miR-193b Modulates Resistance to Doxorubicin in Human Breast Cancer Cells by Downregulating MCL-1

Long, Jingpei; Ji, Zhiwei; Jiang, Kai; Wang, Zhaoyang; Meng, Guanmin

doi:10.1155/2015/373574

Cited by 39 publications

(20 citation statements)

References 26 publications

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“…We propose that miR-193b inhibits a network of genes involved in the complex processes of VM and may be key in modulating tumour growth and development. Previously identified targets of miR-193b are limited, but include cyclinD1 and ETS1 in hepatoma cells 55 , uPA, HSP40 and RAB22A in MDA-MB-231 cells 39 , 52 and MCL-1 in MCF7 cells 72 . Further research is required to determine if other genes involved in the DDAH/ADMA/NO and associated pathways are also targets for miR-193b in cancer.…”

Section: Discussionmentioning

confidence: 99%

MiR-193b regulates breast cancer cell migration and vasculogenic mimicry by targeting dimethylarginine dimethylaminohydrolase 1

Hulin

Tommasi

Elliot

et al. 2017

Sci Rep

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Dimethylarginine dimethylaminohydrolase 1 (DDAH1) is responsible for metabolism of an endogenous inhibitor of nitric oxide synthase (NOS), asymmetric dimethylarginine (ADMA), which plays a key role in modulating angiogenesis. In addition to angiogenesis, tumours can establish a vascular network by forming vessel-like structures from tumour cells; a process termed vasculogenic mimicry (VM). Here, we identified over-expression of DDAH1 in aggressive MDA-MB-231, MDA-MB-453 and BT549 breast cancer cell lines when compared to normal mammary epithelial cells. DDAH1 expression was inversely correlated with the microRNA miR-193b. In DDAH1+ MDA-MB-231 cells, ectopic expression of miR-193b reduced DDAH1 expression and the conversion of ADMA to citrulline. In DDAH1− MCF7 cells, inhibition of miR-193b elevated DDAH1 expression. Luciferase reporter assays demonstrated DDAH1 as a direct target of miR-193b. MDA-MB-231 cells organised into tube structures in an in vitro assay of VM, which was significantly inhibited by DDAH1 knockdown or miR-193b expression. Mechanistically, we found miR-193b regulates cell proliferation and migration of MDA-MB-231 cells, whilst DDAH1 knockdown inhibited cell migration. These studies represent the first evidence for DDAH1 expression, regulation and function in breast cancer cells, and highlights that targeting DDAH1 expression and/or enzymatic activity may be a valid option in the treatment of aggressive breast cancers.

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Section: Discussionmentioning

confidence: 99%

MiR-193b regulates breast cancer cell migration and vasculogenic mimicry by targeting dimethylarginine dimethylaminohydrolase 1

Hulin

Tommasi

Elliot

et al. 2017

Sci Rep

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“…In MDA-MB-231 cells, among upregulated miRNAs there are miR-26a, miR-149, miR-181a, miR-193b, miR-195 and miR-324-3p that increase drug responsiveness. In particular, previous studies showed that miR-26a sensitized gastric cancer to cisplatin targeting NRAS and E 2 F 2 [ 22 ], miR-149 increased chemosensitivity of glioblastoma to Temozolomide treatment through a RAP1B-mediated remodeling of cellular cytoskeleton [ 23 ], miR-181a enhanced Adryamicin-induced apoptosis targeting Bcl-2 [ 24 ], miR-193b sensitized cancer cells to Doxorubicin targeting myeloid cell leukemia-1 (MCL-1) [ 25 ], miR-195 increased Adriamycin sensibility by downregulating RAF [ 26 ], and, finally, miR-324-3p induced drug sensitivity reducing its SMAD7 target mRNA that is associated with lung, pancreas and skin cancer [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

