Long non‐coding <scp>RNA FTH</scp>1P3 activates paclitaxel resistance in breast cancer through miR‐206/<scp>ABCB</scp>1

Wang, Ruoming; Zhang, Tengteng; Yang, Zhen; Jiang, Chunxia; Shen, Jingjing

doi:10.1111/jcmm.13679

Cited by 81 publications

(49 citation statements)

References 29 publications

(29 reference statements)

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“…Particularly, the ceRNA regulatory mechanism has been identified as a canonical theory for lncRNAs to participate in the formation of chemotherapy resistance. For example, in breast cancer cells, the lncRNA FTH1P3 promotes P-gp expression and activates paclitaxel resistance by acting as a molecular sponge of miR-206 (Wang et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Long Non-coding RNA KCNQ1OT1 Contributes to Antiepileptic Drug Resistance Through the miR-138-5p/ABCB1 Axis in vitro

et al. 2019

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Compelling evidence has verified that long non-coding RNAs (lncRNAs) play a critical role on drug resistance in various diseases, especially cancer. However, the role of lncRNAs underlying multidrug resistance in epilepsy remains to be clarified. In the present study, we investigated the potential regulatory mechanism of the lncRNA KCNQ1OT1 in regulating antiepileptic drug (AED) resistance in human brain microvascular endothelial cells (HBMECs). The results revealed that expression of P-glycoprotein (P-gp) and KCNQ1OT1 was significantly elevated in phenytoin-resistant HBMECs (HBMEC/PHT). Meanwhile, the activity of nuclear factor-kappa B (NF-κB) was increased in HBMECs/PHT cells. Microarray analysis indicated that miR-138-5p was downregulated in HBMEC/PHT cells. Interestingly, bioinformatics prediction tools indicated miR-138-5p could directly target the transcripts of KCNQ1OT1 and NF-κB p65, and these results were confirmed by luciferase assays. Moreover, KCNQ1OT1 downregulation or miR-138-5p upregulation in vitro could inhibit P-gp expression and suppress NF-κB signaling pathway activation. Additionally, knockdown of KCNQ1OT1 or overexpression of miR-138-5p could increase the accumulation of rhodamine 123 (Rh123) and AEDs in HBMEC/PHT cells. Collectively, our results suggested that KCNQ1OT1 contributes to AED resistance through the miR-138-5p/NF-κB/ABCB1 axis in HBMEC/PHT cells, and these results provide a promising therapeutic target for the treatment of medically intractable epilepsy.

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Section: Discussionmentioning

confidence: 99%

Long Non-coding RNA KCNQ1OT1 Contributes to Antiepileptic Drug Resistance Through the miR-138-5p/ABCB1 Axis in vitro

et al. 2019

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“…Despite these constraints, several groups have characterized different pseudogenes as miRNA sponges, and a manually curated database (miRsponge) has been created [203]. Thus PMS1 Homolog 2, Mismatch Repair System Component Pseudogene 2 (PMS2L2) has been described as a molecular sponge of miR‐203 in osteoarthritis, with MCL‐1 mRNA being the direct target of miR‐203 [206], ferritin heavy chain 1 pseudogene 3 (FTH1P3) was shown to suppress miR‐206 activity to promote ABCB1 (ATP binding cassette subfamily B member 1) protein expression [207], and to sponge miR‐224‐5p to modulate expression of fizzled 5 [208]. Furthermore, OCT4‐pseudogene 4 was shown to protect OCT4 mRNA from miR‐145 [209], and PTENp1 (PTEN pseudogene 1) was seen to shield PTEN mRNAs from miR‐21 in oral squamous cell carcinoma (OSCC) [210], and from miR‐106b and miR‐93 in gastric tumours [211].…”

