Subpopulations of Stem-like Cells in Side Population Cells from the Human Bladder Transitional Cell Cancer Cell Line T24

Zf, Ning; Yj, Huang; Tx, Lin; Yx, Zhou; Jiang, Cheng; Kw, Xu; Huang, Hongzhang; Xb, Yin; Huang, Junhui

doi:10.1177/147323000903700304

Cited by 44 publications

(38 citation statements)

References 26 publications

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“…Furthermore, expression of the ABC transporters ABCG2 and ABCB1 (also known as MDR1) was confirmed, and side population cells express the stem cell markers POU5F1 and BMI1, implying a stem-like phenotype of side population cells (36). In an independent study, side population cells isolated from the T24 bladder cancer cell line showed a more quiescent cell state, asymmetric cell division, rapid cell growth, and colony formation and chemo-and radioresistance, providing further evidence for CSC enrichment (37). Moreover, side population cells isolated from patient samples have increased clonogenic and proliferative capacity, a higher percentage of quiescent cells, and long-term selfrenewal.…”

Section: Urothelial Stem Cellsmentioning

confidence: 80%

Epithelial Plasticity, Cancer Stem Cells, and the Tumor-Supportive Stroma in Bladder Carcinoma

Horst

Bos

Pluijm

2012

Molecular Cancer Research

142

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High recurrence rates and poor survival rates of metastatic bladder cancer emphasize the need for a drug that can prevent and/or treat bladder cancer progression and metastasis formation. Accumulating evidence suggests that cancer stem/progenitor cells are involved in tumor relapse and therapy resistance in urothelial carcinoma. These cells seem less affected by the antiproliferative therapies, as they are largely quiescent, have an increased DNA damage response, reside in difficult-to-reach, protective cancer stem cell niches and express ABC transporters that can efflux drugs from the cells. Recent studies have shown that epithelial-to-mesenchymal transition (EMT), a process in which sessile, epithelial cells switch to a motile, mesenchymal phenotype may render cancer cells with cancer stem cells properties and/or stimulate the expansion of this malignant cellular subpopulation. As cancer cells undergo EMT, invasiveness, drug resistance, angiogenesis, and metastatic ability seem to increase in parallel, thus giving rise to a more aggressive tumor type. Furthermore, the tumor microenvironment (tumor-associated stromal cells, extracellular matrix) plays a key role in tumorigenesis, tumor progression, and metastasis formation. Taken together, the secret for more effective cancer therapies might lie in developing and combining therapeutic strategies that also target cancer stem/progenitor cells and create an inhospitable microenvironment for highly malignant bladder cancer cells. This review will focus on the current concepts about the role of cancer stem cells, epithelial plasticity, and the supportive stroma in bladder carcinoma. The potential implications for the development of novel bladder cancer therapy will be discussed. Mol Cancer Res; 10(8); 995-1009. Ó2012 AACR. Bladder CancerWorldwide, an estimated number of 386,300 new cases and 150,200 deaths from bladder cancer occurred in 2008, with the majority of cases (77%) occurring in men. Thereby, bladder cancer is the seventh most common cancer and the ninth most common cause of cancer-related death in men. Bladder cancer is most common in developed countries, where 63% of the cases occurred in 2002. In Europe and the United States, for example, bladder cancer is the fourth most common cancer in males. Overall, the 5-year survival rate of bladder cancer is approximately 80%, and it varies with the stage of the tumor, ranging from 97% for carcinoma in situ to 6% for metastatic disease.Urothelial carcinoma is a heterogeneous disease and multifocal tumors can develop in the same patient. Multifocality can be explained by the monoclonal theory, that is, multiple tumors arise from a single transformed cell or by the field cancerization theory (1). In the latter, exposure of the urothelium to important risk factors for bladder cancer, such as occupational carcinogens induces changes at different sites of the urothelium. As described by Cheng and colleagues (1), urothelial carcinoma in situ is a well-established precursor of invasive bladder cancer and may be...

