◽  
Yunfeng Fu ◽  
Rong Gui
Keyword(s):  
Colon Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Quantitative Polymerase Chain Reaction ◽  
Human Colon ◽  
Tumor Xenograft ◽  
Colon Cancer Cells ◽  
Poor Overall Survival ◽  
Sw620 Cell

Abstract Foxp1 is a tumor suppressor in colon cancer. However, circFoxp1 derived from Foxp1 is an oncogene. In this study, we aim to investigate the role of circFoxp1 in colon cancer and the regulatory mechanism between circFoxp1 and Foxp1. 78 human colon tumor tissues and the matched paracancerous tissues were collected. Quantitative polymerase chain reaction, immunohistochemistry, quantitative methylation-specific PCR, chromatin immunoprecipitation assay, CCK-8 assay, and Tumor xenograft in nude mice were performed. The expression of circFoxp1 was increased and Foxp1 was reduced in colon cancer tissues, which were associated with a poor overall survival rate of the patients with colon cancer. CircFoxp1 recruited DNMT1 to the promoter of Foxp1, leading to promotor hypermethylation, thereby inhibiting Foxp1 transcription. Interfering circFoxp1 by siRNA in SW620 cells significantly inhibited cell viability, while knockdown Foxp1 expression partially restored SW620 cell viability. In addition, knockdown of circFoxp1 significantly sensitized colon cancer cells to Capecitabine in vitro and vivo through regulating Foxp1. We discovered a novel epigenetic pathway that circFoxp1 regulated Foxp1 in colon cancer cells. CircFoxp1 may regulate DNA methylation and demethylation to coordinate colon cancer cell proliferation and participate in chemotherapy drug responses. Therefore, circFoxp1 may be a potential therapeutic target for colon cancer.

Cryptotanshinone-Induced p53-Dependent Sensitization of Colon Cancer Cells to Apoptotic Drive by Regulation of Calpain and Calcium Homeostasis

2020 ◽  
Vol 48 (05) ◽  
pp. 1179-1202
Author(s):  
Yue Wang ◽  
Zhu Zhang ◽  
Kathy Ka-Wai Auyeung ◽  
Chi-Hin Cho ◽  
Ken Kin-Lam Yung ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Calcium Homeostasis ◽  
Tumor Xenograft ◽  
Calpain Inhibitor ◽  
Colon Cancer Cells ◽  
Calpain Activity ◽  
Chemotherapeutic Regimen

Over-expression of calpains in tumor tissues can be associated with cancer progression. Thus, inhibition of calpain activity using specific inhibitors has become a novel approach to control tumor growth. In this study, the anticancer potential of cryptotanshinone in combination with calpain inhibitor had been investigated in colon cancer cells and tumor xenograft. Cryptotanshinone elicited an initial endoplasmic reticular (ER) stress response, whereas prolonged stress would result in the promotion of apoptosis. It was then discovered that cryptotanshinone could cause rapid and sustained increase in cytosolic calcium in colon cancer cells accompanied by early GRP78 overexpression, which could be attenuated by pre-treatment of the calcium chelator BAPTA-AM. Cryptotanshinone also facilitated an early increase in calpain activity, which could be blocked by BAPTA-AM or the calpain inhibitor PD150606. A dynamic interaction between GRP78 and calpain during the action of cryptotanshinone was unveiled. This together with the altered NF-[Formula: see text]B signaling could be abolished by calpain inhibitor. GRP78 knockdown increased the sensitivity of cancer cells to cryptotanshinone-evoked apoptosis and reduction of cancer cell colony formation. Such sensitization of drug action had been confirmed to be p53-dependent by using p53-mutated (HT-29) and p53-deficient (HCT116 p53−∕−) cells. The synergistic antitumor effect of cryptotanshinone and calpain inhibitor was further exhibited in vivo. Taken together, findings in this study exemplify a new chemotherapeutic regimen comprising cryptotanshinone and calpain inhibitor by regulation of calpain and calcium homeostasis. This has provided us with new insights in the search of a potential target-specific neoadjuvant therapy against colon cancer.

scholarly journals Expression of carbohydrate-antigen sialyl-Lewis a on colon cancer cells promotes xenograft growth and angiogenesis in nude mice

