Characterization of the conversion between CD133<sup>+</sup>and CD133<sup>-</sup>cells in colon cancer SW620 cell line

Feng, Jianming; Jiang, Yi; Chen, Yi; Li, Jiaxin; Tong, Linjiang; Zhang, Jin; Huang, Yiran; Ding, Jian

doi:10.4161/cbt.22000

Cited by 21 publications

(15 citation statements)

References 29 publications

(41 reference statements)

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“…To study photochemical delivery of the CD133-targeting recombinant IT scFvCD133/-rGelonin (clone 7), the CD133 positive colorectal adenocarcinoma HT29 and WiDr cell lines were used, in addition to the CD133 (clone 7) negative / low-expression murine fibrosarcoma NIH/3T3, human glioblastoma U87, breast cancer MDA-MB-231 and MCF-7 cell lines. Spontaneous conversion of CD133 expression between CD133 positive and negative cells may be a challenge, as reported by Feng et al (Feng et al, 2012). Our FACS sorted CD133-high and -low HT29 cells were confirmed to preserve the CD133 status when investigated for CD133 specificity by PCI of scFvCD133/rGelonin.…”

Section: Cell Linessupporting

confidence: 76%

Development of resistance to photodynamic therapy (PDT) in human breast cancer cells is photosensitizer-dependent: Possible mechanisms and approaches for overcoming PDT-resistance

Olsen

Weyergang

Edwards

et al. 2017

Biochemical Pharmacology

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Here we report on the induction of resistance to photodynamic therapy (PDT) in the ABCG2-high human breast cancer cell line MA11 after repetitive PDT, using either Pheophorbide A (PhA) or di-sulphonated meso-tetraphenylchlorin (TPCS) as photosensitizer. Resistance to PhA-PDT was associated with enhanced expression of the efflux pump ABCG2. TPCS-PDT-resistance was neither found to correspond with lower TPCS-accumulation nor reduced generation of reactive oxygen species (ROS). Cross-resistance to chemotherapy (doxorubicin) or radiotherapy was not observed. TPCS-PDT-resistant cells acquired a higher proliferation capacity and an enhanced expression of EGFR and ERK1/2. p38 MAPK was found to be a death-signalling pathway in the MA11 cells post TPCS-PDT, contrasting the MA11/TR cells in which PDT generated a sustained phosphorylation of p38 that had lost its death-mediated signalling, and an abrogated activation of its downstream effector MAPKAPK2. No difference in apoptosis, necrosis or autophagy responses was found between the treated cell lines. Development of TPCS-PDT resistance in the MDA-MB-231 cell line was also established, however, p38 MAPK did not play a role in the PDT-resistance. MCF-7 cells did not develop TPCS-PDT-resistance. Photochemical internalisation (PCI) of 1 pM of EGF-saporin induced equal strong cytotoxicity in both MA11 and MA11/TR cells. In conclusion, loss of p38 MAPK-inducing death signalling is the main mechanism of resistance to TPCS-PDT in the MA11/TR cell line. This work provides mechanistic knowledge of intrinsic and acquired PDT-resistance which is dependent on choice of photosensitizer, and suggests PCI as a rational therapeutic intervention for the elimination of PDT-resistant cells.

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Section: Cell Linessupporting

confidence: 76%

Development of resistance to photodynamic therapy (PDT) in human breast cancer cells is photosensitizer-dependent: Possible mechanisms and approaches for overcoming PDT-resistance

Olsen

Weyergang

Edwards

et al. 2017

Biochemical Pharmacology

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“…Accordingly, in view of the reported role of CSCs during early stages of tumor initiation, the promotion of self-renewal identified here provides a potential rationale for the proposed role of progastrin overexpression as a risk marker of neoplastic transformation in patients with hyperplastic colonic polyps (46). Homeostatic equilibrium within heterogeneous tumor cell populations involves proliferation and cell death rates of CSCs and non-CSCs, as well as rates of phenotypic transitions between the CSC and non-CSC states (8,32,47). Using ALDH activity as a marker to enrich functional CSCs, our results indicate that progastrin promotes ALDH high CSC survival and self-renewal.…”

Section: Discussionmentioning

confidence: 81%

“…The recent literature suggests that stochastic transitions between non-stem and stem-like cells contribute to the maintenance of phenotypic equilibrium within cancer cell populations (8,32 (Fig. 3C).…”

