Highly tumorigenic lung cancer CD133
            <sup>+</sup>
            cells display stem-like features and are spared by cisplatin treatment

Bertolini, Giulia; Roz, Luca; Perego, Paola; Tortoreto, Monica; Fontanella, Enrico; Gatti, Laura; Pratesi, Graziella; Fabbri, Alessandra; Andriani, Francesca; Tinelli, Stella; Roz, Elena; Caserini, Roberto; Vullo, Salvatore Lo; Camerini, Tiziana; Mariani, Luigi; Delia, Domenico; Calabrò, Elisa; Pastorino, Ugo; Sozzi, Gabriella

doi:10.1073/pnas.0905653106

Cited by 709 publications

(715 citation statements)

References 39 publications

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“…14,28 Our previous results demonstrated that CD133-positive cells isolated from patients with NSCLC exhibit greater chemoradioresistance compared with NSCLC cells of the CD133-negative lineage. 13 To further explore other possible characteristics of CSCs in CD133-positive cells from patients with lung cancer, we isolated CD133-positive cells (Fig.…”

Section: Isolation and Characterization Of Lungmentioning

confidence: 98%

“…Then, the samples were assessed by flow cytometry for purity. 14 The medium was replaced or supplemented with fresh growth factors twice weekly until the cells started to grow and form floating aggregates. Floating sphere cultures were expanded weekly by mechanical dissociation followed by replating of single cells in complete fresh medium.…”

Section: Isolation Of Cd133-positive Cellsmentioning

confidence: 99%

“…13 Consistent with our findings, Bertolini et al also provided evidence that CD133-positive lung tumor cells possessed stemness features and a higher tumorigenic potential than CD133-negative cells in severe combined immunodeficient (SCID) mice. 14 A growing body of evidence indicates the tumor initiation ability and chemoradioresistance of CD133-positive cells in lung CSCs. However, the functional significance of the biomolecular pathways that are overexpressed in lung CSCs remains unclear and needs further clarification.…”

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confidence: 99%

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Cucurbitacin I inhibits tumorigenic ability and enhances radiochemosensitivity in nonsmall cell lung cancer‐derived CD133‐positive cells

Hsu¹,

Huang

Chang

et al. 2011

Cancer

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BACKGROUND: Signal transducer and activator of transcription 3 (STAT3) signaling reportedly promotes tumor malignancy and recurrence in nonsmall cell lung cancer (NSCLC). It was demonstrated previously that the STAT3 pathway maintains the tumorigenicity and therapeutic resistance of malignant tumors as well as cancer stem cells (CSCs). The objective of the current study was to investigate the effect of the strong STAT3 inhibitor, cucurbitacin I, in prominin-1 (CD133)-positive lung cancer cells. METHODS: CD133-positive and CD133-negative NSCLC-derived cells were isolated from 7 patients with NSCLC. CD133-positive NSCLC cells that were treated with or without cucurbitacin I were evaluated for their expression of phosphorylated STAT3 (p-STAT3), tumorigenicity, stemness properties, and resistance to chemotherapeutic drugs and ionizing radiation. RESULTS: Compared with parental or CD133-negative NSCLC cells, CD133-positive NSCLC cells had greater tumorigenicity, greater radioresistance, and higher expression of octamer-binding transcription factor 4 (Oct-4), Nanog homeobox, and sex-determining region Y, box 2 (Sox2) at high p-STAT3 levels. Cucurbitacin I treatment at 100 nM effectively abrogated STAT3 activation, tumorigenic capacity, sphere formation ability, radioresistance, and chemoresistance in CD133-positive NSCLC cells. Microarray data suggested that cucurbitacin I inhibited the stemness gene signature of CD133-positive NSCLC cells and facilitated the differentiation of CD133-positive NSCLC cells into CD133-negative NSCLC cells. It is noteworthy that 150 nM cucurbitacin I effectively blocked STAT3 signaling and downstream survival targets, such as B-cell chronic lymphocytic leukemia/lymphoma 2 (Bcl-2) and Bcl-2-like 1 (Bcl-xL) expression and induced apoptosis in CD133-positive NSCLC cells. Finally, xenotransplantation experiments revealed that cucurbitacin I plus radiotherapy or chemotherapeutic drugs significantly suppressed tumorigenesis and improved survival in NSCLC-CD133-positive-transplanted, immunocompromised mice. CONCLUSIONS: Targeting STAT3 signaling in CD133-positive NSCLC cells with cucurbitacin I suppressed CSC-like properties and enhanced chemoradiotherapy response. The potential of cucurbitacin I should be verified further in future anti-CSC therapy.