2013 ◽  
Vol 45 (12) ◽  
pp. 2796-2800 ◽  
Author(s):  
Laura Terraneo ◽  
Laura Avagliano ◽  
Anna Caretti ◽  
Paola Bianciardi ◽  
Delfina Tosi ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Nude Mice ◽  
Carbohydrate Antigen ◽  
Colon Cancer Cells ◽  
Xenograft Growth ◽  
Sialyl Lewis ◽  
Sialyl Lewis A ◽  
Lewis A

Enantiomeric CopA3 dimer peptide suppresses cell viability and tumor xenograft growth of human gastric cancer cells

Tumor Biology ◽  
2015 ◽  
Vol 37 (3) ◽  
pp. 3237-3245 ◽  
Author(s):  
Joon ha Lee ◽  
In-woo Kim ◽  
Yong pyo Shin ◽  
Ho jin Park ◽  
Young shin Lee ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Tumor Xenograft ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Xenograft Growth ◽  
Tumor Xenograft Growth

The Effects of the Stromal Cell-Derived Cyclooxygenase-2 Metabolite Prostaglandin E2 on the Proliferation of Colon Cancer Cells

2010 ◽  
Vol 336 (2) ◽  
pp. 516-523 ◽  
Author(s):  
Seok-Woo Park ◽  
Hyo-Sun Kim ◽  
Myung-Sun Choi ◽  
Woo-Jin Jeong ◽  
Dae-Seog Heo ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Prostaglandin E2 ◽  
Cancer Cells ◽  
Stromal Cell ◽  
Cyclooxygenase 2 ◽  
Colon Cancer Cells

scholarly journals Novel anti-angiogenic effects of formononetin in human colon cancer cells and tumor xenograft

2012 ◽  
Vol 28 (6) ◽  
pp. 2188-2194 ◽  
Author(s):  
KATHY KA-WAI AUYEUNG ◽  
PUI-CHING LAW ◽  
JOSHUA KA-SHUN KO
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Human Colon ◽  
Tumor Xenograft ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Human Colon Cancer Cells

scholarly journals Hypoxia-induced Fascin-1 upregulation is regulated by Akt/Rac1 axis and enhances malignant properties of liver cancer cells via mediating actin cytoskeleton rearrangement and Hippo/YAP activation

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Jian Pu ◽  
Youguan Huang ◽  
Quan Fang ◽  
Jianchu Wang ◽  
Wenchuan Li ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Actin Cytoskeleton ◽  
Cancer Cells ◽  
Potential Functions ◽  
Tumor Xenograft ◽  
Mesenchymal Transition ◽  
Liver Cancer Cells ◽  
Xenograft Growth ◽  
Tumor Xenograft Growth ◽  
Cytoskeleton Rearrangement

AbstractIn solid tumors, hypoxia facilitates malignant progression of cancer cells by triggering epithelial-mesenchymal transition (EMT) and cancer stemness. Fascin-1, an actin-bundling protein, takes part in the formation of many actin-based cellular structures. In the present study, we explored the potential functions of hypoxia-induced upregulation of Fascin-1 in liver cancer. Transcriptome RNA-sequencing was conducted to identify hypoxia-related genes. The potential functions of Fascin-1 were evaluated by western blot, transwell migration and invasion assays, sphere-formation assay, tumor xenograft growth, gelatin zymography analysis, immunofluorescence, cell viability assay, soft agar assay, and flow cytometry. We found that Fascin-1 was upregulated by hypoxia in liver cancer cell lines, elevated in liver cancer patients and correlated with larger tumor size, lymph node metastasis, distant metastasis, and shorter overall survival. Knockdown of Fascin-1 suppressed migration, invasion, EMT, stemness, and tumor xenograft growth of liver cancer cells under both normoxia and hypoxia conditions, while forced Fascin-1 expression showed opposite effects. Moreover, hypoxia-induced upregulation of Fascin-1 was regulated by the Akt/Rac1 signaling, and inhibition of Akt/Rac1 signaling by EHop-016 and MK-2206 restrained migration, invasion, EMT, and stemness of liver cancer cells under hypoxia. Furthermore, Fascin-1 knockdown suppressed MMP-2 and MMP-9 expression, impaired actin cytoskeleton rearrangement, inactivated Hippo/YAP signaling, and increased Sorafenib sensitivity in liver cancer cells. Our study provided a novel insight of Fascin-1 in regulating migration, invasion, EMT, and stemness of liver cancer cells under normoxia and hypoxia conditions.

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