Long non‐coding <scp>RNA</scp>‐<scp>CTD</scp>‐2108O9.1 represses breast cancer metastasis by influencing leukemia inhibitory factor receptor

Wang, Mozhi; Wang, Mengshen; Wang, Zhenning; Yu, Xiaohui; Song, Yongxi; Wang, Chong; Xu, Yujie; Wei, Fengheng; Zhao, Yi; Xu, Yingying

doi:10.1111/cas.13592

Cited by 17 publications

(11 citation statements)

References 34 publications

(68 reference statements)

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“…56,59 A mechanistic study has shown that lncRNA-CTD-2108O9.1 can effectively suppress tumour activities in breast cancer transformation via the metastasis inhibitory factor LIFR. 57 In our study, the expression levels of LIFR and AC124312.3 were lower in patients with TNBC than those with non-TNBC, and both molecules had been related to TNBC based on GO and OS analysis. Therefore, the results indicated that LIFR is probably targeted by lncRNA AC124312.3 to repress the metastasis of TNBC indirectly by competitive binding with the miR-1-3p, miR-206 and miR-613 families.…”

Section: Dovepresssupporting

confidence: 46%

“…LIFR is a key modulator in the controlling cytokine-cytokine receptor interaction, cell proliferation and signalling pathways regulating the pluripotency of stem cells and Jak-STAT. 56,57 Previous studies have reported that LIFR was regarded as a tumour suppressor and related to pancreatic carcinoma cell metastasis in vitro and in vivo. 58 LIFR, as a breast tumour suppressor, has been related to signal transduction upstream of the Hippo-YAP pathway in human breast cancer migration, and its deregulation may be associated with the metastasis of a considerable proportion of breast cancer.…”

Section: Dovepressmentioning

confidence: 99%

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<p>Construction and Comprehensive Analysis of a ceRNA Network to Reveal Potential Novel Biomarkers for Triple-Negative Breast Cancer</p>

Ma¹,

Song²,

Li³

et al. 2020

CMAR

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Background: Triple-negative breast cancer (TNBC) is the most common and aggressive type of breast cancer with an unfavourable outcome worldwide. Novel therapeutic targets are urgently required to explore this malignancy. This study explored the ceRNA network and the important genes for predicting the therapeutic targets. Methods: It identified the differentially expressed genes of mRNAs, lncRNAs and miRNAs between TNBC and non-TNBC samples in four cohorts (TCGA, GSE38959, GSE45827 and GSE65194) to explore the novel therapeutic targets for TNBC. Downstream analyses, including functional enrichment analysis, ceRNA network, protein-protein interaction and survival analysis, were then conducted by bioinformatics analysis. Finally, the potential core protein of the ceRNA network in TNBC was validated by immunohistochemistry. Results: A total of 1,045 lncRNAs and 28 miRNAs were differentially expressed in the TCGA TNBC samples, and the intersections of 282 mRNAs (176 upregulations and 106 downregulations) between the GEO and TCGA databases were identified. A ceRNA network composed of 7 lncRNAs, 62 mRNAs, 12 miRNAs and 244 edges specific to TNBC was established. The functional assay showed dysregulated genes, and GO, DO and KEGG enrichment analysis were performed. Survival analysis showed that mRNA LIFR and lncRNA AC124312.3 were significantly correlated with the overall survival of patients with TNBC in the TCGA databases (P < 0.05). Finally, the LIFR protein was validated, and immunohistochemical results showed the upregulated expression of LIFR in TNBC tissues. Conclusion: Thus, our study presents an enhanced understanding of the ceRNA network in TNBC, where the key gene LIFR may be a new promising potential therapeutic target for patients with TNBC.

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Section: Dovepresssupporting

confidence: 46%

Section: Dovepressmentioning

confidence: 99%

<p>Construction and Comprehensive Analysis of a ceRNA Network to Reveal Potential Novel Biomarkers for Triple-Negative Breast Cancer</p>

Ma¹,

Song²,

Li³

et al. 2020

CMAR

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“…lncRNAs involved in EMT of TNBC could be assigned to two classes based on the level of expression and molecular regulation. First, lncRNAs LET [21], Xist [22], lncRNA-CTD-2108O9.1 [23], and GAS5 [24] were shown to be downregulated in TNBC cell lines. Upregulation of these lncRNAs attenuates TNBC cell proliferation and viability and enhances apoptosis.…”

Section: Long Non-coding Rnasmentioning

confidence: 99%

“…The mechanisms by which this category of lncRNA acts differ from one lncRNA to another. XIST exerts its suppressive activity via miR-155/CDX1 [22], GAS5 by functioning as a competing endogenous RNA (ceRNA) that antagonizes miR-196a-5p targeting thereby FOXO1/PI3K/AKT signalling [24], lncRNA-CTD-2108O9.1 targets leukemia inhibitory factor receptor LIFR [23], while no specific molecular mechanism for LET is yet defined [21]. (see Figure S1 and Table 1).…”

