HDAC inhibitor suppresses proliferation and invasion of breast cancer cells through regulation of miR-200c targeting CRKL

Bian, Xu-ming; Liang, Zhongxing; Feng, Amber; Salgado, Eric; Shim, Hyunsuk

doi:10.1016/j.bcp.2017.11.008

Cited by 46 publications

(40 citation statements)

References 51 publications

(50 reference statements)

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“…miRNAs are a class of small noncoding RNAs with 18-25 nucleotides, which play as promising targets for diagnosis, prognosis and therapeutics of breast cancer [12]. Previous works have demonstrated that miR-200b and miR-200c could serve as important tumor suppressor by inhibiting cell proliferation, migration and invasion in breast cancer [13][14][15][16][17]. More importantly, the complementary sites between cir-cDENND4C and miR-200b or miR-200c predicted by bioinformatics analysis using starBase stimulated us to hypothesize that miR-200b and miR-200c might be required for circDENND4C-mediated progression of breast cancer.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of circDENND4C inhibits glycolysis, migration and invasion by up-regulating miR-200b/c in breast cancer under hypoxia

Ren

Liu

Feng

et al. 2019

J Exp Clin Cancer Res

138

105

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Background: Hypoxia is a key feature of breast cancer, which affects cancer development, metastasis and metabolism. Previous studies suggested that circular RNAs (circRNAs) could participate in cancer progression and hypoxia regulation. This study aimed to investigate the role of circRNA differentially expressed in normal cells and neoplasia domain containing 4C (circDENND4C) in breast cancer progression under hypoxia. Methods: Forty-three patients with breast cancer were involved in this study. Breast cancer cell lines MDA-MB-453 and SK-BR-3 were cultured under hypoxia (1% O 2) for experiments in vitro. The expression levels of circDENND4C, microRNA-200b (miR-200b) and miR-200c were measured by quantitative real-time polymerase chain reaction. Glycolysis was investigated by glucose consumption, lactate production and hexokinase II (HK2) protein level. Migration and invasion were evaluated via trans-well assay and protein levels of matrix metallopeptidase 9 (MMP9) and MMP2. The interaction between circDENND4C and miR-200b or miR-200c was explored by bioinformatics analysis, luciferase assay and RNA immunoprecipitation. Murine xenograft model was established to investigate the anti-cancer role of circDENND4C in vivo. Results: circDENND4C highly expressed in breast cancer was up-regulated in response to hypoxia. Knockdown of circDENND4C decreased glycolysis, migration and invasion in breast cancer cells under hypoxia. circDENND4C was validated as a sponge of miR-200b and miR-200c. Deficiency of miR-200b or miR-200c reversed the suppressive effect of circDENND4C knockdown on breast cancer progression. Moreover, silence of circDENND4C reduced xenograft tumor growth by increasing miR-200b and miR-200c. Conclusion: circDENND4C silence suppresses glycolysis, migration and invasion in breast cancer cells under hypoxia by increasing miR-200b and miR-200c.

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Section: Introductionmentioning

confidence: 99%

Knockdown of circDENND4C inhibits glycolysis, migration and invasion by up-regulating miR-200b/c in breast cancer under hypoxia

Ren

Liu

Feng

et al. 2019

J Exp Clin Cancer Res

138

105

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“…3 MiRNAs can repress the protein expression via mRNA degradation or translational inhibition through binding to the 3′-untranslated regions (3′-UTRs) of mRNAs. [6][7][8][9][10][11] BMI1 is a member of polycomb repressive complex 1 that has multiple roles in chromatin modification, DNA damage repair, cell cycle regulation, and senescence. Upregulated miRNAs are considered as an oncogene and downregulated miRNAs as a tumor suppressor.…”

Section: Introductionmentioning

confidence: 99%

“…MiR-200c is a tumor suppressor which inhibits the proliferation, EMT, migration, and invasion and induces the apoptosis and chemosensitivity in various cancers, such as renal cell cancer, ovarian cancer, bladder cancer, ovarian cancer, and CRC. [6][7][8][9][10][11] BMI1 is a member of polycomb repressive complex 1 that has multiple roles in chromatin modification, DNA damage repair, cell cycle regulation, and senescence. Furthermore, BMI1 is involved in cancer development.…”

Section: Introductionmentioning

confidence: 99%

Retracted: Anticancer effects of miR‐200c in colorectal cancer through BMI1

Mazraehshah

Tavangar

Saidijam

et al. 2018

J of Cellular Biochemistry

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Colorectal cancer (CRC) is one of the most leading cancer deaths throughout the world. MiR-200c has been shown to have a critical role in cancer initiation and progression. In this study, we investigated the miR-200c expression in CRC tissues and its effects on CRC cell lines which were mediated by polycomb complex protein (BMI1). Quantitative reverse transcription polymerase chain reaction (QRT-PCR) and immunohistochemistry were used to detect miR-200c and BMI1 expression in tumor tissues from 38 patients with CRC and 38 normal colon tissues. HCT-116 and SW-48 cells were transfected by locked nucleic acid (LNA)-anti-miR-200c. Western blot analysis and real-time PCR were applied to determine the BMI1 protein and microRNA (miRNA) levels. The apoptosis was analyzed via annexin/propidium iodide staining, and cell invasion was evaluated by transwell assay. MiR-200c was markedly downregulated in CRC tissues, whereas the protein expression of BMI1 in CRC tissues was upregulated compared with normal colon tissues. In the colon cancer cell lines, transfection of LNA-anti-miR-200c increased BMI1 gene and protein expression as well as the cell invasion. Downregulation of miR-200c by LNA decreased the apoptotic cells. The results from this study revealed that miR-200c may have antitumor effects through inhibition of BMI1 expression.

