scholarly journals Curcumin attenuates resistance to irinotecan via induction of apoptosis of cancer stem cells in chemoresistant colon cancer cells

2018 ◽  
Author(s):  
Pengfei Su ◽  
Yong Yang ◽  
Guoxin Wang ◽  
Xiaowu Chen ◽  
Yongle Ju
Keyword(s):  
Stem Cells ◽  
Colon Cancer ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
Induction Of Apoptosis

pH- and GSH-Sensitive Hyaluronic Acid-MP Conjugate Micelles for Intracellular Delivery of Doxorubicin to Colon Cancer Cells and Cancer Stem Cells

2018 ◽  
Vol 19 (9) ◽  
pp. 3725-3737 ◽  
Author(s):  
Tilahun Ayane Debele ◽  
Lu-Yi Yu ◽  
Cheng-Sheng Yang ◽  
Yao-An Shen ◽  
Chun-Liang Lo
Keyword(s):  
Stem Cells ◽  
Colon Cancer ◽  
Hyaluronic Acid ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Intracellular Delivery ◽  
Colon Cancer Cells

Autophagy of cancer stem cells is involved with chemoresistance of colon cancer cells

2013 ◽  
Vol 434 (4) ◽  
pp. 898-903 ◽  
Author(s):  
Shaobin Wu ◽  
Xianwei Wang ◽  
Jinxiang Chen ◽  
Yuxiang Chen
Keyword(s):  
Stem Cells ◽  
Colon Cancer ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Colon Cancer Cells

Abstract 252: Molecular characterization of cancer stem cells isolated from primary colon cancer cells.

2013 ◽  
Author(s):  
Martin Lange ◽  
Dirk Schumacher ◽  
Thomas Hauling ◽  
Christian Regenbrecht ◽  
Oliver Politz ◽  
...  
Keyword(s):  
Stem Cells ◽  
Colon Cancer ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Molecular Characterization ◽  
Colon Cancer Cells ◽  
Primary Colon Cancer ◽  
Primary Colon

scholarly journals An integrated microfluidic system for screening of phage-displayed peptides specific to colon cancer cells and colon cancer stem cells

2015 ◽  
Vol 9 (5) ◽  
pp. 054121 ◽  
Author(s):  
Yu-Jui Che ◽  
Huei-Wen Wu ◽  
Lien-Yu Hung ◽  
Ching-Ann Liu ◽  
Hwan-You Chang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Colon Cancer ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Microfluidic System ◽  
Colon Cancer Cells ◽  
Colon Cancer Stem Cells

scholarly journals Elevated ATGL in colon cancer cells and cancer stem cells promotes metabolic and tumorigenic reprogramming reinforced by obesity

Oncogenesis ◽  
2021 ◽  
Vol 10 (11) ◽  
Author(s):  
Rida Iftikhar ◽  
Harrison M. Penrose ◽  
Angelle N. King ◽  
Joshua S. Samudre ◽  
Morgan E. Collins ◽  
...  
Keyword(s):  
Stem Cells ◽  
Colon Cancer ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Cancer Progression ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Increased Risk

AbstractObesity is a worldwide epidemic associated with increased risk and progression of colon cancer. Here, we aimed to determine the role of adipose triglyceride lipase (ATGL), responsible for intracellular lipid droplet (LD) utilization, in obesity-driven colonic tumorigenesis. In local colon cancer patients, significantly increased ATGL levels in tumor tissue, compared to controls, were augmented in obese individuals. Elevated ATGL levels in human colon cancer cells (CCC) relative to non-transformed were augmented by an obesity mediator, oleic acid (OA). In CCC and colonospheres, enriched in colon cancer stem cells (CCSC), inhibition of ATGL prevented LDs utilization and inhibited OA-stimulated growth through retinoblastoma-mediated cell cycle arrest. Further, transcriptomic analysis of CCC, with inhibited ATGL, revealed targeted pathways driving tumorigenesis, and high-fat-diet obesity facilitated tumorigenic pathways. Inhibition of ATGL in colonospheres revealed targeted pathways in human colonic tumor crypt base cells (enriched in CCSC) derived from colon cancer patients. In CCC and colonospheres, we validated selected transcripts targeted by ATGL inhibition, some with emerging roles in colonic tumorigeneses (ATG2B, PCK2, PGAM1, SPTLC2, IGFBP1, and ABCC3) and others with established roles (MYC and MUC2). These findings demonstrate obesity-promoted, ATGL-mediated colonic tumorigenesis and establish the therapeutic significance of ATGL in obesity-reinforced colon cancer progression.

