Ephrin type-A receptor 2-antisense RNA1/2 promote proliferation and migration of MDA-MB-231 cells through EPHA2-dependent Ras signaling pathway mediated by MAPK8/JNK1, MAPK9/JNK2-NFATC2/NFAT1 and JUND
Ephrin type-A receptor 2 (EPHA2) is a receptor tyrosine kinase that is overexpressed in a variety of cancers, including breast cancer. EPHA2 expression may be causally related to tumorigenesis; therefore, it is important to understand how EPHA2 expression is regulated. We previously reported that EP...
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| Published in | Frontiers in molecular biosciences Vol. 11; p. 1402354 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
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| Abstract | Ephrin type-A receptor 2 (EPHA2) is a receptor tyrosine kinase that is overexpressed in a variety of cancers, including breast cancer. EPHA2 expression may be causally related to tumorigenesis; therefore, it is important to understand how
EPHA2
expression is regulated. We previously reported that EPHA2 antisense RNA (EPHA2-AS), a natural antisense transcript, is an important modulator of EPHA2 mRNA levels and hence production of EPHA2 protein. EPHA2-AS encodes two splice variants, EPHA2-AS1 and EPHA2-AS2. The two variants are constitutively expressed in a concordant manner with EPHA2 mRNA in human breast adenocarcinoma cell lines and in patient samples, with the highest levels detected in the basal-like/triple-negative molecular subtype of breast cancer cells. In this study, we investigated the mechanism of EPHA2-AS1/2 in triple-negative breast cancer using MDA-MB-231 cells. We performed RNA-seq transcriptome analyses of MDA-MB-231 cells treated with AHCC
®
, which suppressed expression of EPHA2-AS1/2 and EPHA2 mRNA, and EPHA2-AS1/2-silenced MDA-MB-231 cells. Bioinformatics analyses identified 545 overlapping differentially expressed genes that were significantly up- or down-regulated by these treatments. Subsequent functional enrichment analyses of the overlapping genes in combination with
in vitro
assays indicated that EPHA2-AS1/2 may promote the proliferation and migration of MDA-MB-231 cells through the
EPHA2
-dependent Ras signaling pathways mediated by MAPK8/JNK1, MAPK9/JNK2-NFATC2/NFAT1 (proliferation and migration) and JUND (migration). These results thus suggest that EPHA2-AS1/2 may represent a potential molecular target for triple-negative breast cancer treatment. |
|---|---|
| AbstractList | Ephrin type-A receptor 2 (EPHA2) is a receptor tyrosine kinase that is overexpressed in a variety of cancers, including breast cancer. EPHA2 expression may be causally related to tumorigenesis; therefore, it is important to understand how
EPHA2
expression is regulated. We previously reported that EPHA2 antisense RNA (EPHA2-AS), a natural antisense transcript, is an important modulator of EPHA2 mRNA levels and hence production of EPHA2 protein. EPHA2-AS encodes two splice variants, EPHA2-AS1 and EPHA2-AS2. The two variants are constitutively expressed in a concordant manner with EPHA2 mRNA in human breast adenocarcinoma cell lines and in patient samples, with the highest levels detected in the basal-like/triple-negative molecular subtype of breast cancer cells. In this study, we investigated the mechanism of EPHA2-AS1/2 in triple-negative breast cancer using MDA-MB-231 cells. We performed RNA-seq transcriptome analyses of MDA-MB-231 cells treated with AHCC
®
, which suppressed expression of EPHA2-AS1/2 and EPHA2 mRNA, and EPHA2-AS1/2-silenced MDA-MB-231 cells. Bioinformatics analyses identified 545 overlapping differentially expressed genes that were significantly up- or down-regulated by these treatments. Subsequent functional enrichment analyses of the overlapping genes in combination with
in vitro
assays indicated that EPHA2-AS1/2 may promote the proliferation and migration of MDA-MB-231 cells through the
EPHA2
