Abstract 835: Comparison of direct transplantation of colon cancer cells vs. tumor xenografts using orthotopic mouse model for colon cancer progression and metastasis

2016 ◽  
Author(s):  
Anathbandhu Chaudhuri ◽  
Liying Geng ◽  
Jing Wang
Keyword(s):  
Colon Cancer ◽  
Mouse Model ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Colon Cancer Cells ◽  
Orthotopic Mouse Model ◽  
Tumor Xenografts ◽  
Colon Cancer Progression

scholarly journals LINC01123 facilitates proliferation, invasion and chemoresistance of colon cancer cells

2020 ◽  
Vol 40 (8) ◽  
Author(s):  
Shicai Ye ◽  
Bilan Sun ◽  
Weiyun Wu ◽  
Caiyuan Yu ◽  
Ting Tian ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Colon Adenocarcinoma ◽  
Colon Cancer Cells ◽  
Prognostic Signature ◽  
Small Cell Lung ◽  
Non Coding Rna ◽  
Colon Cancer Progression ◽  
Long Non Coding Rna

Abstract Colon cancer is one of the major causes of cancer-related deaths worldwide. Long non-coding RNA (lncRNA) LINC01123 has been suggested to act as an oncogene in non-small cell lung cancer and a prognostic signature in head and neck squamous cell carcinoma. However, its role in colon cancer remains obscure. From TCGA database, LINC01123 was observed to be up-regulated in colon adenocarcinoma (COAD). Subsequently, the up-regulated LINC01123 was also detected in colon cancer cells. Functionally, LINC01123 could enhance cell proliferation, migration, invasion and angiogenesis. Moreover, the chemoresistance of colon cancer cells was verified to be promoted by LINC01123. Afterward, LINC01123 was found to bind with Ago2 and miR-34c-5p. Besides, miR-34c-5p was confirmed to inhibit the cellular process and chemoresistance of colon cancer cells. Then, VEGFA was disclosed to coexist with LINC01123 and miR-34c-5p in RNA-induced silencing complex. And TCGA database suggested that its expression was correlated with different stages of COAD. Moreover, it was uncovered that VEGFA could bind with miR-34c-5p and its expression positively correlated with LINC01123 expression. Finally, LINC01123 was proofed to regulate colon cancer progression and cells chemoresistance via VEGFA. In conclusion, LINC01123/miR-34c-5p/VEGFA axis promotes colon cancer malignancy and cells chemoresistance.

scholarly journals Colon Cancer and Perturbations of the Sphingolipid Metabolism

2019 ◽  
Vol 20 (23) ◽  
pp. 6051 ◽  
Author(s):  
Miroslav Machala ◽  
Jiřina Procházková ◽  
Jiřina Hofmanová ◽  
Lucie Králiková ◽  
Josef Slavík ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Human Colon ◽  
Sphingolipid Metabolism ◽  
Western World ◽  
Colon Cancer Cells ◽  
Colon Tumors ◽  
Metabolism Enzymes

The development and progression of colon cancer (CRC), a major cause of cancer-related death in the western world, is accompanied with alterations of sphingolipid (SL) composition in colon tumors. A number of enzymes involved in the SL metabolism have been found to be deregulated in human colon tumors, in experimental rodent studies, and in human colon cancer cells in vitro. Therefore, the enzymatic pathways that modulate SL levels have received a significant attention, due to their possible contribution to CRC development, or as potential therapeutic targets. Many of these enzymes are associated with an increased sphingosine-1-phosphate/ceramide ratio, which is in turn linked with increased colon cancer cell survival, proliferation and cancer progression. Nevertheless, more attention should also be paid to the more complex SLs, including specific glycosphingolipids, such as lactosylceramides, which can be also deregulated during CRC development. In this review, we focus on the potential roles of individual SLs/SL metabolism enzymes in colon cancer, as well as on the pros and cons of employing the current in vitro models of colon cancer cells for lipidomic studies investigating the SL metabolism in CRC.

scholarly journals Matrilysin (MMP-7) induces homotypic adhesion of human colon cancer cells and enhances their metastatic potential in nude mouse model

Oncogene ◽  
2003 ◽  
Vol 22 (54) ◽  
pp. 8662-8670 ◽  
Author(s):  
Mitomu Kioi ◽  
Kazuhiro Yamamoto ◽  
Shouichi Higashi ◽  
Naohiko Koshikawa ◽  
Kiyohide Fujita ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Mouse Model ◽  
Cancer Cells ◽  
Nude Mouse ◽  
Human Colon ◽  
Metastatic Potential ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Nude Mouse Model ◽  
Human Colon Cancer Cells

scholarly journals Antiproliferative Effects of Fluoxetine on Colon Cancer Cells and in a Colonic Carcinogen Mouse Model

PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e50043 ◽  
Author(s):  
Vinicius Kannen ◽  
Henning Hintzsche ◽  
Dalila L. Zanette ◽  
Wilson A. Silva ◽  
Sérgio B. Garcia ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Mouse Model ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
Antiproliferative Effects

scholarly journals LINC02418 promotes colon cancer progression by suppressing apoptosis via interaction with miR-34b-5p/BCL2 axis

