A Synthetic Binder of Breast Cancer Stem Cells

Chen, Luxi; Long, Chao; Tran, Kha A.; Lee, Jiyong

doi:10.1002/chem.201705663

Cited by 3 publications

(2 citation statements)

References 27 publications

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“…One of the hypotheses to explain cancer resistance to therapy is cancer stem cells, or cancer-initiating cells. Although they are more recognized as a phenotypic status or mode rather than a fixed subset of cancer cells, various authors distinguish certain populations of cells within a tumor that propagate cancer [83][84][85][86][87]. The main trick regarding those cells is that when they are asleep, they evade chemotherapy; when they wake up, they cause cancer recurrence.…”

Section: Models Of Cancer Treatment Predictionmentioning

confidence: 99%

Recent Approaches Encompassing the Phenotypic Cell Heterogeneity for Anticancer Drug Efficacy Evaluation

Stulpinas¹,

Imbrasaitė²,

Krestnikova³

et al. 2020

Tumor Progression and Metastasis

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Despite the advancements in biomarker-based personalized cancer therapy, the inadequacy of molecular and genetic profiling in identifying effective drug combinations was defined in most cases. Drug resistance remains a major limitation of the current predictive oncology. Emerging reports indicate that the success of anticancer therapy is usually limited by intratumoral heterogeneity which is not captured by the existing cancer cell biomarker-based approaches. Cell heterogeneity, not only genetic but also phenotypic, is considered to be the root cause of resistance to anticancer treatment, cancer progression, and the presence of cancer stem cells. Therefore, functional testing of live cells representing various cell types within the tumor exposed to potential therapies is needed for identification of effective drug combinations. Here we look at the different existing model systems, including ex vivo models of the patient's tumor cells, 2D/3D in vitro cultures/cocultures, patient-derived cellular organoids, single-cell models, ex vivo tumor platforms containing tumor microenvironment and extracellular matrix, etc., scoping at drug efficacy evaluation and solving the problem of cancer resistance.

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Section: Models Of Cancer Treatment Predictionmentioning

confidence: 99%

Recent Approaches Encompassing the Phenotypic Cell Heterogeneity for Anticancer Drug Efficacy Evaluation

Stulpinas¹,

Imbrasaitė²,

Krestnikova³

et al. 2020

Tumor Progression and Metastasis

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“… 13 – 15 Numerous studies have documented the existence of CSCs in various types of human cancers including NSCLC. 16 , 17 Additionally, emerging evidence has validated the clinical relevance of CSCs, including an initial positive response to therapy and resistance to currently used chemotherapy and radiotherapy. 18 Chemotherapeutic agents are widely accepted as the standard therapy for patients with advanced NSCLC.…”

Section: Introductionmentioning

confidence: 99%

lincROR influences the stemness and crizotinib resistance in EML–ALK<sup>+</sup> non-small-cell lung cancer cells

Yang¹,

Huang²,

Xie³

et al. 2018

OTT

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IntroductionEchinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4–ALK) is identified as an important pathogenic factor in patients with non-small-cell lung cancer (NSCLC) and could induce a stem-like phenotype in NSCLC cells. Crizotinib is commonly used for EML4–ALK+ NSCLC treatment, but its acquired resistance results in tumor recurrence. Long intergenic noncoding RNA, regulator of reprogramming (lincROR) is related to the acquisition and maintenance of self-renewal and stemness features of cancer stem cells. It has been documented that lincROR is implicated in chemoresistance. However, the correlations of lincROR and EML4–ALK in stem cell-like properties and of lincROR and crizotinib resistance in NSCLC cells are yet to be elucidated.Patients and methodsIn the present study, we investigated the expression profile of lincROR in EML–ALK NSCLC tissues, and the potential role of lincROR in prognosis was then analyzed. Subsequently, its association with stem cell-like properties of EML–ALK+ NSCLC cells was determined. Furthermore, the correlation of lincROR with crizotinib and the effects of lincROR and crizotinib on cell viability of EML4–ALK+ NSCLC cells were all explored.ResultsThe results showed that lincROR expression was upregulated in EML4–ALK+ NSCLC tissues relative to EML4–ALK− NSCLC tissues. Low-expressed lincROR was related to a favorable prognosis of patients with EML–ALK NSCLC. lincROR overexpression could enhance the stemness features of EML–ALK+ NSCLC cells which were repressed by ALK knockdown.ConclusionWe found that lincROR expression was significantly inhibited because of the increased concentration of crizotinib in EML4–ALK+ NSCLC cells. Furthermore, lincROR overexpression increased cell viability of EML4–ALK+ NSCLC cells, which was impaired by crizotinib. Conjointly, these results suggested the important role of lincROR in EML–ALK+ NSCLC. lincROR may serve as a potential therapeutic target to overcome chemotherapy resistance in EML–ALK+ NSCLC.

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Cancer Stem Cell for Tumor Therapy

Huang

Yan

2021

Cancers

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Tumors pose a significant threat to human health. Although many methods, such as operations, chemotherapy and radiotherapy, have been proposed to eliminate tumor cells, the results are unsatisfactory. Targeting therapy has shown potential due to its specificity and efficiency. Meanwhile, it has been revealed that cancer stem cells (CSCs) play a crucial role in the genesis, development, metastasis and recurrence of tumors. Thus, it is feasible to inhibit tumors and improve prognosis via targeting CSCs. In this review, we provide a comprehensive understanding of the biological characteristics of CSCs, including mitotic pattern, metabolic phenotype, therapeutic resistance and related mechanisms. Finally, we summarize CSCs targeted strategies, including targeting CSCs surface markers, targeting CSCs related signal pathways, targeting CSC niches, targeting CSC metabolic pathways, inducing differentiation therapy and immunotherapy (tumor vaccine, CAR-T, oncolytic virus, targeting CSCs–immune cell crosstalk and immunity checkpoint inhibitor). We highlight the potential of immunity therapy and its combinational anti-CSC therapies, which are composed of different drugs working in different mechanisms.

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A Synthetic Binder of Breast Cancer Stem Cells

Cited by 3 publications

References 27 publications

Recent Approaches Encompassing the Phenotypic Cell Heterogeneity for Anticancer Drug Efficacy Evaluation

Recent Approaches Encompassing the Phenotypic Cell Heterogeneity for Anticancer Drug Efficacy Evaluation

lincROR influences the stemness and crizotinib resistance in EML–ALK<sup>+</sup> non-small-cell lung cancer cells

Cancer Stem Cell for Tumor Therapy

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A Synthetic Binder of Breast Cancer Stem Cells

Cited by 3 publications

References 27 publications

Recent Approaches Encompassing the Phenotypic Cell Heterogeneity for Anticancer Drug Efficacy Evaluation

Recent Approaches Encompassing the Phenotypic Cell Heterogeneity for Anticancer Drug Efficacy Evaluation

lincROR influences the stemness and crizotinib resistance in EML&ndash;ALK<sup>+</sup> non-small-cell lung cancer cells

Cancer Stem Cell for Tumor Therapy

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lincROR influences the stemness and crizotinib resistance in EML–ALK<sup>+</sup> non-small-cell lung cancer cells