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“…Exposure to ZEA, OTA, and AFB1 may increase the incidence of human breast cancer (Yip, Wan, Wong, Korach, & El‐Nezami, ; Yu, Zhang, Wu, & Liu, ), and a metabolite of ZEA, α‐ZAL, may play a key role in the development of breast cancer (Belhassen et al., ). Further, miR‐21, let‐7, miR‐200c, and miR‐199a can regulate the development of breast cancer, thus, they may function as feasible diagnostic biomarkers and therapeutic targets for mycotoxin‐induced breast cancer (Bian, Liang, Feng, Salgado, & Shim, ; Elghoroury et al., ; Xu et al., ).…”

Section: Mirna and Diseases: Are They Related To Mycotoxins?mentioning

confidence: 99%

“…Since the known molecular mechanisms underlying the pathogenicity and carcinogenicity of mycotoxin are mostly at the protein level, very few examinations on miRNAs (likely the aberrant expressed miRNAs) can be found for early diagnosis of acute toxicity induced by mycotoxin. -122, miR-34a, miR-192, miR-26b, miR-761, miR-21, miR-199a ZEA, AOH, 3-ADON, 15-ADON, AFB1, FB1 (Gazzah et al, 2013;Juan-García et al, 2015;Qian et al, 2016;Girard et al, 2008;Brzuzan et al, 2015;Zhao et al, 2014;Zhou et al, 2016;Amr et al, 2016) Breast cancer miR-21, let-7, miR-200c, miR-199a ZEA, OTA, AFB1, α-ZAL (Yip et al, 2017;Yu et al, 2005;Belhassen et al, 2015;Bian et al, 2017;Elghoroury et al, 2017;Xu et al, 2017) Colon carcinoma miR-378-3a, miR-21, miR-34a, miR-299-3p, miR-495, miR-199a-5p, miR-375, miR-136, miR-15a, miR-192 DON, ZEA (Bensassi et al, 2009;Abassi et al, 2016;Fang et al, 2017;Kara et al, 2015;Wang et al, 2017;Yan et al, 2017;Yuan et al, 2017;Brzuzan et al, 2015) Inflammation-related diseases miR-21, miR-130a, miR-132, miR-155, miR-221 ZEA, DON, OTA, Patulin (Fan et al, 2018;Tardivel et al, 2015;Marin et al, 2017;Kim et al, 2015;McDonald et al, 2015;Croston et al, 2018;Qi et al, 2014;Valencia-Quintana et al, 2014) Apoptosis-induced diseases…”

Section: Mycotoxins and Mirnasmentioning

confidence: 99%

The Significance of Regulatory MicroRNAs: Their Roles in Toxicodynamics of Mycotoxins and in the Protection Offered by Dietary Therapeutics Against Mycotoxin‐Induced Toxicity

Xue

Sun‐Waterhouse

Wang

et al. 2018

Comp Rev Food Sci Food Safe

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Mycotoxins are contaminants commonly found in foods and represent a worldwide threat to human health and welfare. Efforts have been undertaken to reduce mycotoxins and their toxicity, including the introduction of good agricultural practices, appropriate food processing, specific biotransformation approaches, and pursue therapeutic agents to counteract mycotoxins. Efficient and predictive tools are required for investigations on mycotoxins and their toxicodynamics, and strategies for mycotoxin reduction. Gene expression and transcriptome analysis can unravel the mode of action, transformation and combined toxicity of mycotoxins, or mycotoxin's interactions with food components including dietary therapeutics, at the cellular level and from a molecular perspective. MicroRNAs (miRNAs) regulate endogenously and posttranscriptionally the expression of target genes and enzymes involved in physiological, disease and toxicological responses, and the metabolism of therapeutic agents. Accordingly, this review aimed to collect up‐to‐date information on (1) the regulatory role of miRNAs in mycotoxin‐initiated toxicological processes and (2) the protective role of active ingredients from plants on mycotoxin‐induced toxicity. Through such a review of published evidence, we found some common signal pathways involving miRNAs shared by these two types of biological events. This finding indicates the possibility of using miRNAs as biomarkers in assessing and controlling mycotoxins in food via cellular mechanisms.

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HDAC inhibitor suppresses proliferation and invasion of breast cancer cells through regulation of miR-200c targeting CRKL

Cited by 46 publications

References 51 publications

Knockdown of circDENND4C inhibits glycolysis, migration and invasion by up-regulating miR-200b/c in breast cancer under hypoxia

Knockdown of circDENND4C inhibits glycolysis, migration and invasion by up-regulating miR-200b/c in breast cancer under hypoxia

Retracted: Anticancer effects of miR‐200c in colorectal cancer through BMI1

The Significance of Regulatory MicroRNAs: Their Roles in Toxicodynamics of Mycotoxins and in the Protection Offered by Dietary Therapeutics Against Mycotoxin‐Induced Toxicity

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