LncRNA-ATB promotes trastuzumab resistance and invasion-metastasis cascade in breast cancer

Shi, Shengjia; Wang, Lijuan; Yu, Bo; Li, Yunhui; Jin, Yong; Bai, Xiaozhong

doi:10.18632/oncotarget.3457

Cited by 287 publications

(245 citation statements)

References 37 publications

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“…24 Lnc-ATB was the most remarkably up-regulated lncRNA in the tissues of breast cancer patients with trastuzumab resistance and could induce invasion-metastasis cascade in breast cancer. 25 We here in Wilms tumour found that LINC00473…”

mentioning

confidence: 85%

LINC00473 antagonizes the tumour suppressor miR‐195 to mediate the pathogenesis of Wilms tumour via IKKα

Zhu

Zhang

et al. 2017

Cell Proliferation

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Objectives: Although dramatic improvements of overall survival has achieved in patients with favourable histology Wilms tumour, disease recurrence is still the main cause of cancer-related death in childhood. Long non-coding RNAs (lncRNAs) as oncogenes or tumour suppressors are dysregulated during carcinogenesis. However, the role of lncRNAs in the pathogenesis of Wilms tumour is unknown. Here, an lncRNA LINC00473 signature that functioned as oncogene was identified in Wilms tumour.

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mentioning

confidence: 85%

LINC00473 antagonizes the tumour suppressor miR‐195 to mediate the pathogenesis of Wilms tumour via IKKα

Zhu

Zhang

et al. 2017

Cell Proliferation

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“…Trastuzumab (Herceptin) was obtained from Roche (Basel, Switzerland) and dissolved in sterile water. Trastuzumab‐resistant SKBR‐3/Tr and BT474/Tr cells were obtained by continuous culture with 5 mg/mL trastuzumab for 6 months as previously reported,11, 12 and were cultured in RPMI 1640 medium with 250 μg/mL trastuzumab.…”

Section: Methodsmentioning

confidence: 99%

“…In recent years, emerging evidence indicates that they play important roles in regulating cellular and biological functions. LncRNAs can regulate gene expression at post‐transcriptional level via sponging microRNAs10 and modulate transcriptional gene silencing via the chromatin regulation 11, 12. Thus, the investigation of the role of lncRNAs in breast cancer could help with the understanding of tumorigenesis and the identification of novel diagnostic and therapeutic targets.…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA SNHG14 induces trastuzumab resistance of breast cancer via regulating PABPC1 expression through H3K27 acetylation

Huang

Wang

et al. 2018

J Cellular Molecular Medi

101

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Currently, resistance to trastuzumab, a human epidermal growth factor receptor 2 (HER2) inhibitor, has become one major obstacle for improving the clinical outcome of patients with advanced HER2+ breast cancer. While cell behaviour can be modulated by long non‐coding RNAs (lncRNAs), the contributions of lncRNAs in progression and trastuzumab resistance of breast cancer are largely unknown. To this end, the involvement and regulatory functions of lncRNA SNHG14 in human breast cancer were investigated. RT‐qPCR assay showed that SNHG14 was up‐regulated in breast cancer tissues and associated with trastuzumab response. Gain‐ and loss‐of‐function experiments revealed that overexpression of SNHG14 promotes cell proliferation, invasion and trastuzumab resistance, whereas knockdown of SNHG14 showed an opposite effect. PABPC1 gene was identified as a downstream target of SNHG14, and PABPC1 mediates the SNHG14‐induced oncogenic effects. More importantly, ChIP assays demonstrated that lncRNA SNHG14 may induce PABPC1 expression through modulating H3K27 acetylation in the promoter of PABPC1 gene, thus resulting in the activation of Nrf2 signalling pathway. These data suggest that lncRNA SNHG14 promotes breast cancer tumorigenesis and trastuzumab resistance through regulating PABPC1 expression through H3K27 acetylation. Therefore, SNHG14 may serve as a novel diagnostic and therapeutic target for breast cancer patients.

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“…Furthermore, miR-200c treatment of xenografts of a trastuzumab-resistant breast cancer cell line leads to re-gain of trastuzumab sensitivity [88]. In the same scenario, another level of regulation comes from a long non-coding RNA, Lnc-ATB, which is expressed at the downstream of TGF-β signaling and competitively binds to miR-200c conferring ZEB1 and ZNF217 (upregulation)-mediated trastuzumab resistance [89]. In summary, these studies clearly provide the cue that miR-200c could efficiently control the response of cancer cells to anti-cancer therapies through EMT-dependent and EMT-independent pathways.…”

Section: Mir-200c Emt and Targeted Therapy Resistancementioning

confidence: 99%

miR-200c: a versatile watchdog in cancer progression, EMT, and drug resistance

et al. 2016

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MicroRNAs (miRNAs) are 20-22-nucleotide small endogenous non-coding RNAs which regulate gene expression at post-transcriptional level. In the last two decades, identification of almost 2600 miRNAs in human and their potential to be modulated opened a new avenue to target almost all hallmarks of cancer. miRNAs have been classified as tumor suppressors or oncogenes depending on the phenotype they induce, the targets they modulate, and the tissue where they function. miR-200c, an illustrious tumor suppressor, is one of the highly studied miRNAs in terms of development, stemness, proliferation, epithelial-mesenchymal transition (EMT), therapy resistance, and metastasis. In this review, we first focus on the regulation of miR-200c expression and its role in regulating EMT in a ZEB1/E-cadherin axis-dependent and ZEB1/E-cadherin axis-independent manner. We then describe the role of miR-200c in therapy resistance in terms of multidrug resistance, chemoresistance, targeted therapy resistance, and radiotherapy resistance in various cancer types. We highlight the importance of miR-200c at the intersection of EMT and chemoresistance. Furthermore, we show how miR-200c coordinates several important signaling cascades such as TGF-β signaling, PI3K/Akt signaling, Notch signaling, VEGF signaling, and NF-κB signaling. Finally, we discuss miR-200c as a potential prognostic/diagnostic biomarker in several diseases, but mainly focusing on cancer and its potential application in future therapeutics.

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LncRNA-ATB promotes trastuzumab resistance and invasion-metastasis cascade in breast cancer

Cited by 287 publications

References 37 publications

LINC00473 antagonizes the tumour suppressor miR‐195 to mediate the pathogenesis of Wilms tumour via IKKα

LINC00473 antagonizes the tumour suppressor miR‐195 to mediate the pathogenesis of Wilms tumour via IKKα

Long non‐coding RNA SNHG14 induces trastuzumab resistance of breast cancer via regulating PABPC1 expression through H3K27 acetylation

miR-200c: a versatile watchdog in cancer progression, EMT, and drug resistance

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