Analysis of miRNA expression profile induced by short term starvation in breast cancer cells treated with doxorubicin

et al. 2017

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Recent studies showed that dietary approaches restricting food intake can be helpful to hinder tumor progression. To date, the molecular mechanisms are unclear and a key role seems to be exerted by nutrient-related signaling pathways. Since several evidences showed that non-coding small RNAs, including microRNAs, are correlated to cancer progression and antiblastic treatment response, our work aims to study their involvement in a triple negative breast cancer (TNBC) cell line treated with doxorubicin under Short Term Starvation (STS) condition.Human TNBC cell line MDA-MB-231 and healthy breast cell line MCF10A were treated with 1 μM doxorubicin for 24 h under STS condition for 48 h and miRNA expression profiles were analyzed using Taqman® Low Density Array A human microRNA microfluidic cards. In addition, the expression of specific mRNAs and miRNAs differentially expressed under STS was analyzed using Real-time PCR analyses.MiRNA expression profile analysis in MDA-MB-231 and MCF10A cells treated with doxorubicin under STS for 48 h could explain the molecular mechanisms underlying anticancer effects associated to STS. Among deregulated miRNAs, a subset, including miR-15b, miR-23a, miR-26a, miR-29a, miR-106b, miR-128, miR-149, miR-181a, miR-192, miR-193b, miR-195, miR-324-3p and miR-494, has been shown to be involved in pathways related to drug sensitivity/resistance.The obtained data from our study suggest a potential involvement of some miRNAs in molecular pathways mediating the anticancer effects of STS in doxorubicin-treated breast cancer cells. Preliminary results seem to be encouraging and, in future, could allow the discovery of new potential targets useful for the development of new therapeutic approaches.

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“…It drives urgent need to detect new targets and treatment strategies. MiRNAs play a vital role in tumorigenesis, angiogenesis and drug resistance [32–34], and are proved to be a useful biomarker in the diagnosis and prognosis of cancer. Recently, miRNAs or anti-miRNAs trafficked by microvesicles (MV) or other plasmids have been used for the treatment of various diseases in mouse models, including cancers [22, 35, 36].…”

Section: Discussionmentioning

confidence: 99%

Onco-miR-130 promotes cell proliferation and migration by targeting TGFβR2 in gastric cancer

Duan

Zhang

et al. 2016

Oncotarget

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MicroRNAs (miRNAs) have been proved to play crucial roles in tumorigenesis. TGFβ signal pathway abnormality is found in various cancers and correlates with tumor proliferation and metastasis. However, the mechanisms underlying the dys-regulation of TGFβR2 expression in GC have not been investigated yet. In this study, we found that the TGFβR2 protein was clearly repressed in tumor tissues, while miR-130 expression level was dramatically increased in GC tissues. Firefly luciferase activity assay revealed that miR-130 could directly bind to 3′UTR of TGFβR2 mRNA. Meanwhile, miR-130 mimics lead to the decreased TGFβR2 protein levels, while miR-130 inhibitors enhanced TGFβR2 expression in SGC7901 cells. Subsequent functional experiments showed that overexpressed miR-130 could promote proliferation and migration of SGC7901 cells. And siRNA-mediated TGFβR2 down-regulation could simulate the effects of miR-130 mimics on phenotypes of SGC7901 cells. Furthermore, there existed intense relationship between the expression level of miR-130 and epithelial-mesenchymal markers. Our results demonstrated that miR-130 was an oncogene by directly targeting TGFβR2 in GC.

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miR-193b Modulates Resistance to Doxorubicin in Human Breast Cancer Cells by Downregulating MCL-1

Cited by 39 publications

References 26 publications

MiR-193b regulates breast cancer cell migration and vasculogenic mimicry by targeting dimethylarginine dimethylaminohydrolase 1

MiR-193b regulates breast cancer cell migration and vasculogenic mimicry by targeting dimethylarginine dimethylaminohydrolase 1

Analysis of miRNA expression profile induced by short term starvation in breast cancer cells treated with doxorubicin

Onco-miR-130 promotes cell proliferation and migration by targeting TGFβR2 in gastric cancer

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