Effects of notch-1 down-regulation on malignant behaviors of breast cancer stem cells

Peng, Gongling; Lu, Chong; Guo, Hui; Zhao, Xiangwang; Guo, Yinglu; Wang, Longqiang; Du, Qiuli; Liu, Chunping

doi:10.1007/s11596-014-1258-4

Cited by 8 publications

(9 citation statements)

References 20 publications

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“…This is consistent with the finding that MDA-9/Syntenin is highly expressed in the reservoir of interfollicular stem cells [82]. However, the relationship between MDA-9/Syntenin and Notch signaling has not been fully explored in other settings, including breast cancer, in which this pathway can be a promoter of tumor stem cell activity and invasion [92,93]. …”

Section: Directing Cellular Traffic: Role As Intracellular Adaptersupporting

confidence: 84%

Targeting tumor invasion: the roles of MDA-9/Syntenin

Kegelman

Das

Emdad

et al. 2014

Expert Opinion on Therapeutic Targets

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Introduction Melanoma differentiation-associated gene – 9 (MDA-9)/Syntenin has become an increasingly popular focus for investigation in numerous cancertypes. Originally implicated in melanoma metastasis, it has diverse cellular roles and is consistently identified as a regulator of tumor invasion and angiogenesis. As a potential target for inhibiting some of the most lethal aspects of cancer progression, further insight into the function of MDA-9/Syntenin is mandatory. Areas covered Recent literature and seminal articles were reviewed to summarize the latest collective understanding of MDA-9/Syntenin’s role in normal and cancerous settings. Insights into its participation in developmental processes are included, as is the functional significance of the N- and C-terminals and PDZ domains of MDA-9/Syntenin. Current reports highlight the clinical significance of MDA-9/Syntenin expression level in a variety of cancers, often correlating directly with reduced patient survival. Also presented are assessments of roles of MDA-9/Syntenin in cancer progression as well as its functions as an intracellular adapter molecule. Expert opinion Multiple studies demonstrate the importance of MDA-9/ Syntenin in tumor invasion and progression. Through the use of novel drug design approaches, this protein may provide a worthwhile therapeutic target. As many conventional therapies do not address, or even enhance, tumor invasion, an anti-invasive approach would be a worthwhile addition in cancer therapy.

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Section: Directing Cellular Traffic: Role As Intracellular Adaptersupporting

confidence: 84%

Targeting tumor invasion: the roles of MDA-9/Syntenin

Kegelman

Das

Emdad

et al. 2014

Expert Opinion on Therapeutic Targets

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“…Notch-1 was linked to diverse cellular processes including cell proliferation, apoptosis, and cancer metastasis and angiogenesis [44]. Recently, Notch-1 was reported to take part in the regulation of malignant behaviors of breast cancer stem-like cells [45]. Moreover, Xu et al [46] demonstrated that by interacting with the Akt signaling pathways, Notch-1 is involved in the growth and tumorgenesis of GSCs in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

miR-92a-3p Exerts Various Effects in Glioma and Glioma Stem-Like Cells Specifically Targeting CDH1/β-Catenin and Notch-1/Akt Signaling Pathways

Song

Zhang

Liu

et al. 2016

IJMS

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MicroRNAs (miRNAs) are implicated in the regulation of tumor progression and stemness of cancer stem-like cells. Recently, miR-92a-3p was reported to be up-regulated in human glioma samples. Nevertheless, the precise role of miR-92a-3p in glioma cells and glioma stem-like cells (GSCs) has not been fully elucidated. It is necessary to clarify the function of miR-92a-3p in glioma and GSCs to develop novel therapeutic approaches for glioma patients. In the present study, we applied methyl-thiazolyl-tetrazolium (MTT) assay and Transwell assay to measure the proliferation rate and metastatic potential of glioma cells. Meanwhile, the self-renewal ability of GSCs was detected by tumor sphere formation assay. The results revealed that down-regulation of miR-92a-3p suppressed the glioma cell malignancy in vitro. Moreover, knockdown of miR-92a-3p led to a reduction of tumorgenesis in vivo. Interestingly, we also observed that up-regulation of miR-92a-3p could inhibit the stemness of GSCs. Subsequent mechanistic investigation indicated that cadherin 1 (CDH1)/β-catenin signaling and Notch-1/Akt signaling were the downstream pathways of miR-92a-3p in glioma cells and GSCs, respectively. These results suggest that miR-92a-3p plays different roles in glioma cells and GSCs through regulating different signaling pathways.

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“…TGF-β induces cell cycle to arrest in G0/G1 phase, and in the TGF-β signaling pathway STIM1 and store-operated calcium entry (SOCE) play an anti-proliferative role in breast cancer [15]. In addition, more and more evidences have shown that Notch1 overexpression is strongly associated with breast cancer invasion, which is an important factor in maintaining the malignant phenotype of breast cancer stem cells [16]. Notchl signaling also correlates with self-renewal and differentiation of breast cancer stem cells (CSCs) and their malignant behaviors [17].…”

Section: Introductionmentioning

confidence: 99%

MFAP5 promotes basal-like breast cancer progression by activating the EMT program

Wu²,

Zhang

et al. 2019

Cell Biosci

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Purpose Human basal-like breast cancer (BLBC) is an aggressive malignancy with poor prognosis. Since most current treatments are ineffective, there is an urgent need to identify therapeutic targets for BLBC. Microfibrillar-associated protein 5 (MFAP5) plays an important role in the integration of elastic microfibers and the regulation of endothelial cell behaviors. We previously demonstrated that MFAP5 was significantly overexpressed in BLBC tissues and associated with poor metastasis-free survival of patients with BLBC. However, the detailed role of MFAP5 in BLBC is unclear. Thereby, the current study aimed to investigate the underlying function of MFAP5 in BLBC. Method Functional analyses were conducted for the role of MFAP5 in BLBC in vitro and in vivo. Results Overexpression of MFAP5 resulted in a significant increase in the proliferation, migration, invasion and epithelial–mesenchymal transition (EMT) markers in BLBC in vitro and in vivo. In addition, other metastasis animal models by tail intravenous injection of BT20 cells further confirmed that MFAP5 overexpression promoted BLBC proliferation and BT20 cells metastasis. We found that the TGF-β or Notch inhibitor significantly reversed the tumorigenicity and metastasis of MFAP5-induced BLBC cells. Conclusion Our findings suggest that MFAP5 may promote EMT in BLBC metastasis via the TGF-β/Notch pathway. Electronic supplementary material The online version of this article (10.1186/s13578-019-0284-0) contains supplementary material, which is available to authorized users.

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Effects of notch-1 down-regulation on malignant behaviors of breast cancer stem cells

Cited by 8 publications

References 20 publications

Targeting tumor invasion: the roles of MDA-9/Syntenin

Targeting tumor invasion: the roles of MDA-9/Syntenin

miR-92a-3p Exerts Various Effects in Glioma and Glioma Stem-Like Cells Specifically Targeting CDH1/β-Catenin and Notch-1/Akt Signaling Pathways

MFAP5 promotes basal-like breast cancer progression by activating the EMT program

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