Chemical approaches to targeting drug resistance in cancer stem cells

Sotiropoulou, Panagiota A.; Christodoulou, Michael S.; Silvani, Alessandra; Herold‐Mende, Christel; Passarella, Daniele

doi:10.1016/j.drudis.2014.05.002

Cited by 88 publications

(70 citation statements)

References 163 publications

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“…Cancer stem cells (CSCs) are reported as vital factor for treatment resistance in cancer therapy (40)(41)(42)(43). however, we found no reliable changes of CSC markers in our DDX6 K/D cells (data not shown, in 8 CSC markers of GBM).…”

Section: Discussioncontrasting

confidence: 48%

Involvement of DDX6 gene in radio- and chemoresistance in glioblastoma

Cho

Kang

Kim

et al. 2016

International Journal of Oncology

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Abstract. CCRT (concomitant chemotherapy and radiation therapy) is often used for glioblastoma multiforme (GBM) treatment after surgical therapy, however, patients treated with CCRT undergo poor prognosis due to development of treatment resistant recurrence. Many studies have been performed to overcome these problems and to discover genes influencing treatment resistance. To discover potential genes inducing CCRT resistance in GBM, we used whole genome screening by infecting shRNA pool in patient-derived cell. The cells infected ~8,000 shRNAs were implanted in mouse brain and treated RT/TMZ as in CCRT treated patients. We found DDX6 as the candidate gene for treatment resistance after screening and establishing DDX6 knock down cells for functional validation. Using these cells, we confirmed tumor associated ability of DDX6 in vitro and in vivo. Although proliferation improvement was not found, decreased DDX6 influenced upregulated clonogenic ability and resistant response against radiation treatment in vivo and in vitro. Taken together, we suggest that DDX6 discovered by using whole genome screening was responsible for radio-and chemoresistance in GBM.

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Section: Discussioncontrasting

confidence: 48%

Involvement of DDX6 gene in radio- and chemoresistance in glioblastoma

Cho

Kang

Kim

et al. 2016

International Journal of Oncology

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“…Tyrosine kinase c-Yes overexpressed in these quiescent CSCs provided a therapeutic target to eliminate quiescent CSCs during 5FU chemotherapy. On the other hand, hypoxic and 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 perivascular niches also contributed to CSC multidrug resistance phenotype [35]. For example, CSCs increasing in hypoxic niche could decrease their sensitivity to antiangiogenic agents in breast cancer [36].…”

Section: Implications Of Csc Heterogeneity In Csc Targeted Therapymentioning

confidence: 97%

“…For instance, in squamous cell carcinomas, two CSC subclones differing in CD34 expression levels could interchange their phenotype according to different microenvironments [34]. In addition, hypoxic and perivascular niches are also vital conditions for the maintenance of CSC properties [35]. Conley et al showed that hypoxic niche increased the CSC fraction in breast cancer [36].…”

Section: Sources Of Heterogeneity In Cancer Stem Cellsmentioning

confidence: 98%

“…It is widely believed that more effective therapies are needed to eradicate CSCs. Cell quiescence, protective microenvironment, high expression of drug efflux pumps, more efficient DNA repair, miRNA regulation and anti-apoptosis system are potential resistance mechanisms of CSCs [26,35]. It would be productive to develop CSC targeted therapies based on its resistance mechanisms.…”

Section: Implications Of Csc Heterogeneity In Csc Targeted Therapymentioning

confidence: 99%

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Heterogeneity in cancer stem cells

Wang

Chen

et al. 2015

Cancer Letters

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“…Cancer development could be due to the fact that CSCs are associated with tumor initiation, progression, and metastasis as well as treatment resistance. Thus, CSCs have been discovered to be a suitable therapeutic target for prevention and treatment of cancer (Soltanian and Matin, 2011;Sotiropoulou et al, 2014). Breast CSCs are multiple, distinct, and nonoverlapping populations coexisting within the tumor mass (Wright et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Effects of celecoxib and L-NAME on apoptosis and cell cycle ofMCF-7 CD44+/CD24–/low subpopulation

Majdzadeh¹,

Aliebrahimi²,

Vatankhah³

et al. 2017

Turk J Biol

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IntroductionBreast cancer is the primary cause of death in malignancies among females (Regulski et al., 2016). It is suggested that a major population of breast tumor was incapable of further growth but only a minute fraction was able to seed new cancers, called cancer stem cells (CSCs) (Al-Hajj et al., 2003). During recent years, studies have identified CSCs as the subpopulation of tumor cells with a unique capacity for self-renewal and the ability to give rise to a heterogeneous population of cancer cells to form tumors. Genomic instability via several gene mutations has been reported to form CSCs from normal stem cells, progenitor cells, or differentiated cells. Cancer development could be due to the fact that CSCs are associated with tumor initiation, progression, and metastasis as well as treatment resistance. Thus, CSCs have been discovered to be a suitable therapeutic target for prevention and treatment of cancer (Soltanian and Matin, 2011;Sotiropoulou et al., 2014). Breast CSCs are multiple, distinct, and nonoverlapping populations coexisting within the tumor mass (Wright et al., 2008). In 2003, breast CSCs with CD44 + /CD24 -/low / ESA + cell surface markers were isolated for the first time by Al-Hajj et al. (2003). Additionally, ALDH1, which belongs to the aldehyde dehydrogenase family, is a putative CSC marker, including breast cancer. To date, several breast cancer stem cell markers have been proposed (CD133, CD29, and CD49f), of which CD44 + /CD24 -/low and ALDH1 are used exclusively to identify these highly tumorigenic cells (Carrasco et al., 2014).The cyclooxygenase enzyme, which mediates prostaglandin production, consists of three isoforms, COX-1, COX-2, and COX-3. COX-1, a house-keeping enzyme, has a crucial role for internal homeostasis. Conversely, COX-2 is undetectable in normal tissues while it is inducible in the setting of neoplasia and inflammation (Regulski et al., 2016). COX-2 upregulation by modulating various signaling pathways can enhance production of prostaglandins, which promote tumor growth, invasion, angiogenesis, and apoptosis resistance. Recent studies have also attributed the overexpression of COX-2 to breast cancer stem-like cell (CSC-LCs) properties and cancer development (Jeong et al., 2010;Singh et al., 2011).

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Chemical approaches to targeting drug resistance in cancer stem cells

Cited by 88 publications

References 163 publications

Involvement of DDX6 gene in radio- and chemoresistance in glioblastoma

Involvement of DDX6 gene in radio- and chemoresistance in glioblastoma

Heterogeneity in cancer stem cells

Effects of celecoxib and L-NAME on apoptosis and cell cycle ofMCF-7 CD44+/CD24–/low subpopulation

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