-dependent Ras signaling pathways mediated by MAPK8/JNK1, MAPK9/JNK2-NFATC2/NFAT1 (proliferation and migration) and JUND (migration). These results thus suggest that EPHA2-AS1/2 may represent a potential molecular target for triple-negative breast cancer treatment. Ephrin type-A receptor 2 (EPHA2) is a receptor tyrosine kinase that is overexpressed in a variety of cancers, including breast cancer. EPHA2 expression may be causally related to tumorigenesis; therefore, it is important to understand how expression is regulated. We previously reported that EPHA2 antisense RNA (EPHA2-AS), a natural antisense transcript, is an important modulator of EPHA2 mRNA levels and hence production of EPHA2 protein. EPHA2-AS encodes two splice variants, EPHA2-AS1 and EPHA2-AS2. The two variants are constitutively expressed in a concordant manner with EPHA2 mRNA in human breast adenocarcinoma cell lines and in patient samples, with the highest levels detected in the basal-like/triple-negative molecular subtype of breast cancer cells. In this study, we investigated the mechanism of EPHA2-AS1/2 in triple-negative breast cancer using MDA-MB-231 cells. We performed RNA-seq transcriptome analyses of MDA-MB-231 cells treated with AHCC , which suppressed expression of EPHA2-AS1/2 and EPHA2 mRNA, and EPHA2-AS1/2-silenced MDA-MB-231 cells. Bioinformatics analyses identified 545 overlapping differentially expressed genes that were significantly up- or down-regulated by these treatments. Subsequent functional enrichment analyses of the overlapping genes in combination with assays indicated that EPHA2-AS1/2 may promote the proliferation and migration of MDA-MB-231 cells through the -dependent Ras signaling pathways mediated by MAPK8/JNK1, MAPK9/JNK2-NFATC2/NFAT1 (proliferation and migration) and JUND (migration). These results thus suggest that EPHA2-AS1/2 may represent a potential molecular target for triple-negative breast cancer treatment. Ephrin type-A receptor 2 (EPHA2) is a receptor tyrosine kinase that is overexpressed in a variety of cancers, including breast cancer. EPHA2 expression may be causally related to tumorigenesis; therefore, it is important to understand how EPHA2 expression is regulated. We previously reported that EPHA2 antisense RNA (EPHA2-AS), a natural antisense transcript, is an important modulator of EPHA2 mRNA levels and hence production of EPHA2 protein. EPHA2-AS encodes two splice variants, EPHA2-AS1 and EPHA2-AS2. The two variants are constitutively expressed in a concordant manner with EPHA2 mRNA in human breast adenocarcinoma cell lines and in patient samples, with the highest levels detected in the basal-like/triple-negative molecular subtype of breast cancer cells. In this study, we investigated the mechanism of EPHA2-AS1/2 in triple-negative breast cancer using MDA-MB-231 cells. We performed RNA-seq transcriptome analyses of MDA-MB-231 cells treated with AHCC®, which suppressed expression of EPHA2-AS1/2 and EPHA2 mRNA, and EPHA2-AS1/2-silenced MDA-MB-231 cells. Bioinformatics analyses identified 545 overlapping differentially expressed genes that were significantly up- or down-regulated by these treatments. Subsequent functional enrichment analyses of the overlapping genes in combination with in vitro assays indicated that EPHA2-AS1/2 may promote the proliferation and migration of MDA-MB-231 cells through the EPHA2-dependent Ras signaling pathways mediated by MAPK8/JNK1, MAPK9/JNK2-NFATC2/NFAT1 (proliferation and migration) and JUND (migration). These results thus suggest that EPHA2-AS1/2 may represent a potential molecular target for triple-negative breast cancer treatment. Ephrin type-A receptor 2 (EPHA2) is a receptor tyrosine kinase that is overexpressed in a variety of cancers, including breast cancer. EPHA2 expression may be causally related to tumorigenesis; therefore, it is important to understand how EPHA2 expression is regulated. We previously reported that EPHA2 antisense RNA (EPHA2-AS), a natural antisense transcript, is an important modulator of EPHA2 mRNA levels and hence production of EPHA2 protein. EPHA2-AS encodes two splice variants, EPHA2-AS1 and EPHA2-AS2. The two variants are