Long non-coding RNA NONHSAT101069 promotes epirubicin resistance, migration, and invasion of breast cancer cells through NONHSAT101069/miR-129-5p/Twist1 axis

Yao, Na; Fu, Yue; Chen, Lie; Liu, Zhao; He, Jing; Zhu, Yichao; Xia, Tiansong; Wang, Shui

doi:10.1038/s41388-019-0904-5

Cited by 91 publications

(66 citation statements)

References 50 publications

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“…In our finding, we assured that MEG3 blocked the proliferation, invasion, and migration of glioma cells, which was in line with previously published data [7,11,20]. Moreover, it has been reported that cancer cells can be mechanically guided by EMT processes, which play key roles in the invasion, migration, and metastasis of multiple malignancies [21]. EMT, known as epithelial to mesenchymal transformation, could increase individual cell motility [22].…”

Section: Discussionsupporting

confidence: 91%

Tumor-Suppressive Function of lncRNA-MEG3 in Glioma Cells by Regulating miR-6088/SMARCB1 Axis

Gong

Huang

2020

BioMed Research International

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Objective. Mounting evidence has elaborated the implication of long noncoding RNAs (lncRNAs) in tumorigenesis of several cancers, including glioma. However, little was known about the mechanism of lncRNA maternally expressed gene 3 (MEG3) in the development and progression of glioma. This work is designed to explore the effect of MEG3 on glioma progression and its possible mechanism. Methods. Expressions of lncRNA-MEG3 and SMARCB1 were detected in human glioblastoma U87 and U251 cell lines. Gain and loss of function of MEG3 or/and miR-6088 was performed in U87 and U251 cells to observe its effect on cell proliferation and migration as well as on epithelial-mesenchymal transition (EMT) related markers. Luciferase reporter gene assay was employed to inspect the interactions among MEG3, miR-6088, and SMARCB1. Results. MEG3 and SMARCB1 expressions were downregulated in glioma cells. Transfection of pcDNA3.1-MEG3 or pcDNA3.1-SMARCB1 plasmids could clearly block cell proliferation, migration, and EMT progression. MEG3 functions as a sponge for miR-6088, while SMARCB1 is a downstream protein of miR-6088. Transfection of miR-6088 mimic or si-SMARCB1 could obviously reverse the favorable effect of pcDNA3.1-MEG3 on glioma progression. Conclusion. Collectively, the evidence in this study indicated that MEG3 was downregulated in glioma cells and inhibited proliferation and migration of glioma cells via regulating miR-6088/SMARCB1 axis.

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Section: Discussionsupporting

confidence: 91%

Tumor-Suppressive Function of lncRNA-MEG3 in Glioma Cells by Regulating miR-6088/SMARCB1 Axis

Gong

Huang

2020

BioMed Research International

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“…They have been extensively studied in the carcinogenesis of many diseases, including cancer. Moreover, recent findings manifested that lncR-NAs are involved in a series of biological processes, such as cell proliferation, apoptosis, invasion and migration [9,10]. Furthermore, lncRNAs have been identified as new biomarkers of many malignancies, since they are associated with the complicated pathogenesis of malignancies [11,12].…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA RHPN1-AS1 promotes colorectal cancer progression via targeting miR-7-5p/OGT axis

