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      Long noncoding RNA LINC00115 promotes breast cancer metastasis by inhibiting miR‐7

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          Abstract

          Breast cancer is the second leading cause of cancer‐related deaths in women. The long noncoding RNA LINC00115 has been reported to be involved in the poor outcome of patients with breast cancer, but the biological function and underlying mechanism remain unclear. Here, we report that LINC00115 expression is increased in triple‐negative breast cancer tissue compared with matched normal tissue, and LINC00115 knockdown suppresses breast cancer cell migration and invasion. Furthermore, we show that LINC00115 directly targets miR‐7 and inhibits its expression. LINC00115 also reduces the expression of KLF4, which is a direct target of miR‐7 and is involved in breast cancer metastasis. Together, our findings suggest that LINC00115 promotes breast cancer metastasis through modulating the expression of miR‐7 and KLF4.

          Abstract

          LINC00115 expression is increased in breast cancer tissue and promotes tumor cell migration and invasion by inhibiting miR‐7 expression. This miRNA has been identified as a tumor suppressor in breast cancer, and one of its direct targets, KLF4, is an oncogene in breast cancer.

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          GAS5, a non-protein-coding RNA, controls apoptosis and is downregulated in breast cancer.

          M. Mourtada-Maarabouni, M Pickard, V. L. Hedge … (2009)
          Effective control of both cell survival and cell proliferation is critical to the prevention of oncogenesis and to successful cancer therapy. Using functional expression cloning, we have identified GAS5 (growth arrest-specific transcript 5) as critical to the control of mammalian apoptosis and cell population growth. GAS5 transcripts are subject to complex post-transcriptional processing and some, but not all, GAS5 transcripts sensitize mammalian cells to apoptosis inducers. We have found that, in some cell lines, GAS5 expression induces growth arrest and apoptosis independently of other stimuli. GAS5 transcript levels were significantly reduced in breast cancer samples relative to adjacent unaffected normal breast epithelial tissues. The GAS5 gene has no significant protein-coding potential but expression encodes small nucleolar RNAs (snoRNAs) in its introns. Taken together with the recent demonstration of tumor suppressor characteristics in the related snoRNA U50, our observations suggest that such snoRNAs form a novel family of genes controlling oncogenesis and sensitivity to therapy in cancer.
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            JAK2-binding long noncoding RNA promotes breast cancer brain metastasis.

            Shouyu Wang, Ke Liang, Qingsong Hu … (2017)
            Conventional therapies for breast cancer brain metastases (BCBMs) have been largely ineffective because of chemoresistance and impermeability of the blood-brain barrier. A comprehensive understanding of the underlying mechanism that allows breast cancer cells to infiltrate the brain is necessary to circumvent treatment resistance of BCBMs. Here, we determined that expression of a long noncoding RNA (lncRNA) that we have named lncRNA associated with BCBM (Lnc-BM) is prognostic of the progression of brain metastasis in breast cancer patients. In preclinical murine models, elevated Lnc-BM expression drove BCBM, while depletion of Lnc-BM with nanoparticle-encapsulated siRNAs effectively treated BCBM. Lnc-BM increased JAK2 kinase activity to mediate oncostatin M- and IL-6-triggered STAT3 phosphorylation. In breast cancer cells, Lnc-BM promoted STAT3-dependent expression of ICAM1 and CCL2, which mediated vascular co-option and recruitment of macrophages in the brain, respectively. Recruited macrophages in turn produced oncostatin M and IL-6, thereby further activating the Lnc-BM/JAK2/STAT3 pathway and enhancing BCBM. Collectively, our results show that Lnc-BM and JAK2 promote BCBMs by mediating communication between breast cancer cells and the brain microenvironment. Moreover, these results suggest targeting Lnc-BM as a potential strategy for fighting this difficult disease.
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              Oncogenic long noncoding RNA landscape in breast cancer

