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      Crosstalk between long noncoding RNA and microRNA in Cancer

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          Abstract

          miRNAs and lncRNAs play a central role in cancer-associated gene regulations. The dysregulated expression of lncRNAs has been reported as a hallmark of cancer progression, acting as an independent prediction marker for an individual cancer patient. The interplay of miRNA and lncRNA decides the variation of tumorigenesis that could be mediated by acting as sponges for endogenous RNAs, regulating miRNA decay, mediating intra-chromosomal interactions, and modulating epigenetic components. This paper focuses on the influence of crosstalk between lncRNA and miRNA on cancer hallmarks such as epithelial-mesenchymal transition, hijacking cell death, metastasis, and invasion. Other cellular roles of crosstalks, such as neovascularization, vascular mimicry, and angiogenesis were also discussed. Additionally, we reviewed crosstalk mechanism with specific host immune responses and targeting interplay (between lncRNA and miRNA) in cancer diagnosis and management.

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          Analyzing MiRNA-LncRNA Interactions.

          Long noncoding RNAs (lncRNAs) are noncoding transcripts usually longer than 200 nts that have recently emerged as one of the largest and significantly diverse RNA families. The biological role and functions of lncRNAs are still mostly uncharacterized. Their target-mimetic, sponge/decoy function on microRNAs was recently uncovered. miRNAs are a class of noncoding RNA species (~22 nts) that play a central role in posttranscriptional regulation of protein coding genes by mRNA cleavage, direct translational repression and/or mRNA destabilization. LncRNAs can act as miRNA sponges, reducing their regulatory effect on mRNAs. This function introduces an extra layer of complexity in the miRNA-target interaction network. This chapter focuses on the study of miRNA-lncRNA interactions with either in silico or experimentally supported analyses. The proposed methodologies can be appropriately adapted in order to become the backbone of advanced multistep functional miRNA analyses.
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            MicroRNA expressions associated with progression of prostate cancer cells to antiandrogen therapy resistance

            Background Development of resistance to androgen deprivation therapy (ADT) is a major obstacle for the management of advanced prostate cancer. Therapies with androgen receptor (AR) antagonists and androgen withdrawal initially regress tumors but development of compensatory mechanisms including AR bypass signaling leads to re-growth of tumors. MicroRNAs (miRNAs) are small regulatory RNAs that are involved in maintenance of cell homeostasis but are often altered in tumor cells. Results In this study, we determined the association of genome wide miRNA expression (1113 unique miRNAs) with development of resistance to ADT. We used androgen sensitive prostate cancer cells that progressed to ADT and AR antagonist Casodex (CDX) resistance upon androgen withdrawal and treatment with CDX. Validation of expression of a subset of 100 miRNAs led to identification of 43 miRNAs that are significantly altered during progression of cells to treatment resistance. We also show a correlation of altered expression of 10 proteins targeted by some of these miRNAs in these cells. Conclusions We conclude that dynamic alterations in miRNA expression occur early on during androgen deprivation therapy, and androgen receptor blockade. The cumulative effect of these altered miRNA expression profiles is the temporal modulation of multiple signaling pathways promoting survival and acquisition of resistance. These early events are driving the transition to castration resistance and cannot be studied in already developed CRPC cell lines or tissues. Furthermore our results can be used a prognostic marker of cancers with a potential to be resistant to ADT.
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              Functional role of a long non-coding RNA LIFR-AS1/miR-29a/TNFAIP3 axis in colorectal cancer resistance to pohotodynamic therapy