constitutively expressed in a concordant manner with EPHA2 mRNA in human breast adenocarcinoma cell lines and in patient samples, with the highest levels detected in the basal-like/triple-negative molecular subtype of breast cancer cells. In this study, we investigated the mechanism of EPHA2-AS1/2 in triple-negative breast cancer using MDA-MB-231 cells. We performed RNA-seq transcriptome analyses of MDA-MB-231 cells treated with AHCC®, which suppressed expression of EPHA2-AS1/2 and EPHA2 mRNA, and EPHA2-AS1/2-silenced MDA-MB-231 cells. Bioinformatics analyses identified 545 overlapping differentially expressed genes that were significantly up- or down-regulated by these treatments. Subsequent functional enrichment analyses of the overlapping genes in combination with in vitro assays indicated that EPHA2-AS1/2 may promote the proliferation and migration of MDA-MB-231 cells through the EPHA2-dependent Ras signaling pathways mediated by MAPK8/JNK1, MAPK9/JNK2-NFATC2/NFAT1 (proliferation and migration) and JUND (migration). These results thus suggest that EPHA2-AS1/2 may represent a potential molecular target for triple-negative breast cancer treatment.Ephrin type-A receptor 2 (EPHA2) is a receptor tyrosine kinase that is overexpressed in a variety of cancers, including breast cancer. EPHA2 expression may be causally related to tumorigenesis; therefore, it is important to understand how EPHA2 expression is regulated. We previously reported that EPHA2 antisense RNA (EPHA2-AS), a natural antisense transcript, is an important modulator of EPHA2 mRNA levels and hence production of EPHA2 protein. EPHA2-AS encodes two splice variants, EPHA2-AS1 and EPHA2-AS2. The two variants are constitutively expressed in a concordant manner with EPHA2 mRNA in human breast adenocarcinoma cell lines and in patient samples, with the highest levels detected in the basal-like/triple-negative molecular subtype of breast cancer cells. In this study, we investigated the mechanism of EPHA2-AS1/2 in triple-negative breast cancer using MDA-MB-231 cells. We performed RNA-seq transcriptome analyses of MDA-MB-231 cells treated with AHCC®, which suppressed expression of EPHA2-AS1/2 and EPHA2 mRNA, and EPHA2-AS1/2-silenced MDA-MB-231 cells. Bioinformatics analyses identified 545 overlapping differentially expressed genes that were significantly up- or down-regulated by these treatments. Subsequent functional enrichment analyses of the overlapping genes in combination with in vitro assays indicated that EPHA2-AS1/2 may promote the proliferation and migration of MDA-MB-231 cells through the EPHA2-dependent Ras signaling pathways mediated by MAPK8/JNK1, MAPK9/JNK2-NFATC2/NFAT1 (proliferation and migration) and JUND (migration). These results thus suggest that EPHA2-AS1/2 may represent a potential molecular target for triple-negative breast cancer treatment. |
| Author | Sakamoto, Ryou Nishizawa, Mikio Odaka, Tokifumi Okuma, Kazu Kimura, Tominori Kumagai, Kazuhiro |
| AuthorAffiliation | 2 Department of Microbiology , Faculty of Medicine , Kansai Medical University , Hirakata , Japan 3 Medical Chemistry Laboratory , Department of Biomedical Sciences , College of Life Sciences , Ritsumeikan University , Kusatsu , Japan 1 Laboratory of Microbiology and Cell Biology , Department of Pharmacy , College of Pharmaceutical Sciences , Ritsumeikan University , Kusatsu , Japan |
| AuthorAffiliation_xml | – name: 2 Department of Microbiology , Faculty of Medicine , Kansai Medical University , Hirakata , Japan – name: 3 Medical Chemistry Laboratory , Department of Biomedical Sciences , College of Life Sciences , Ritsumeikan University , Kusatsu , Japan – name: 1 Laboratory of Microbiology and Cell Biology , Department of Pharmacy , College of Pharmaceutical Sciences , Ritsumeikan University , Kusatsu , Japan |
