Role of CD44high/CD133high HCT-116 cells in the tumorigenesis of colon cancer

Zhou, Jin‐Yong; Chen, Min; Ma, Long; Wang, Xiaoxiao; Chen, Yugen; Liu, Shenlin

doi:10.18632/oncotarget.7084

Cited by 63 publications

(53 citation statements)

References 33 publications

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“…Emerging evidence has shown that a subpopulation of cells, cancer stem cells (CSCs) or tumor-initiating cells, displays stem cell characteristics that influence tumorigenesis [2]. These cells possess specific properties, including self-renewal, differentiation potential, resistance to chemotherapy and high tumorigenicity.…”

Section: Introductionmentioning

confidence: 99%

“…CSCs have been prospectively identified in colorectal cancer by their expression of specific surface markers, such as leucine-rich-repeat-containing G-protein-coupled receptor 5 (Lgr5), CD133, CD44, CD166, EpCAM (epithelial cell adhesion molecule), CD24, CD29, and aldehyde dehydrogenase (ALDH), among others [2, 8-10]. More recently, it was reported that Lgr5 showed promise as a biomarker for colorectal CSCs [9, 11, 12].…”

Section: Introductionmentioning

confidence: 99%

“…CD44 overexpression increases tumor growth and anti-apoptotic properties. A recent study showed that CD133+CD44+ cells isolated from human colorectal cancer cell line exhibited CSC properties [2]. …”

Section: Introductionmentioning

confidence: 99%

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Lgr5+CD44+EpCAM+ Strictly Defines Cancer Stem Cells in Human Colorectal Cancer

Leng

Xia

Chen

et al. 2018

Cell Physiol Biochem

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Background/Aims: Although EpCAM+CD44+ cells exhibit more stem-like properties than did EpCAM-CD44- cells, the specificity of EpCAM combined with CD44 in defining CSCs needs further improvement. Lgr5 is used as a biomarker to isolate cancer stem cells (CSCs) in colorectal cancer. However, it remains unclear whether Lgr5, along with EpCAM and CD44, can further identify and define CSCs in colorectal cancer. Methods: Lgr5+CD44+EpCAM+, Lgr5+CD44+EpCAM-, Lgr5+CD44-EpCAM+, Lgr5-CD44+EpCAM+, and Lgr5-CD44-EpCAM-cells were separately isolated using fluorescence-activated cell sorting (FACS). Colony formation, self-renewal, differentiation, and tumorigenic properties of these cells were investigated through in vitro experiments and in vivo tumor xenograft models. The expression of stemness genes and CSC- and epithelial-mesenchymal transition (EMT)-related genes, such as KLF4, Oct4, Sox2, Nanog, CD133, CD44, CD166, ALDH1, Lgr5, E-cadherin, ZO-1, Vimentin, Snail, Slug, and Twist, was examined using real-time PCR. Results: Lgr5-positive subpopulations exhibited higher capacities for colony formation, self-renewal, differentiation, and tumorigenicity as well as higher expression of stemness genes and mesenchymal genes and lower expression of epithelial genes than did Lgr5-negative subpopulations. Conclusion: Our data revealed that tumorigenic cells were highly restricted to Lgr5-positive subpopulations. Most importantly, Lgr5+CD44+EpCAM+ cells exhibited more pronounced CSC-like traits than did any other subpopulation, indicating that Lgr5 combined with CD44 and EpCAM can further improve the stem-like traits of CSCs in colorectal cancer.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Lgr5+CD44+EpCAM+ Strictly Defines Cancer Stem Cells in Human Colorectal Cancer

Leng

Xia

Chen

et al. 2018

Cell Physiol Biochem

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“…In this context, it is noteworthy that CD44 + and CD133 + stem cells have been documented in several human colon carcinoma-derived cell lines (31)(32)(33), and positive expression of these markers in colon carcinoma-derived HCT-116 cells have been correlated with the metastatic phenotype (31). In addition, as regards the upregulated expression of CD44 and c-Myc, supportive lines of evidence suggest that these Apc target genes are upregulated in colon cancer stem cells (20)(21)(22)(31)(32)(33). Furthermore, the SUL-R phenotype also raises the possibility that these resistant cells may display altered expression of non-COX targets, such as β-catenin, E-cadherin, mitochondrial apoptotic proteins, cyclin-dependent kinase inhibitor p21 WAF1/CIP1 and peroxisome proliferator-activated receptor-γ (PPAR-γ).…”

Section: Discussionmentioning

confidence: 99%

“…It is noteworthy that drug-resistant cancer stem cells have been isolated and characterized from colon carcinoma-derived cell culture models (31)(32)(33) and from luminal A and triple-negative breast carcinoma-derived cell culture models (43,44).…”

Section: Discussionmentioning

confidence: 99%

Anti‑inflammatory drug resistance selects putative cancer stem cells in a cellular model for genetically predisposed colon cancer

Telang¹

2017

Oncol Lett

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-/-cells with SUL and CLX resulted in inhibition of anchorage-independent colony formation in vitro, which is indicative of reduced cancer risk in vivo. Mechanistically, SUL and CLX suppressed the expression of the Apc target genes β-catenin, cyclin D1, c-Myc and cyclooxygenase-2. Long-term treatment with high concentrations of SUL and CLX led to the selection of hyper-proliferative drug-resistant phenotypes. The Apc -/-SUL-resistant phenotype displayed spheroid formation and enhanced the expression of the stem cell-specific molecular markers CD44, CD133 and c-Myc. These data demonstrated the growth-inhibitory efficacy of SUL and CLX and indicated that drug resistance leads to the selection of a putative cancer stem cell phenotype. The study outcome validates a stem cell-targeted mechanistic approach to identify testable alternative leads for chemotherapy-resistant colon cancer.

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Molecular characterization of an MLL1 fusion and its role in chromosomal instability

et al. 2018

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Chromosomal rearrangements involving the mixed‐lineage leukemia (MLL1) gene are common in a unique group of acute leukemias, with more than 100 fusion partners in this malignancy alone. However, do these fusions occur or have a role in solid tumors? We performed extensive network analyses of MLL1‐fusion partners in patient datasets, revealing that multiple MLL1‐fusion partners exhibited significant interactions with the androgen‐receptor signaling pathway. Further exploration of tumor sequence data from TCGA predicts the presence of MLL1 fusions with truncated SET domain in prostate tumors. To investigate the physiological relevance of MLL1 fusions in solid tumors, we engineered a truncated version of MLL1 by fusing it with one of its known fusion partners, ZC3H13, to use as a model system. Functional characterization with cell‐based assays revealed that MLL1‐ZC3H13 fusion induced chromosomal instability, affected mitotic progression, and enhanced tumorsphere formation. The MLL1‐ZC3H13 chimera consistently increased the expression of a cancer stem cell marker (CD44); in addition, we detected potential collateral lethality between DOT1L and MLL1 fusions. Our work reveals that MLL1 fusions are likely prevalent in solid tumors and exhibit a potential pro‐tumorigenic role.

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Role of CD44high/CD133high HCT-116 cells in the tumorigenesis of colon cancer

Cited by 63 publications

References 33 publications

Lgr5+CD44+EpCAM+ Strictly Defines Cancer Stem Cells in Human Colorectal Cancer

Lgr5+CD44+EpCAM+ Strictly Defines Cancer Stem Cells in Human Colorectal Cancer

Anti‑inflammatory drug resistance selects putative cancer stem cells in a cellular model for genetically predisposed colon cancer

Molecular characterization of an MLL1 fusion and its role in chromosomal instability

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