Breast Cancer Stem Cells

Crabtree, Judy S.; Miele, Lucio

doi:10.3390/biomedicines6030077

Cited by 69 publications

(55 citation statements)

References 126 publications

(139 reference statements)

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“…In addition, the analysis of the expression level of these markers (MFC, mean fluorescence channel) indicates that, along with an increase of expression of CD24, treated mammospheres show a reduced expression of CD44. Moreover, expression of pluripotency-related transcription factors involved in self-renewal Nanog, Oct3/4, and stem cell markers ALDH1, and CD44 [ 34 – 36 ] were also reduced ( Fig 2B ). Together, these results suggested that c-Src functionality is relevant for MCF7-mammosphere renewal.…”

Section: Resultsmentioning

confidence: 99%

“…In this respect, we previously observed that SrcDN expression and selective c-Src tyrosine-kinase inhibitors diminish cyclin D1 expression and cell cycle progression at G1-phase in breast cancer cells [ 24 , 43 , 44 ]. Moreover, these mammosphere cells also showed expression of Oct3/4, Nanog pluripotency-associated transcription factors, ALDH1, and CD44 stem-cell markers [ 34 – 36 ], which were reduced upon SrcDN induction. These pluripotency-associated transcription factors are required for embryonic stem cell self-renewal [ 34 ], and they are also involved in tumorigenesis and metastasis [ 45 ].…”

Section: Discussionmentioning

confidence: 99%

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c-Src functionality controls self-renewal and glucose metabolism in MCF7 breast cancer stem cells

et al. 2020

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Deregulation of Src kinases is associated with cancer. We previously showed that SrcDN conditional expression in MCF7 cells reduces tumorigenesis and causes tumor regression in mice. However, it remained unclear whether SrcDN affected breast cancer stem cell functionality or it reduced tumor mass. Here, we address this question by isolating an enriched population of Breast Cancer Stem Cells (BCSCs) from MCF7 cells with inducible expression of SrcDN. Induction of SrcDN inhibited self-renewal, and stem-cell marker expression (Nanog, Oct3-4, ALDH1, CD44). Quantitative proteomic analyses of mammospheres from MCF7-Tet-On-SrcDN cells (data are available via ProteomeXchange with identifier PXD017789, project DOI: 10.6019/PXD017789 ) and subsequent GSEA showed that SrcDN expression inhibited glycolysis. Indeed, induction of SrcDN inhibited expression and activity of hexokinase, pyruvate kinase and lactate dehydrogenase, resulting in diminished glucose consumption and lactate production, which restricted Warburg effect. Thus, c-Src functionality is important for breast cancer stem cell maintenance and renewal, and stem cell transcription factor expression, effects linked to glucose metabolism reduction.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

c-Src functionality controls self-renewal and glucose metabolism in MCF7 breast cancer stem cells

et al. 2020

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“…However, breast cancer still is the most frequently diagnosed cancer and the leading cause of cancer-related death in women worldwide 2. In 2018, estimated 260,000 new cases diagnosed with breast cancer and that breast cancer caused over 40,000 deaths in the United States 3. However, the molecular mechanism of breast cancer development is not fully understood.…”

Section: Introductionmentioning

confidence: 99%

miR-1307-3p Stimulates Breast Cancer Development and Progression by Targeting SMYD4

et al. 2019

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Recent studies show that dysregulated miRNAs play an important role in breast cancer initiation and progression. Here, we identified upregulated expression of miR-1307-3p in breast cancer tissues and that increased level of miR-1307-3p was closely correlated with lower survival rate in breast cancer patients. Consistent with clinical data, our in vitro data show that expression level of miR-1307-3p was significantly increased in breast cancer cell lines compared to human mammary epithelial cell line MCF10A. Overexpression of miR-1307-3p in MCF10A stimulated cell proliferation and caused their growth in soft agar and tumor formation in nude mice. In contrast, inhibition of miR-1307-3p suppressed breast cancer cell proliferation and their growth in soft agar and inhibited tumor formation in nude mice. Further, we identified that miR-1307-3p plays its oncogenic role through targeting SET and MYND domain-containing 4 (SMYD4) expression in breast cancer. Taken together, our findings suggest that miR-1307-3p is a oncogenic miRNA that significantly contributes to breast cancer development and progression, and inhibition of miR-1307-3p may be a novel strategy for inhibits breast cancer initiation and progression.

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“…Cancer stem cells (CSCs) are assumed to be a group of cells with the ability to initiate tumour growth, self‐renew and differentiate and are implicated in tumour initiation, progression, metastasis, recurrence and resistance to therapy . Researchers have now provided evidence of the existence of CSCs that were isolated from several types of human tumours, such as brain tumours, breast cancer and colon cancer . It has been previously shown that stem cells cultured in suspension could generate non‐adherent spherical clusters of cells composed of stem cells and progenitor cells .…”

Section: Discussionmentioning

confidence: 99%

“…[13][14][15][16] Researchers have now provided evidence of the existence of CSCs that were isolated from several types of human tumours, such as brain tumours, breast cancer and colon cancer. [17][18][19] It has been previously shown that stem cells cultured in suspension could generate nonadherent spherical clusters of cells composed of stem cells and progenitor cells. 20,21 We showed that the overexpression of CPA4 causes a more dramatic induction of sphere clonogenicity, whereas repression of CPA4 leads to a reduction in sphere clonogenicity.…”

Section: Discussionmentioning

confidence: 99%

Carboxypeptidase A4 promotes proliferation and stem cell characteristics of hepatocellular carcinoma

Zhang

Wang

Shang

et al. 2019

Int J Experimental Path

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Summary Carboxypeptidase A4 (CPA4), a member of the metallo‐carboxypeptidase family, is overexpressed in liver cancer and is associated with cancer progression. The role of CPA4 in hepatocellular carcinoma (HCC) remains unclear. In this study, we aimed to evaluate the relevance of CPA4 to the proliferation and expression of stem cell characteristics of hepatocellular carcinoma cells. Western blot analysis showed high CPA4 expression in the liver cancer cell line Bel7402 and low expression in HepG2 cells. Knock‐down of CPA4 decreased cancer cell proliferation as detected by MTT and clone formation assays. The serum‐free culture system revealed that downregulated CPA4 suppressed the sphere formation capacities of tumour cells. However, upregulated CPA4 increased the proliferation and sphere formation capacity. In addition, the protein expression of CD133, ALDH1 and CD44 also increased in cells with upregulated CPA4. In vivo, the overexpression of CPA4 in tumour cells that were subcutaneously injected into nude mice markedly increased the growth of the tumours. These data suggest that CPA4 expression leads to poor prognoses by regulating tumour proliferation and the expression of stem cell characteristics and may therefore serve as a potential therapeutic target of HCC.

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Breast Cancer Stem Cells

Cited by 69 publications

References 126 publications

c-Src functionality controls self-renewal and glucose metabolism in MCF7 breast cancer stem cells

c-Src functionality controls self-renewal and glucose metabolism in MCF7 breast cancer stem cells

miR-1307-3p Stimulates Breast Cancer Development and Progression by Targeting SMYD4

Carboxypeptidase A4 promotes proliferation and stem cell characteristics of hepatocellular carcinoma

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