              Colorectal Cancer (CRC) is one of the most common digestive system malignant tumors. Recently, PDT has been used as a first-line treatment for colon cancer; however, limited curative effect was obtained due to resistance of CRC to PDT. During the past decades, accumulating CRC-related long non-coding RNAs (lncRNAs), microRNAs (miRNAs) and mRNAs have been reported to exert diverse functions through various biological processes; their dysregulation might trigger and/or promote the pathological changes. Herein, we performed microarrays analysis to identify dysregulated lncRNAs, miRNAs and mRNAs in PDT-treated HCT116 cells to figure out the lncRNA-miRNA interactions related to the resistance of CRC to PDT treatment, and the downstream mRNA target, as well as the molecular mechanism. We found a total of 1096 lncRNAs dysregulated in PDT-treated CRC HCT116 cells; among them, LIFR-AS1 negatively interacted with miR-29a, one of the dysregulated miRNAs in PDT-treated CRC cells, to affect the resistance of CRC to PDT. LIFR-AS1 knockdown attenuated, whereas miR-29a inhibition enhanced the cellular effect of PDT on HCT116 cell proliferation and apoptosis. Furthermore, among the dysregulated mRNAs, TNFAIP3 was confirmed to be a direct target of miR-29a and exerted a similar effect to LIFR-AS1 on the cellular effects of PDT. In summary, LIFR-AS1 serves as a competitive endogenous RNA (ceRNA) for miR-29a to inhibit its expression and up-regulate downstream target TNFAIP3 expression, finally modulating the resistance of CRC to PDT. We provide an experimental basis for this lncRNA/miRNA/mRNA network being a promising target in CRC resistance to PDT treatment.
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                Author and article information

                Contributors
                arvindnegi2301@gmail.com
                nirajkumarjha2011@gmail.com
                kavindra.kesari@helsinki.fi , kavindra.kesari@aalto.fi
                Journal
                Cell Oncol (Dordr)
                Cell Oncol (Dordr)
                Cellular Oncology (Dordrecht)
                Springer Netherlands (Dordrecht )
                2211-3428
                2211-3436
                28 May 2023
                28 May 2023
                2023
                : 46
                : 4
                : 885-908
                Affiliations
                [1 ]GRID grid.412122.6, ISNI 0000 0004 1808 2016, KIIT School of Biotechnology, , Kalinga Institute of Industrial Technology (KIIT-DU), ; Bhubaneswar, Odisha India
                [2 ]GRID grid.9026.d, ISNI 0000 0001 2287 2617, Present Address: Centre for Structural System Biology, Department of Physics, , University of Hamburg, ; c/o DESY, Building 15, Notkestr. 852267, Hamburg, Germany
                [3 ]GRID grid.462378.c, ISNI 0000 0004 1764 2464, School of Biology, , Indian Institute of Science Education and Research, ; Thiruvananthapuram, India
                [4 ]GRID grid.444644.2, ISNI 0000 0004 1805 0217, Amity Institute of Biotechnology, , Amity University Jharkhand, ; Ranchi, Jharkhand, 834001 India
                [5 ]GRID grid.444415.4, ISNI 0000 0004 1759 0860, School of Health Sciences and Technology (SoHST), , UPES University, ; Dehradun, Uttarakhand India
                [6 ]GRID grid.5373.2, ISNI 0000000108389418, Department of Applied Physics, School of Science, , Aalto University, ; Espoo, 00076 Finland
                [7 ]GRID grid.5373.2, ISNI 0000000108389418, Department of Bioproducts and Biosystems, School of Chemical Engineering, , Aalto University, ; Espoo, 00076 Finland
                [8 ]GRID grid.412552.5, ISNI 0000 0004 1764 278X, Department of Biotechnology, School of Engineering and Technology (SET), , Sharda University, ; Greater Noida, 201310 UP India
                [9 ]GRID grid.449005.c, School of Bioengineering & Biosciences, , Lovely Professional University, ; Phagwara, 144411 India
                [10 ]GRID grid.449906.6, ISNI 0000 0004 4659 5193, Department of Biotechnology, School of Applied & Life Sciences (SALS), , Uttaranchal University, ; Dehradun, 248007 India
                [11 ]GRID grid.7737.4, ISNI 0000 0004 0410 2071, Faculty of Biological and Environmental Sciences, , University of Helsinki, ; Biocentre 3, Helsinki, Finland
                [12 ]GRID grid.13797.3b, ISNI 0000 0001 2235 8415, Pharmacy, , Abo Akademi University, ; Tykistökatu 6A, Turku, Finland
                Author information
                http://orcid.org/0000-0003-3622-9555
                Article
                806
                10.1007/s13402-023-00806-9
                10356678
                37245177
                89325f33-38d7-4d40-a069-511035c25bc0
                © The Author(s) 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 26 March 2023
                Funding
                Funded by: Aalto University
                Categories
                Review
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                © Springer Nature Switzerland AG 2023

                Oncology & Radiotherapy
                microrna,long-noncoding rna,cancer,epithelial-mesenchymal transition,metastasis,angiogenesis,neovascularization,vascular mimicry

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