miRNA‐215‐5p suppresses the aggressiveness of breast cancer cells by targeting Sox9

Gao, Jia Bao; Zhu, Ming; Zhu, Xiaoliang

doi:10.1002/2211-5463.12733

Cited by 36 publications

(22 citation statements)

References 24 publications

(29 reference statements)

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“…Also, many articles indicate the anti-migratory role of miR-214. For instance, in an article, it was shown that miRNA-214-5p suppresses the aggressiveness of breast cancer cells through targeting Sox9 [ 56 ]. It was also shown that miR-214 inhibits the migration of trophoblast cells [ 57 ].…”

Section: Discussionmentioning

confidence: 99%

Silencing ZEB2 Induces Apoptosis and Reduces Viability in Glioblastoma Cell Lines

et al. 2021

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Background: Glioma is an aggressive type of brain tumor that originated from neuroglia cells, accounts for about 80% of all malignant brain tumors. Glioma aggressiveness has been associated with extreme cell proliferation, invasion of malignant cells, and resistance to chemotherapies. Due to resistance to common therapies, glioma affected patients’ survival has not been remarkably improved. ZEB2 (SIP1) is a critical transcriptional regulator with various functions during embryonic development and wound healing that has abnormal expression in different malignancies, including brain tumors. ZEB2 overexpression in brain tumors is attributed to an unfavorable state of the malignancy. Therefore, we aimed to investigate some functions of ZEB2 in two different glioblastoma U87 and U373 cell lines. Methods: In this study, we investigated the effect of ZEB2 knocking down on the apoptosis, cell cycle, cytotoxicity, scratch test of the two malignant brain tumor cell lines U87 and U373. Besides, we investigated possible proteins and microRNA, SMAD2, SMAD5, and miR-214, which interact with ZEB2 via in situ analysis. Then we evaluated candidate gene expression after ZEB2-specific knocking down. Results: We found that ZEB2 suppression induced apoptosis in U87 and U373 cell lines. Besides, it had cytotoxic effects on both cell lines and reduced cell migration. Cell cycle analysis showed cell cycle arrest in G0/G1 and apoptosis induction in U87 and U373 cell lines receptively. Also, we have found that SAMAD2/5 expression was reduced after ZEB2-siRNA transfection and miR-214 upregulated after transfection. Conclusions: In line with previous investigations, our results indicated a critical oncogenic role for ZEB2 overexpression in brain glioma tumors. These properties make ZEB2 an essential molecule for further studies in the treatment of glioma cancer.

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Section: Discussionmentioning

confidence: 99%

Silencing ZEB2 Induces Apoptosis and Reduces Viability in Glioblastoma Cell Lines

et al. 2021

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“…Similarly, in the same study, another p53-dependent miR-215 was shown to significantly reduce levels of mRNA and protein of Zeb2 in cells of the colorectal cancer lines SW620 and DLD-1. Importantly, the observation of EMTsuppressing activity of miR-215 was confirmed in breast cancer cells 42 . However, in this case, the authors focused on Sox-9 as the main target of miR-215.…”

Section: Mir-192/215 Familymentioning

confidence: 77%

Interplay between p53 and non-coding RNAs in the regulation of EMT in breast cancer

et al. 2021

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The epithelial–mesenchymal transition (EMT) plays a pivotal role in the differentiation of vertebrates and is critically important in tumorigenesis. Using this evolutionarily conserved mechanism, cancer cells become drug-resistant and acquire the ability to escape the cytotoxic effect of anti-cancer drugs. In addition, these cells gain invasive features and increased mobility thereby promoting metastases. In this respect, the process of EMT is critical for dissemination of solid tumors including breast cancer. It has been shown that miRNAs are instrumental for the regulation of EMT, where they play both positive and negative roles often as a part of a feed-back loop. Recent studies have highlighted a novel association of p53 and EMT where the mutation status of p53 is critically important for the outcome of this process. Interestingly, p53 has been shown to mediate its effects via the miRNA-dependent mechanism that targets master-regulators of EMT, such as Zeb1/2, Snail, Slug, and Twist1. This regulation often involves interactions of miRNAs with lncRNAs. In this review, we present a detailed overview of miRNA/lncRNA-dependent mechanisms that control interplay between p53 and master-regulators of EMT and their importance for breast cancer.

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“…Upregulation of miR-204-5p significantly inhibits the viability, proliferation, and migration capacity of BC cells through regulating various cancer-related pathways and the expression of key cytokines, and high miR-204-5p expression is associated with better survival status of patients with BC ( 30 ). miR-215-5p overexpression inhibits the aggressive abilities of BC cells by targeting SOX9 ( 31 ), while overexpression of miR-20a-5p promotes the migration and invasion of BC cells through reducing RUNX3 expression ( 32 ). We identified miR-497-5p as the key miRNA in the lncRNA-miRNA-hub gene sub-network.…”

Section: Discussionmentioning

confidence: 99%

Identification of DGUOK-AS1 as a Prognostic Factor in Breast Cancer by Bioinformatics Analysis

Liang

et al. 2020

Front. Oncol.

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Background: Significant developments have been made in breast cancer diagnosis and treatment, yet the prognosis remains unsatisfactory. Accumulating evidence indicates that long non-coding RNAs (lncRNAs) play pivotal roles in the development and progression of human tumors. However, the regulatory mechanisms and clinical significance of most lncRNAs in breast cancer remain poorly understood. Methods: The lncRNA, miRNA, and mRNA expression profiles were obtained from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases. A lncRNA-miRNA-mRNA regulatory network was constructed and visualized using Cytoscape. The protein-protein interaction (PPI) network was constructed using the STRING database and hub genes were extracted using the cytoHubba plugin. Gene Ontology and Kyoto Encyclopedia of Gene and Genomes analyses identified the functions and signaling pathways associated with these differentially expressed mRNAs (DEmRNAs). Expression of the key lncRNA and the relationship with prognosis of patients with breast cancer were evaluated. Results: Six differentially expressed lncRNAs (DElncRNAs), 29 differentially expressed miRNAs (DEmiRNAs), and 253 DEmRNAs were selected to construct the regulatory network. A PPI network was established and seven hub genes were identified. A lncRNA-miRNA-hub gene regulatory sub-network was established containing two DElncRNAs, five DEmiRNAs, and seven DEmRNAs. Hub genes were associated with breast cancer onset and progression. The upregulated DGUOK-AS1 was identified as the key lncRNA in breast cancer based on the competing endogenous RNA network. High DGUOK-AS1 expression was associated with adverse prognosis in patients with breast cancer and a prognostic nomogram built on Grade, LN status, and DGUOK-AS1 expression shows significant prognostic value. Conclusions: Our results reveal the significant roles of lncRNA/miRNA/mRNA regulatory networks in breast cancer and identified a novel prognosis predictor and promising therapeutic target for patients with breast cancer.

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miRNA‐215‐5p suppresses the aggressiveness of breast cancer cells by targeting Sox9

Cited by 36 publications

References 24 publications

Silencing ZEB2 Induces Apoptosis and Reduces Viability in Glioblastoma Cell Lines

Silencing ZEB2 Induces Apoptosis and Reduces Viability in Glioblastoma Cell Lines

Interplay between p53 and non-coding RNAs in the regulation of EMT in breast cancer

Identification of DGUOK-AS1 as a Prognostic Factor in Breast Cancer by Bioinformatics Analysis

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