scholarly journals Registered report: Wnt activity defines colon cancer stem cells and is regulated by the microenvironment

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
James Evans ◽  
Anthony Essex ◽  
Hong Xin ◽  
Nurith Amitai ◽  
Lindsey Brinton ◽  
...  
Keyword(s):  
Stem Cells ◽  
Colon Cancer ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Cell Biology ◽  
Cancer Biology ◽  
Stem Cell Markers ◽  
Colon Cancer Cells ◽  
Colon Cancer Stem Cells

The Reproducibility Project: Cancer Biology seeks to address growing concerns about reproducibility in scientific research by replicating selected results from a substantial number of high-profile papers in the field of cancer biology. The papers, which were published between 2010 and 2012, were selected on the basis of citations and Altmetric scores (<xref ref-type="bibr" rid="bib5">Errington et al., 2014</xref>). This Registered report describes the proposed replication plan of key experiments from ‘Wnt activity defines colon cancer stem cells and is regulated by the microenvironment’ by Vermeulen and colleagues, published in Nature Cell Biology in 2010 (<xref ref-type="bibr" rid="bib20">Vermeulen et al., 2010</xref>). The key experiments that will be replicated are those reported in Figures 2F, 6D, and 7E. In these experiments, Vermeulen and colleagues utilize a reporter for Wnt activity and show that colon cancer cells with high levels of Wnt activity also express cancer stem cell markers (Figure 2F; <xref ref-type="bibr" rid="bib20">Vermeulen et al., 2010</xref>). Additionally, treatment either with conditioned medium derived from myofibroblasts or with hepatocyte growth factor restored clonogenic potential in low Wnt activity colon cancer cells in vitro (Figure 6D; <xref ref-type="bibr" rid="bib20">Vermeulen et al., 2010</xref>) and in vivo (Figure 7E; <xref ref-type="bibr" rid="bib20">Vermeulen et al., 2010</xref>). The Reproducibility Project: Cancer Biology is a collaboration between the Center for Open Science and Science Exchange and the results of the replications will be published in eLife.

scholarly journals E2F7 Transcriptionally Inhibits MicroRNA-199b Expression to Promote USP47, Thereby Enhancing Colon Cancer Tumor Stem Cell Activity and Promoting the Occurrence of Colon Cancer

2021 ◽  
Vol 10 ◽  
Author(s):  
Xiong Guo ◽  
Ling Liu ◽  
Qi Zhang ◽  
Weiming Yang ◽  
Yang Zhang
Keyword(s):  
Stem Cells ◽  
Colon Cancer ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Cell Activity ◽  
Luciferase Reporter ◽  
Tumor Stem Cell ◽  
Colon Cancer Cells ◽  
Loss Of Function ◽  
Colon Cancer Stem Cells

microRNAs (miRNAs) can modulate the expression level of genes in a post-transcription manner, which are closely related to growth and metastasis of colon cancer. Herein, we aimed to explore how miR-199b influences colon cancer and to characterize its underlying molecular mechanism associating with E2F transcription factor 7 (E2F7). Assays of RT-qPCR, Western blot, and immunohistochemistry were utilized to detect the expression of E2F7 in the tissue samples collected from 30 patients diagnosed with colon cancer. Flow analysis was utilized to detect the ratio of ALDH1+ and CD133+ colon cancer stem cells. The interaction between E2F7, miR-199b, USP47, and MAPK was identified by ChIP-Seq analysis, luciferase reporter, RNA pull-down, co-immunoprecipitation, as well as glutathione-S-transferase (GST) pull-down experiments. Based on the gain- and loss-of-function approaches, the cellular functions of colon cancer cells by the E2F7-regulated miR-199b/USP47/MAPK axis were assessed. It was identified that E2F7 are expressed highly in the collected colon cancer tissues. E2F7 silencing reduced the production of ALDH1+ and CD133+ colon cancer stem cells and antagonized the effects of 5-fluorouracil (5-FU) treatment. Besides, the silencing of E2F7 was observed to suppress the oxidative stress, proliferation, migration, as well as invasion of ALDH1+ cells in vitro and tumorigenesis of colon cancer cells in vivo. Our findings reveal the pro-oncogenic effect of E2F7 on colon cancer development, highlighting E2F7 as a novel target for therapeutic strategy for colon cancer.

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