Section: Long Non-coding Rnasmentioning

confidence: 99%

New Insights into the Implication of Epigenetic Alterations in the EMT of Triple Negative Breast Cancer

Khaled

Bidet

2019

Cancers

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Breast cancer is the most common cancer and leading cause of cancer death among women worldwide, encompassing a wide heterogeneity of subtypes with different clinical features. During the last two decades, the use of targeted therapies has emerged in clinical research in order to increase treatment efficiency, improve prognosis and reduce recurrence. However, the triple negative breast cancer (TNBC) subtype remains a clinical challenge, with poor prognosis since no therapeutic targets have been identified. This aggressive breast cancer entity lacks expression of oestrogen receptor (ER) and progesterone receptor (PR), and it does not overexpress human epidermal growth factor receptor 2 (HER2). The major reason for TNBC poor prognosis is early therapeutic escape from conventional treatments, leading to aggressive metastatic relapse. Metastases occur after an epithelial-mesenchymal transition EMT of epithelial cells, allowing them to break free from the primary tumour site and to colonize distant organs. Cancer-associated EMT consists not only of acquired migration and invasion ability, but involves complex and comprehensive reprogramming, including changes in metabolism, expression levels and epigenetic. Recently, many studies have considered epigenetic alterations as the primary initiator of cancer development and metastasis. This review builds a picture of the epigenetic modifications implicated in the EMT of breast cancer. It focuses on TNBC and allows comparisons with other subtypes. It emphasizes the role of the main epigenetic modifications lncRNAs, miRNAs, histone and DNA- modifications in tumour invasion and appearance of metastases. These epigenetic alterations can be considered biomarkers representing potential diagnostic and prognostic factors in order to define a global metastatic signature for TNBC.

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“…Aberrant expression of several lncRNAs has been reported in human diseases, including breast cancer (11,12). However, the number of lncRNAs that have been experimentally identified as oncogenes or tumor suppressors in breast cancer is considerably low (13)(14)(15). lncRNAs can regulate gene expression by sponging miRNAs, binding to promoters or directly interacting with proteins (16)(17)(18).…”

Section: Introductionmentioning

confidence: 99%

Long non‑coding RNA SNHG1 promotes breast cancer progression by regulation of LMO4

Xiong

Feng

et al. 2020

Oncol Rep

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Long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) was reported to be a critical regulator of tumorigenesis and is frequently deregulated in several cancer types. However, the exact mechanism by which SNHG1 contributes to breast cancer progression has not been fully elucidated. The identification of the molecular mechanism of SNHG1 is important for understanding the development of breast cancer and for improving the prognosis of the patients with this disease. In the present study, increased expression levels of SNHG1 were noted in breast cancer tumors following analysis of differentially expressed lncRNAs between 1,063 tumor and 102 normal tissues derived from The Cancer Genome Atlas Breast Invasive Carcinoma (TCGA-BRCA) dataset. This finding was further validated using 50 pairs of normal and tumor tissues that were collected from patients with breast cancer. Notably, SNHG1 expression was significantly correlated with estrogen receptor (ER)/progesterone receptor (PR) negative status (ER -/PR -) and advanced clinical stage in breast cancer tissues. Knockdown of SNHG1 led to cell growth arrest, cell cycle redistribution and cell migration inhibition of breast cancer cells. The miRDB database predicted that miR-573 interacts with SNHG1. RT-PCR confirmed the negative regulation of miR-573 levels by SNHG1 in breast cancer cells and the Dual-luciferase reporter assay confirmed their complementary binding. The repression of miR-573 by SNGH1 decreased LIM domain only 4 (LMO4) mRNA and protein expression levels in the breast cancer cell lines tested and induced the expression of cyclin D1 and cyclin E. In vitro experiments indicated that LMO4 overexpression could reverse siSNHG1-induced cell growth arrest, cell cycle redistribution and inhibition of cell migration in breast cancer cells. Moreover, the tumor xenograft model indicated that SNHG1 knockdown inhibited MDA-MB-231 growth in vivo and LMO4 overexpression reversed the tumor growth inhibition induced by SNHG1 knockdown. The present study demonstrated that SNHG1 acts as a novel oncogene in breast cancer via the SNHG/miR-573/LMO4 axis and that it could be a promising therapeutic target for patients with breast cancer.

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Long non‐coding RNA‐CTD‐2108O9.1 represses breast cancer metastasis by influencing leukemia inhibitory factor receptor

Cited by 17 publications

References 34 publications

<p>Construction and Comprehensive Analysis of a ceRNA Network to Reveal Potential Novel Biomarkers for Triple-Negative Breast Cancer</p>

<p>Construction and Comprehensive Analysis of a ceRNA Network to Reveal Potential Novel Biomarkers for Triple-Negative Breast Cancer</p>

New Insights into the Implication of Epigenetic Alterations in the EMT of Triple Negative Breast Cancer

Long non‑coding RNA SNHG1 promotes breast cancer progression by regulation of LMO4

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