| Author_xml | – sequence: 1 givenname: Tokifumi surname: Odaka fullname: Odaka, Tokifumi – sequence: 2 givenname: Ryou surname: Sakamoto fullname: Sakamoto, Ryou – sequence: 3 givenname: Kazuhiro surname: Kumagai fullname: Kumagai, Kazuhiro – sequence: 4 givenname: Kazu surname: Okuma fullname: Okuma, Kazu – sequence: 5 givenname: Mikio surname: Nishizawa fullname: Nishizawa, Mikio – sequence: 6 givenname: Tominori surname: Kimura fullname: Kimura, Tominori |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38855323$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1016_j_heliyon_2025_e42293 |
| Cites_doi | 10.1016/j.devcel.2004.09.006 10.1007/s11033-018-4190-z 10.1158/1541-7786.Mcr-06-0321 10.18632/oncotarget.26047 10.1038/nrm1662 10.1002/jemt.10177 10.1038/sj.emboj.7600476 10.1159/000333833 10.1172/jci33154 10.1038/onc.2017.170 10.1038/nrc904 10.1096/fj.05-4038fje 10.1002/cncr.22254 10.1038/nrm856 10.1038/sj.onc.1207247 10.1007/s00262-005-0111-9 10.1128/mmbr.00043-14 10.2310/7200.2008.0022 10.1093/nar/gkac194 10.1016/s0168-8278(02)00091-0 10.1038/nrclinonc.2015.73 10.3389/fmolb.2020.605623 10.1186/s13058-020-01296-5 10.1016/j.bbcan.2014.07.009 10.1016/j.biochi.2020.10.002 10.1101/cshperspect.a000034 10.1016/j.ccr.2005.07.005 10.3892/mmr.2020.11384 10.1073/pnas.0712168105 10.1186/s13045-020-00944-9 10.1007/s00018-012-1216-x 10.7554/eLife.40474 10.3390/biomedicines11020315 10.1007/s00018-015-1875-5 10.1158/0008-5472.Can-05-0530 10.1371/journal.pgen.1007802 10.1093/emboj/18.23.6694 |
| ContentType | Journal Article |
| Copyright | Copyright © 2024 Odaka, Sakamoto, Kumagai, Okuma, Nishizawa and Kimura. Copyright © 2024 Odaka, Sakamoto, Kumagai, Okuma, Nishizawa and Kimura. 2024 Odaka, Sakamoto, Kumagai, Okuma, Nishizawa and Kimura |
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| Keywords | MAPK8/JNK1 JUND proliferation MAPK9/JNK2 NFATC2/NFAT1 migration EPHA2-AS1/2 EPHA2 |
| Language | English |
| License | Copyright © 2024 Odaka, Sakamoto, Kumagai, Okuma, Nishizawa and Kimura. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Reviewed by: Anindhya Sundar Das, Brown University, United States Tianqi Li, University of Florida, United States These authors have contributed equally to this work Present address: Ryou Sakamoto, Department of Infection Control, Kansai Medical University Hospital, Hirakata, Japan Kazuhiro Kumagai, Department of Immunology, Nagoya University Graduate School of Medicine, Nagoya, Japan Edited by: Upendar Rao Golla, The Pennsylvania State University, United States |
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| References | Pasquale (B23) 2005; 6 Sherman (B29) 2022; 50 Larsen (B13) 2007; 5 Brantley-Sieders (B3) 2008; 118 Gao (B6) 2006; 55 Mach (B14) 2008; 6 Landen (B12) 2005; 65 Salic (B28) 2008; 105 Zago (B39) 2018; 7 Zardavas (B35) 2015; 12 Song (B31) 2017; 36 Dan (B4) 2020; 7 Duxbury (B5) 2004; 23 Zelinski (B37) 2001; 61 Kimura (B10) 2015; 72 Ibrahim (B7) 2018; 9 Qin (B27) 2014; 1846 Shukla (B30) 2018; 45 Oeckinghaus (B20) 2009; 1 Kimura (B9) 2013; 70 Matsui (B16) 2002; 37 Jadaliha (B8) 2018; 14 Zeke (B36) 2016; 80 Xiao (B33) 2020; 13 Pomerantz (B26) 1999; 18 Essers (B38) 2004; 23 Kullander (B11) 2002; 3 Poliakov (B25) 2004; 7 Arora (B1) 2023; 11 Mstsui (B17) 2011; 47 Macrae (B15) 2005; 8 Nakamoto (B18) 2002; 59 Okuyama (B21) 2020; 179 Wei (B32) 2020; 22 Pelengaris (B24) 2002; 2 Yin (B34) 2020; 22 Brantley-Sieders (B2) 2005; 19 Nasreen (B19) 2006; 107 |
| References_xml | – volume: 7 start-page: 465 year: 2004 ident: B25 article-title: Diverse roles of eph receptors and ephrins in the regulation of cell migration and tissue assembly publication-title: Dev. Cell doi: 10.1016/j.devcel.2004.09.006 – volume: 45 start-page: 533 year: 2018 ident: B30 article-title: Level of hydrogen peroxide affects expression and sub-cellular localization of Pax6 publication-title: Mol. Biol. Rep. doi: 10.1007/s11033-018-4190-z – volume: 5 start-page: 283 year: 2007 ident: B13 article-title: Activation of the EGFR gene target EphA2 inhibits epidermal growth factor-induced cancer cell motility publication-title: Mol. Cancer Res. doi: 10.1158/1541-7786.Mcr-06-0321 – volume: 9 start-page: 34259 year: 2018 ident: B7 article-title: The role of AP-1 in self-sufficient proliferation