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Section: Isolation and Characterization Of Lungmentioning

confidence: 98%

Section: Isolation Of Cd133-positive Cellsmentioning

confidence: 99%

mentioning

confidence: 99%

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Cucurbitacin I inhibits tumorigenic ability and enhances radiochemosensitivity in nonsmall cell lung cancer‐derived CD133‐positive cells

Hsu¹,

Huang

Chang

et al. 2011

Cancer

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“…CD133‐positive CSCs have demonstrated resistance to traditional chemotherapies,36, 37 and quantitative polymerase chain reaction analyses indicate that high CD133 expression is a marker for a poor prognosis 34. In addition, CD44 is expressed in up to 80% of primary gastric cancer resection specimens and is associated with more advanced clinicopathologic features and a poorer prognosis 21.…”

Section: Cancer Stem Cellsmentioning

confidence: 99%

Identifying and targeting cancer stem cells in the treatment of gastric cancer

Bekaii‐Saab

El‐Rayes²

2017

Cancer

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Current treatment regimens for gastric cancer are not adequate. Cancer stem cells (CSCs) may be a key driving factor for growth and metastasis of this tumor type. In contrast to the conventional clonal evolution hypothesis, CSCs can initiate tumor formation, self‐renew, and differentiate into tumor‐propagating cells. Because gastric cancer can originate from CSCs, it is necessary to review current targets of signaling pathways for CSCs in gastric cancer that are being studied in clinical trials. These pathways are known to regulate the self‐renewal and differentiation process in gastric CSCs. A better understanding of the clinical results of trials that target gastric CSCs will lead to better outcomes for patients with gastric cancer. Cancer 2017;123:1303–1312. © 2017 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society. This is an open access article under the terms of the Creative Commons Attribution NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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“…Until now, CSCs have been reported in several types of solid tumors, including colorectal, breast, pancreatic, lung, and hepatocellular 49, 50, 51, 52. More and more in vivo evidence demonstrated that CSCs could promote MDR.…”

Section: Mechanisms Of Cancer Multidrug Resistancementioning

confidence: 99%

Inorganic Nanocarriers Overcoming Multidrug Resistance for Cancer Theranostics

et al. 2016

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Cancer multidrug resistance (MDR) could lead to therapeutic failure of chemotherapy and radiotherapy, and has become one of the main obstacles to successful cancer treatment. Some advanced drug delivery platforms, such as inorganic nanocarriers, demonstrate a high potential for cancer theranostic to overcome the cancer‐specific limitation of conventional low‐molecular‐weight anticancer agents and imaging probes. Specifically, it could achieve synergetic therapeutic effects, demonstrating stronger killing effects to MDR cancer cells by combining the inorganic nanocarriers with other treatment manners, such as RNA interference and thermal therapy. Moreover, the inorganic nanocarriers could provide imaging functions to help monitor treatment responses, e.g., drug resistance and therapeutic effects, as well as analyze the mechanism of MDR by molecular imaging modalities. In this review, the mechanisms involved in cancer MDR and recent advances of applying inorganic nanocarriers for MDR cancer imaging and therapy are summarized. The inorganic nanocarriers may circumvent cancer MDR for effective therapy and provide a way to track the therapeutic processes for real‐time molecular imaging, demonstrating high performance in studying the interaction of nanocarriers and MDR cancer cells/tissues in laboratory study and further shedding light on elaborate design of nanocarriers that could overcome MDR for clinical translation.

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Highly tumorigenic lung cancer CD133 ⁺ cells display stem-like features and are spared by cisplatin treatment

Cited by 709 publications

References 39 publications

Cucurbitacin I inhibits tumorigenic ability and enhances radiochemosensitivity in nonsmall cell lung cancer‐derived CD133‐positive cells

Cucurbitacin I inhibits tumorigenic ability and enhances radiochemosensitivity in nonsmall cell lung cancer‐derived CD133‐positive cells

Identifying and targeting cancer stem cells in the treatment of gastric cancer

Inorganic Nanocarriers Overcoming Multidrug Resistance for Cancer Theranostics

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Highly tumorigenic lung cancer CD133 + cells display stem-like features and are spared by cisplatin treatment

Cited by 709 publications

References 39 publications

Cucurbitacin I inhibits tumorigenic ability and enhances radiochemosensitivity in nonsmall cell lung cancer‐derived CD133‐positive cells

Cucurbitacin I inhibits tumorigenic ability and enhances radiochemosensitivity in nonsmall cell lung cancer‐derived CD133‐positive cells

Identifying and targeting cancer stem cells in the treatment of gastric cancer

Inorganic Nanocarriers Overcoming Multidrug Resistance for Cancer Theranostics

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Product

Resources

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Highly tumorigenic lung cancer CD133 ⁺ cells display stem-like features and are spared by cisplatin treatment