2020 ◽  
Author(s):  
Jun Tian ◽  
Peng Cui ◽  
Yifei Li ◽  
Xuequan Yao ◽  
Xiaoyu Wu ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Human Colon ◽  
Luciferase Assay ◽  
Colon Cancer Cells ◽  
Multiple Cancer ◽  
Human Colon Cancer ◽  
Prediction Of Prognosis

Abstract Background LncRNAs have been demonstrated to be functional regulators in tumor progression through interaction with various signaling pathways in multiple cancer types. However, the effect of LINC02418 on CRC progression still remains unclear. Methods LncRNA expression profile in CRC tissues was explored by using the TCGA database. The expressional level of LINC02418 in CRC patients was confirmed by qRT-PCR. Kaplan-Meier analyses was used to investigate the correlations between LINC02418 and OS of patients with CRC. After stably transducing sh-LINC02418 and sh-NC into HCT116 and LoVo cells, cell proliferative, migratory and invasive abilities were detected by CCK-8 assay, colony formation assay and trans-well assay, respectively. The binding between LINC02418 and miR-34b-5p, and the interaction between miR-34b-5p and BCL2 were determined by dual-luciferase assay. Western blot experiments were conducted to further explore the effect of miR-34b-5p on BCL2 signaling pathway. Rescue experiments were performed to uncover the role of LINC02418 /miR-34b-5p/ BCL2 axis in CRC progression. Results LINC02418 was upregulated in human colon cancer samples and its high expression correlated with poor prognosis. LINC02418 promoted cancer progression by enhancing tumor growth, cell mobility and invasiveness of colon cancer cells. Additionally, LINC02418 could physically bind to miR-34b-5p and subsequently interact with BCL2 signaling pathway. Down-regulation of LINC02418 reduced cell proliferation, but transfection of miR-34b-5p inhibitor or BCL2 in LINC02418-silenced colon cancer cells significantly promoted cell growth. Conclusions LINC02418 was upregulated in human colon cancer samples and could be used as indicator for prediction of prognosis. LINC02418 acted as a tumor driver by negatively regulating cell apoptosis through LINC02418 /miR-34b-5p/ BCL2 axis and in colorectal cancer.

scholarly journals Correction: Anti-cancer effects of Bifidobacterium species in colon cancer cells and a mouse model of carcinogenesis

PLoS ONE ◽  
2020 ◽  
Vol 15 (6) ◽  
pp. e0234777
Author(s):  
Parisa Asadollahi ◽  
Roya Ghanavati ◽  
Mahdi Rohani ◽  
Shabnam Razavi ◽  
Maryam Esghaei ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Mouse Model ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
Bifidobacterium Species ◽  
Anti 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 SLC6A14, a Na+/Cl−-coupled amino acid transporter, functions as a tumor promoter in colon and is a target for Wnt signaling

2020 ◽  
Vol 477 (8) ◽  
pp. 1409-1425 ◽  
Author(s):  
Mohd O. F. Sikder ◽  
Sathish Sivaprakasam ◽  
Timothy P. Brown ◽  
Muthusamy Thangaraju ◽  
Yangzom D. Bhutia ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Amino Acid ◽  
Wnt Signaling ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Critical Role ◽  
The Cancer Genome Atlas ◽  
Tumor Promoter ◽  
Mouse Tumor ◽  
Colon Cancer Cells

SLC6A14 is a Na+/Cl−-coupled transporter for neutral and cationic amino acids. It is expressed at basal levels in the normal colon but is up-regulated in colon cancer. However, the relevance of this up-regulation to cancer progression and the mechanisms involved in the up-regulation remain unknown. Here, we show that SLC6A14 is essential for colon cancer and that its up-regulation involves, at least partly, Wnt signaling. The up-regulation of the transporter is evident in most human colon cancer cell lines and also in a majority of patient-derived xenografts. These findings are supported by publicly available TCGA (The Cancer Genome Atlas) database. Treatment of colon cancer cells with α-methyltryptophan (α-MT), a blocker of SLC6A14, induces amino acid deprivation, decreases mTOR activity, increases autophagy, promotes apoptosis, and suppresses cell proliferation and invasion. In xenograft and syngeneic mouse tumor models, silencing of SLC6A14 by shRNA or blocking its function by α-MT reduces tumor growth. Similarly, the deletion of Slc6a14 in mice protects against colon cancer in two different experimental models (inflammation-associated colon cancer and genetically driven colon cancer). In colon cancer cells, expression of the transporter is reduced by Wnt antagonist or by silencing of β-catenin whereas Wnt agonist or overexpression of β-catenin shows the opposite effect. Finally, SLC6A14 as a target for β-catenin is confirmed by chromatin immunoprecipitation. These studies demonstrate that SLC6A14 plays a critical role in the promotion of colon cancer and that its up-regulation in cancer involves Wnt signaling. These findings identify SLC6A14 as a promising drug target for the treatment of colon cancer.

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