              Shouping Xu, Dejia Kong, Qianlin Chen … (2017)
              Background Few long noncoding RNAs (lncRNAs) that act as oncogenic genes in breast cancer have been identified. Methods Oncogenic lncRNAs associated with tumourigenesis and worse survival outcomes were examined and validated in Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA), respectively. Then, the potential biological functions and expression regulation of these lncRNAs were studied via bioinformatics and genome data analysis. Moreover, progressive breast cancer subtype-specific lncRNAs were investigated via high-throughput sequencing in our cohort and TCGA validation. To elucidate the mechanisms of the regulation of these lncRNAs, genomic alterations from the TCGA, Broad, Sanger and BCCRC data, as well as epigenetic modifications from GEO data, were then applied and examined to meet this objective. Finally, cell proliferation assays, flow cytometry analyses and TUNEL assays were applied to validate the oncogenic roles of these lncRNAs in vitro. Results A cluster of oncogenic lncRNAs that was upregulated in breast cancer tissue and was associated with worse survival outcomes was identified. These oncogenic lncRNAs are involved in regulating immune system activation and the TGF-beta and Jak-STAT signalling pathways. Moreover, TINCR, LINC00511, and PPP1R26-AS1 were identified as subtype-specific lncRNAs associated with HER-2, triple-negative and luminal B subtypes of breast cancer, respectively. The up-regulation of these oncogenic lncRNAs is mainly caused by gene amplification in the genome in breast cancer and other solid tumours. Finally, the knockdown of TINCR, DSCAM-AS1 or HOTAIR inhibited breast cancer cell proliferation, increased apoptosis and inhibited cell cycle progression in vitro. Conclusions These findings enhance the landscape of known oncogenic lncRNAs in breast cancer and provide insights into their roles. This understanding may potentially aid in the comprehensive management of breast cancer. Electronic supplementary material The online version of this article (doi:10.1186/s12943-017-0696-6) contains supplementary material, which is available to authorized users.
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                Author and article information

                Contributors
                Chunlei Yuan:
                ORCID: https://orcid.org/0000-0002-7212-1747
                1554597615@qq.com
                Liangyun Guo: gly_0417@126.com
                Journal
                Journal ID (nlm-ta): FEBS Open Bio
                Journal ID (iso-abbrev): FEBS Open Bio
                Journal ID (doi): 10.1002/(ISSN)2211-5463
                Journal ID (publisher-id): FEB4
                Title: FEBS Open Bio
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Electronic): 2211-5463
                Publication date (Electronic): 11 June 2020
                Publication date Collection: July 2020
                Volume: 10
                Issue: 7 ( doiID: 10.1002/feb4.v10.7 )
                Pages: 1230-1237
                Affiliations
                [ 1 ] Department of Breast the Second Affiliated Hospital of Nanchang University China
                [ 2 ] Department of Ultrasound the Second Affiliated Hospital of Nanchang University China
                Author notes
                [*] [* ] Correspondence

                L. Guo, Department of Ultrasound, the Second Affiliated Hospital of Nanchang University, Nanchang 330031, China

                E‐mail: gly_0417@ 123456126.com

                and

                C. Yuan, Department of Breast, the Second Affiliated Hospital of Nanchang University, Nanchang 330031, China

                E‐ mail: 1554597615@ 123456qq.com

                Author information
                https://orcid.org/0000-0002-7212-1747
                Article
                Publisher ID: FEB412842
                DOI: 10.1002/2211-5463.12842
                PMC ID: 7327907
                PubMed ID: 32175684
                SO-VID: 596faa95-7445-4c00-bb0b-bb9d2616967b
                Copyright © © 2020 The Second Affiliated Hospital of Nanchang University. FEBS Open Bio published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 12 November 2019
                Date revision received : 06 February 2020
                Date accepted : 12 March 2020
                Page count
                Figures: 4, Tables: 0, Pages: 8, Words: 4109
                Funding
                Funded by: the Jiangxi provincial health department project
                Award ID: 20151081
                Categories
                Subject: Research Article
                Subject: Research Articles
                Custom metadata
                source-schema-version-number 2.0
                cover-date July 2020
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.5 mode:remove_FC converted:01.07.2020

                Keywords: linc00115,metastasis,mir‐7,triple‐negative breast cancer
                Data availability:
                Keywords: linc00115, metastasis, mir‐7, triple‐negative breast cancer

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