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Section: Urothelial Stem Cellsmentioning

confidence: 80%

Epithelial Plasticity, Cancer Stem Cells, and the Tumor-Supportive Stroma in Bladder Carcinoma

Horst

Bos

Pluijm

2012

Molecular Cancer Research

142

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“…Subpopulations of stem-like cells expressing BCRP were found in cell lines or primary tumor samples from a wide assortment of solid tumors, including head and neck cancer [205–207], breast carcinoma [202], small cell and non-small cell lung cancer [208–212], gastrointestinal cancers including pancreatic [213, 214], colon [215, 216] and hepatocellular [217–219], ovarian cancer [220], gliomas [221, 222], malignant peripheral nerve sheath tumors [223], osteosarcoma [224, 225], prostate cancer [226], Ewing’s sarcoma [227], odontogenic tumors [228], transitional cell carcinoma of the bladder [229], and neuroblastoma [230]. Details of these findings will be discussed within individual tumor types in the ensuing paragraphs.…”

Section: Section 5 Recent Findings In Solid Tumorsmentioning

confidence: 99%

“…In malignant amelioblastic (odontogenic) tumors, CD133, BMI-1 and ABCG2 were found to be expressed; BCRP expression was higher in the neoplastic tissue than in tooth germ tissues [228]. Evidence for SP cells that overexpress BCRP/ABCG2 was found in the bladder transitional cell carcinoma cell line T24 [229]. Evidence for a stem cell population was found in 4 of 8 neuroblastoma cell lines which expressed the stem cell markers CD133, ABCG2 and nestin [230].…”

Section: Section 5 Recent Findings In Solid Tumorsmentioning

confidence: 99%

Role of breast cancer resistance protein (BCRP/ABCG2) in cancer drug resistance

Natarajan¹,

Xie²,

Baer³

et al. 2012

Biochemical Pharmacology

356

273

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Since cloning of the ATP-binding cassette (ABC) family member breast cancer resistance protein (BCRP/ABCG2) and its characterization as a multidrug resistance efflux transporter in 1998, BCRP has been the subject of more than two thousand scholarly articles. In normal tissues, BCRP functions as a defense mechanism against toxins and xenobiotics, with expression in the gut, bile canaliculi, placenta, blood-testis and blood-brain barriers facilitating excretion and limiting absorption of potentially toxic substrate molecules, including many cancer chemotherapeutic drugs. BCRP also plays a key role in heme and folate homeostasis, which may help normal cells survive under conditions of hypoxia. BCRP expression appears to be a characteristic of certain normal tissue stem cells termed “side population cells,” which are identified on flow cytometric analysis by their ability to exclude Hoechst 33342, a BCRP substrate fluorescent dye. Hence, BCRP expression may contribute to the natural resistance and longevity of these normal stem cells. Malignant tissues can exploit the properties of BCRP to survive hypoxia and to evade exposure to chemotherapeutic drugs. Evidence is mounting that many cancers display subpopulations of stem cells that are responsible for tumor self-renewal. Such stem cells frequently manifest the “side population” phenotype characterized by expression of BCRP and other ABC transporters. Along with other factors, these transporters may contribute to the inherent resistance of these neoplasms and their failure to be cured.

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“…Our results showed that Sal significantly reduced the percentage of CD44 + /CD24 À cell population in a dose dependent manner. Recent studies have shown that high ALDH activity is an additional defining marker of BCSCs [37][38][39][40] and can serve as a useful biomarker for CSCs [25]. Thus, levels of ALDH1 mRNA and protein are relevant in the evaluation of the ability of Sal to specifically target BCSCs.…”

Section: Discussionmentioning

confidence: 99%

Salinomycin exerts anticancer effects on human breast carcinoma MCF-7 cancer stem cells via modulation of Hedgehog signaling

Lü

Murata

et al. 2015

Chemico-Biological Interactions

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Subpopulations of Stem-like Cells in Side Population Cells from the Human Bladder Transitional Cell Cancer Cell Line T24

Cited by 44 publications

References 26 publications

Epithelial Plasticity, Cancer Stem Cells, and the Tumor-Supportive Stroma in Bladder Carcinoma

Epithelial Plasticity, Cancer Stem Cells, and the Tumor-Supportive Stroma in Bladder Carcinoma

Role of breast cancer resistance protein (BCRP/ABCG2) in cancer drug resistance

Salinomycin exerts anticancer effects on human breast carcinoma MCF-7 cancer stem cells via modulation of Hedgehog signaling

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