Section: Long Non‐coding Rnas (Lncrnas) and Their Functional Relationmentioning

confidence: 99%

Unveiling ncRNA regulatory axes in atherosclerosis progression

Navarro

Mallén

Cruzado

et al. 2020

Clinical & Translational Med

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Completion of the human genome sequencing project highlighted the richness of the cellular RNA world, and opened the door to the discovery of a plethora of short and long non‐coding RNAs (the dark transcriptome) with regulatory or structural potential, which shifted the balance of pathological gene alterations from coding to non‐coding RNAs. Thus, disease risk assessment currently has to also evaluate the expression of new RNAs such as small micro RNAs (miRNAs), long non‐coding RNAs (lncRNAs), circular RNAs (circRNAs), competing endogenous RNAs (ceRNAs), retrogressed elements, 3′UTRs of mRNAs, etc. We are interested in the pathogenic mechanisms of atherosclerosis (ATH) progression in patients suffering Chronic Kidney Disease, and in this review, we will focus in the role of the dark transcriptome (non‐coding RNAs) in ATH progression. We will focus in miRNAs and in the formation of regulatory axes or networks with their mRNA targets and with the lncRNAs that function as miRNA sponges or competitive inhibitors of miRNA activity. In this sense, we will pay special attention to retrogressed genomic elements, such as processed pseudogenes and Alu repeated elements, that have been recently seen to also function as miRNA sponges, as well as to the use or miRNA derivatives in gene silencing, anti‐ATH therapies. Along the review, we will discuss technical developments associated to research in lncRNAs, from sequencing technologies to databases, repositories and algorithms to predict miRNA targets, as well as new approaches to miRNA function, such as integrative or enrichment analysis and their potential to unveil RNA regulatory networks.

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“…8 Emerging studies have validated the participation of lncRNAs in the formation of PTX chemoresistance in BC. For example, lncRNA FTH1P3 was shown to expedite PTX resistance in BC via the miR-206/ABCB1 axis; 9 Han et al illuminated that lncRNA H19 activated PTX resistance in BC through inhibiting apoptosis and the regulation of Akt pathway; 10 Zheng et al asserted that CASC2 generated the promotion of PTX resistance of BC by regulating miR-18a-5p/CDK19. 11 Recently, urothelial carcinoma-associated 1 (UCA1) was reported to be dysregulated in BC and involved in the multiple resistance regulation.…”

Section: Introductionmentioning

confidence: 99%

<p>Long Non-Coding RNA UCA1 Modulates Paclitaxel Resistance in Breast Cancer via miR-613/CDK12 Axis</p>

Liu¹,

Jiang²,

Zhang³

et al. 2020

CMAR

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Background: Paclitaxel (PTX) occupies a considerable status in the chemotherapies of breast cancer (BC), but the drug resistance keeps an obstructive factor of PTX treatment. This study was designed to explore the molecular mechanism of long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) in PTX resistance of BC. Methods: UCA1, microRNA-613 (miR-613) and cyclin-dependent kinase 12 (CDK12) expression was assayed through quantitative real-time polymerase chain reaction (qRT-PCR). Cell Counting Kit-8 (CCK-8) assay was implemented for evaluating the half inhibitory concentrations (IC 50) of PTX and cell viability. Cell apoptosis was examined by flow cytometry. The target relationship was explored using dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. CDK12 protein level was detected through Western blot. Xenograft tumor assay was applied for assessing the influence of UCA1 on PTX resistance of BC in vivo. Results: UCA1 expressed highly in PTX-resistant BC tissues and cells and regulated PTX resistance in BC cells by affecting cell viability and apoptosis in part. UCA1 negatively interacted with miR-613 and modulated PTX resistance via sponging miR-613. CDK12 was a downstream gene of miR-613 and miR-613 exerted the modulation of PTX resistance via targeting CDK12. Furthermore, UCA1 regulated CDK12 level through interacting with miR-613. The regulatory role of UCA1 in PTX resistance of BC was achieved by miR-613/ CDK12 axis in vivo. Conclusion: UCA1 mediated PTX resistance in BC through the miR-613/CDK12 axis, manifesting that UCA1 might improve the PTX treatment of BC as a significant therapeutic biomarker.

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Long non‐coding RNA FTH1P3 activates paclitaxel resistance in breast cancer through miR‐206/ABCB1

Cited by 81 publications

References 29 publications

Long Non-coding RNA KCNQ1OT1 Contributes to Antiepileptic Drug Resistance Through the miR-138-5p/ABCB1 Axis in vitro

Long Non-coding RNA KCNQ1OT1 Contributes to Antiepileptic Drug Resistance Through the miR-138-5p/ABCB1 Axis in vitro

Unveiling ncRNA regulatory axes in atherosclerosis progression

<p>Long Non-Coding RNA UCA1 Modulates Paclitaxel Resistance in Breast Cancer via miR-613/CDK12 Axis</p>

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