LncRNA H19 confers chemoresistance in ERα-positive breast cancer through epigenetic silencing of the pro-apoptotic gene BIK

Si, Xinxin; Zang, Ruochen; Zhang, Erbao; Liu, Yue; Shi, Xiao; Zhang, Er-Shao; Shao, Lipei; Li, Andi; Yang, Nan; Han, Xiao; Pan, Beijing; Zhang, Zhihong; Sun, Luan; Sun, Yujie

doi:10.18632/oncotarget.13263

Cited by 126 publications

(79 citation statements)

References 42 publications

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“…The development of chemoresistance in certain cases also requires the involvement of lncRNAs (17,18). In the present study the upregulation of lncRNA CASC11 was demonstrated in HCC, indicating its oncogenic role.…”

Section: Discussionsupporting

confidence: 59%

Overexpression of long non‑coding RNA cancer susceptibility�11 is involved in the development of chemoresistance to carboplatin in hepatocellular carcinoma

Liu

Zhou

et al. 2020

Oncol Lett

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The long non-coding (lnc)RNA cancer susceptibility 11 (CASC11) promotes gastric cancer, however its role in other diseases is unknown. The present study demonstrated upregulation of lncRNA CASC11 and microRNA (miR)-21 in hepatocellular carcinoma (HCC). Furthermore, the expression of CASC11 was positively correlated with that of miR-21 in HCC tumors. Moreover, overexpression of lncRNA CASC11 led to upregulation of miR-21 in HCC cells, whereas overexpression of miR-21 had no effect on CASC11 levels. The levels of lncRNA CASC11 and miR-21 were found to be upregulated in the plasma of patients with HCC during chemotherapy. In vitro cell experiments demonstrated upregulation of lncRNA CASC11 in HCC cells treated with carboplatin. Additionally, overexpression of lncRNA CASC11 promoted, whereas its knockdown inhibited the viability of HCC cells following carboplatin treatment. Finally, overexpression of miR-21 ameliorated the effects of lncRNA CASC11 knockdown on cell viability. Thus, these findings suggest that upregulation of lncRNA CASC11 is involved in the development of chemoresistance to carboplatin in patients with HCC, via the upregulation of miR-21.

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Section: Discussionsupporting

confidence: 59%

Overexpression of long non‑coding RNA cancer susceptibility�11 is involved in the development of chemoresistance to carboplatin in hepatocellular carcinoma

Liu

Zhou

et al. 2020

Oncol Lett

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“…Si et al . () detected that H19 attenuated cell apoptosis in response to paclitaxel treatment by inhibiting the transcription of pro‐apoptotic genes BIK and NOXA. As reported by Vennin et al .…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, Sun et al (2015) described H19 as an estrogen-inducible gene that plays a key role in survival and estrogeninduced proliferation of MCF-7 cells. Si et al (2016) detected that H19 attenuated cell apoptosis in response to paclitaxel treatment by inhibiting the transcription of pro-apoptotic genes BIK and NOXA. As reported by Vennin et al (2015), the aggressive phenotype of BC cells may depend on the increased cell proliferation and migration in vitro, as well as the increased tumor growth and metastasis in vivo by the overexpression of H19/miR-675.…”

Section: Discussionmentioning

confidence: 99%

Interplay of lncRNA H19/miR‐675 and lncRNA NEAT1/miR‐204 in breast cancer

et al. 2019

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Long noncoding RNAs (lncRNAs) are frequently precursor RNAs of microRNAs (miRNAs) or act as competing endogenous RNAs (ceRNAs) to interact with miRNAs. To better understand the shared impact of lncRNAs and miRNAs in the regulatory post‐transcriptional network, we focused here on the relationships between (a) lncRNA H19 and miR‐675, (b) NEAT1 and miR‐204, and (c) HOTAIR and miR‐331 in plasma of early breast cancer (BC) patients. We quantified each RNA in plasma samples of 63 BC patients and 10 healthy women by quantitative real‐time PCR. In cell culture experiments, the influence of these noncoding RNAs (ncRNAs) on proliferation and apoptosis of BC cell line MCF‐7 was examined. Plasma levels of H19 ( P = 0.030), NEAT1 ( P = 0.030), and miR‐331 ( P = 0.012) were deregulated in BC patients compared with healthy women. In both cohorts, the concentrations of H19 correlated with those of miR‐675 ( P = 0.0001). Higher H19 ( P = 0.001) along with lower miR‐675 ( P = 0.007) levels and higher miR‐204 ( P = 0.017) along with lower NEAT1 ( P = 0.030) levels were detected in plasma of HER2‐positive patients compared with the other BC subgroups. Whereas the expression of HOTAIR was below the detection level, miR‐331 levels correlated with nodal status ( P = 0.002) and recurrence ( P = 0.012). In cell culture experiments, a competitive impact on cell proliferation and apoptosis by these ncRNAs was also documented. Our findings describe a relationship of the plasma levels of H19/miR‐675 and NEAT1/miR‐204 in the different BC subtypes; in addition, they reveal an interplay between these lncRNAs and miRNAs in the regulatory network in MCF‐7 cells, which should also be considered in the search for new diagnostic and therapeutic markers.

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“…Paclitaxel is one of the first‐line chemotherapy drugs for multiple human cancers, including breast cancer . Paclitaxel could induce the cell cycle arrest at G2/M phase and induce the cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

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

Wang

Zhang

Yang

et al. 2018

J Cellular Molecular Medi

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Emerging evidence has indicated the important function of long non‐coding RNAs (lncRNAs) in tumour chemotherapy resistance. However, the underlying mechanism is still ambiguous. In this study, we investigate the physiopathologic role of lncRNA ferritin heavy chain 1 pseudogene 3 (FTH1P3) on the paclitaxel (PTX) resistance in breast cancer. Results showed that lncRNA FTH1P3 was up‐regulated in paclitaxel‐resistant breast cancer tissue and cells (MCF‐7/PTX and MDA‐MB‐231/PTX cells) compared with paclitaxel‐sensitive tissue and parental cell lines (MCF‐7, MDA‐MB‐231). Gain‐ and loss‐of‐function experiments revealed that FTH1P3 silencing decreased the 50% inhibitory concentration (IC50) value of paclitaxel and induced cell cycle arrest at G2/M phase, while FTH1P3‐enhanced expression exerted the opposite effects. In vivo, xenograft mice assay showed that FTH1P3 silencing suppressed the tumour growth of paclitaxel‐resistant breast cancer cells and ABCB1 protein expression. Bioinformatics tools and luciferase reporter assay validated that FTH1P3 promoted ABCB1 protein expression through targeting miR‐206, acting as a miRNA “sponge.” In summary, our results reveal the potential regulatory mechanism of FTH1P3 on breast cancer paclitaxel resistance through miR‐206/ABCB1, providing a novel insight for the breast cancer chemoresistance.

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LncRNA H19 confers chemoresistance in ERα-positive breast cancer through epigenetic silencing of the pro-apoptotic gene BIK

Cited by 126 publications

References 42 publications

Overexpression of long non‑coding RNA cancer susceptibility�11 is involved in the development of chemoresistance to carboplatin in hepatocellular carcinoma

Overexpression of long non‑coding RNA cancer susceptibility�11 is involved in the development of chemoresistance to carboplatin in hepatocellular carcinoma

Interplay of lncRNA H19/miR‐675 and lncRNA NEAT1/miR‐204 in breast cancer

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

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