Section: Progastrin Promotes the Self-renewal Of Colorectal Cells In mentioning

confidence: 99%

Autocrine Secretion of Progastrin Promotes the Survival and Self-Renewal of Colon Cancer Stem–like Cells

et al. 2016

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Subpopulations of cancer stem-like cells (CSC) are thought to drive tumor progression and posttreatment recurrence in multiple solid tumors. However, the mechanisms that maintain stable proportions of self-renewing CSC within heterogeneous tumors under homeostatic conditions remain poorly understood. Progastrin is a secreted peptide that exhibits tumorforming potential in colorectal cancer, where it regulates pathways known to modulate colon CSC behaviors. In this study, we investigated the role of progastrin in regulating CSC phenotype in advanced colorectal cancer. Progastrin expression and secretion were highly enriched in colon CSC isolated from human colorectal cancer cell lines and colon tumor biopsies.Progastrin expression promoted CSC self-renewal and survival, whereas its depletion by RNA interference-mediated or antibody-mediated strategies altered the homeostatic proportions of CSC cells within heterogeneous colorectal cancer tumors. Progastrin downregulation also decreased the frequency of ALDH high cells, impairing their tumor-initiating potential, and inhibited the high glycolytic activity of ALDH high CSC to limit their self-renewal capability. Taken together, our results show how colorectal CSC maintain their tumor-initiating and selfrenewal capabilities by secreting progastrin, thereby contributing to the tumor microenvironment to support malignancy.

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“…Interestingly, we noticed down-regulation of CD133 when treated with high doses of VCR and CDDP, which should not be interpreted to mean that CD133 permanently disappeared, because the same cells were able to significantly express CD133 when combined with VPA. This variability in CD133 expression is under control of the epigenetic modification which could explain why sorted CD133− cells can acquire the CD133 surface marker or CD133+ cells can lose it in some tumors [ 56 ].…”

Section: Discussionmentioning

confidence: 99%

Valproic Acid Increases CD133 Positive Cells that Show Low Sensitivity to Cytostatics in Neuroblastoma

Khalil

Hraběta

Groh³

et al. 2016

PLoS ONE

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Valproic acid (VPA) is a well-known antiepileptic drug that exhibits antitumor activities through its action as a histone deacetylase inhibitor. CD133 is considered to be a cancer stem cell marker in several tumors including neuroblastoma. CD133 transcription is strictly regulated by epigenetic modifications. We evaluated the epigenetic effects of treatment with 1mM VPA and its influence on the expression of CD133 in four human neuroblastoma cell lines. Chemoresistance and cell cycle of CD133+ and CD133− populations were examined by flow cytometry. We performed bisulfite conversion followed by methylation-sensitive high resolution melting analysis to assess the methylation status of CD133 promoters P1 and P3. Our results revealed that VPA induced CD133 expression that was associated with increased acetylation of histones H3 and H4. On treatment with VPA and cytostatics, CD133+ cells were mainly detected in the S and G2/M phases of the cell cycle and they showed less activated caspase-3 compared to CD133− cells. UKF-NB-3 neuroblastoma cells which express CD133 displayed higher colony and neurosphere formation capacities when treated with VPA, unlike IMR-32 which lacks for CD133 protein. Induction of CD133 in UKF-NB-3 was associated with increased expression of phosphorylated Akt and pluripotency transcription factors Nanog, Oct-4 and Sox2. VPA did not induce CD133 expression in cell lines with methylated P1 and P3 promoters, where the CD133 protein was not detected. Applying the demethylating agent 5-aza-2’-deoxycytidine to the cell lines with methylated promoters resulted in CD133 re-expression that was associated with a drop in P1 and P3 methylation level. In conclusion, CD133 expression in neuroblastoma can be regulated by histone acetylation and/or methylation of its CpG promoters. VPA can induce CD133+ cells which display high proliferation potential and low sensitivity to cytostatics in neuroblastoma. These results give new insight into the possible limitations to use VPA in cancer therapy.

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Characterization of the conversion between CD133⁺and CD133^-cells in colon cancer SW620 cell line

Cited by 21 publications

References 29 publications

Development of resistance to photodynamic therapy (PDT) in human breast cancer cells is photosensitizer-dependent: Possible mechanisms and approaches for overcoming PDT-resistance

Development of resistance to photodynamic therapy (PDT) in human breast cancer cells is photosensitizer-dependent: Possible mechanisms and approaches for overcoming PDT-resistance

Autocrine Secretion of Progastrin Promotes the Survival and Self-Renewal of Colon Cancer Stem–like Cells

Valproic Acid Increases CD133 Positive Cells that Show Low Sensitivity to Cytostatics in Neuroblastoma

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Characterization of the conversion between CD133+and CD133-cells in colon cancer SW620 cell line

Cited by 21 publications

References 29 publications

Development of resistance to photodynamic therapy (PDT) in human breast cancer cells is photosensitizer-dependent: Possible mechanisms and approaches for overcoming PDT-resistance

Development of resistance to photodynamic therapy (PDT) in human breast cancer cells is photosensitizer-dependent: Possible mechanisms and approaches for overcoming PDT-resistance

Autocrine Secretion of Progastrin Promotes the Survival and Self-Renewal of Colon Cancer Stem–like Cells

Valproic Acid Increases CD133 Positive Cells that Show Low Sensitivity to Cytostatics in Neuroblastoma

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Characterization of the conversion between CD133⁺and CD133^-cells in colon cancer SW620 cell line