Zheng

Zhang

et al. 2020

Cancer Cell Int

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Background: Rhophilin Rho GTPase binding protein 1 antisense RNA 1 (RHPN1-AS1) is a newly discovered oncogene in several diseases, such as breast cancer, non-small cell lung cancer and uveal melanoma. Nevertheless, its molecular role in colorectal cancer (CRC) remains unknown. This paper explored the role of RHPN1-AS1 in CRC progression.Methods: qRT-PCR was used to detect relevant RNAs expression. CCK-8, EdU, flow cytometry, Transwell and western blot assays were performed to investigate the function of RHPN1-AS1 in CRC cells. Xenograft model was constructed to evaluate the effects of RHPN1-AS1 on tumor growth in vivo. Mechanical experiments were performed to investigate the relationship between relative genes.Results: RHPN1-AS1 was significantly overexpressed in CRC cell lines. Knockdown of RHPN1-AS1 could inhibit cell proliferation, while stimulating cell apoptosis in vitro. Cell migration and invasion abilities were greatly suppressed after silencing RHPN1-AS1. Besides, signal transducer and activator of transcription 3 (STAT3) served as transcription factor of RHPN1-AS1. Moreover, miR-7-5p was identified as a target of RHPN1-AS1 and was negatively regulated by RHPN1-AS1 in CRC. MiR-7-5p inhibition rescued the oncogenic function of RHPN1-AS1. Additionally, O-GlcNAcylation transferase (OGT) was the downstream target of miR-7-5p. OGT overexpression could abrogate the anti-tumor effects of RHPN1-AS1 knockdown on CRC.Conclusion: RHPN1-AS1 regulates CRC by mediating OGT through sponging miR-7-5p, suggesting that RHPN1-AS1 might be a potential therapeutic target for CRC.

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“…CeRNAs also play speci c roles in BRCA drug resistance. LncRNA NONHSAT101069 was upregulated in BRCA tissues and promoted epirubicin resistance via regulation of the NONHSAT101069/miR-129-5p/Twist1 axis, highlighting its potential as an oncogene and therapeutic biomarker for BRCA [37]. The lncRNA regulator of reprogramming promotes the progression of BRCA and decreases sensitivity to rapamycin through miR-194-3p targeting of MECP2 [38].…”

Section: Discussionmentioning

confidence: 99%

Inferences From Dysregulated Long Non-Coding RNA-Mediated Competing Endogenous RNAs in Various Chemotherapy Drugs and Evaluation of Drug Response in Breast Cancer

Zhang¹,

Li²,

Zhang³

et al. 2020

Preprint

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Backgroud: Differences in individual drug response, especially drug resistance, present an obstacle to the treatment of breast cancer (BRCA). Thus, the ability to predict drug response would contribute to developing novel treatment strategies. Accumulating evidence have suggested that tumor molecular profiles and drug response data provide opportunities and challenges for the discovery of new molecular characteristics and mechanisms of drug response in BRCA. Methods: In the present study, an integrated pipeline was developed to explore drug response-related long non-coding RNA (lncRNA)-mediated competing endogenous RNAs (ceRNAs) motifs in BRCA. Results: Drug response-specific ceRNAs indicated that lncRNAs play an essential role in various drug treatments for BRCA. Several key drug-resistant and -sensitive dysregulated ceRNAs were identified in Adriamycin, Cytoxan, and Tamoxifen. The interactions in these ceRNAs showed strong correlations in BRCA. Most drug response-related dysregulated ceRNAs were only present in one kind of drug. A number of drug response-related ceRNAs presented diverse dysregulation patterns. We also extracted some key drug response-related lncRNAs, such as HCP5 and FAM182A. These lncRNAs were associated with certain cancer hallmarks and survival in BRCA. Conclusions: Ultimately, understanding the underlying lncRNA-mediated ceRNAs in drug responses will facilitate improved individual reactions to chemotherapy and overall outcomes of BRCA treatment.

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Long non-coding RNA NONHSAT101069 promotes epirubicin resistance, migration, and invasion of breast cancer cells through NONHSAT101069/miR-129-5p/Twist1 axis

Cited by 91 publications

References 50 publications

Tumor-Suppressive Function of lncRNA-MEG3 in Glioma Cells by Regulating miR-6088/SMARCB1 Axis

Tumor-Suppressive Function of lncRNA-MEG3 in Glioma Cells by Regulating miR-6088/SMARCB1 Axis

Long noncoding RNA RHPN1-AS1 promotes colorectal cancer progression via targeting miR-7-5p/OGT axis

Inferences From Dysregulated Long Non-Coding RNA-Mediated Competing Endogenous RNAs in Various Chemotherapy Drugs and Evaluation of Drug Response in Breast Cancer

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