and migration of cancer cells and its potential impact on an autocrine/paracrine loop publication-title: Oncotarget doi: 10.18632/oncotarget.26047 – volume: 6 start-page: 462 year: 2005 ident: B23 article-title: Eph receptor signalling casts a wide net on cell behaviour publication-title: Nat. Rev. Mol. Cell Biol. doi: 10.1038/nrm1662 – volume: 59 start-page: 58 year: 2002 ident: B18 article-title: Diverse roles for the Eph family of receptor tyrosine kinases in carcinogenesis publication-title: Microsc. Res. Tech. doi: 10.1002/jemt.10177 – volume: 23 start-page: 4802 year: 2004 ident: B38 article-title: FOXO transcription factor activation by oxidative stress mediated by the small GTPase Ral and JNK publication-title: Embo. j. doi: 10.1038/sj.emboj.7600476 – volume: 61 start-page: 2301 year: 2001 ident: B37 article-title: EphA2 overexpression causes tumorigenesis of mammary epithelial cells publication-title: Cancer Res. – volume: 47 start-page: 274 year: 2011 ident: B17 article-title: Active hexose correlated compound inhibits the expression of proinflammatory biomarker iNOS in hepatocytes publication-title: Eur. Surg. Res. doi: 10.1159/000333833 – volume: 118 start-page: 64 year: 2008 ident: B3 article-title: The receptor tyrosine kinase EphA2 promotes mammary adenocarcinoma tumorigenesis and metastatic progression in mice by amplifying ErbB2 signaling publication-title: J. Clin. Invest. doi: 10.1172/jci33154 – volume: 36 start-page: 5620 year: 2017 ident: B31 article-title: Targeting EphA2 impairs cell cycle progression and growth of basal-like/triple-negative breast cancers publication-title: Oncogene doi: 10.1038/onc.2017.170 – volume: 2 start-page: 764 year: 2002 ident: B24 article-title: c-MYC: more than just a matter of life and death publication-title: Nat. Rev. Cancer doi: 10.1038/nrc904 – volume: 19 start-page: 1884 year: 2005 ident: B2 article-title: Impaired tumor microenvironment in EphA2-deficient mice inhibits tumor angiogenesis and metastatic progression publication-title: Faseb J. doi: 10.1096/fj.05-4038fje – volume: 107 start-page: 2425 year: 2006 ident: B19 article-title: Silencing the receptor EphA2 suppresses the growth and haptotaxis of malignant mesothelioma cells publication-title: Cancer doi: 10.1002/cncr.22254 – volume: 3 start-page: 475 year: 2002 ident: B11 article-title: Mechanisms and functions of Eph and ephrin signalling publication-title: Nat. Rev. Mol. Cell Biol. doi: 10.1038/nrm856 – volume: 23 start-page: 1448 year: 2004 ident: B5 article-title: EphA2: a determinant of malignant cellular behavior and a potential therapeutic target in pancreatic adenocarcinoma publication-title: Oncogene doi: 10.1038/sj.onc.1207247 – volume: 55 start-page: 1258 year: 2006 ident: B6 article-title: Active hexose correlated compound enhances tumor surveillance through regulating both innate and adaptive immune responses publication-title: Cancer Immunol. Immunother. doi: 10.1007/s00262-005-0111-9 – volume: 80 start-page: 793 year: 2016 ident: B36 article-title: JNK signaling: regulation and functions based on complex protein-protein partnerships publication-title: Microbiol. Mol. Biol. Rev. doi: 10.1128/mmbr.00043-14 – volume: 6 start-page: 105 year: 2008 ident: B14 article-title: Evaluation of active hexose correlated compound hepatic metabolism and potential for drug interactions with chemotherapy agents publication-title: J. Soc. Integr. Oncol. doi: 10.2310/7200.2008.0022 – volume: 50 start-page: W216 year: 2022 ident: B29 article-title: DAVID: a web server for functional enrichment analysis and functional annotation of gene lists (2021 update) publication-title: Nucleic Acids Res. doi: 10.1093/nar/gkac194 – volume: 37 start-page: 78 year: 2002 ident: B16 article-title: Improved prognosis of postoperative hepatocellular carcinoma patients when treated with functional foods: a prospective cohort study publication-title: J. Hepatol. doi: 10.1016/s0168-8278(02)00091-0 – volume: 12 start-page: 381 year: 2015 ident: B35 article-title: Clinical management of breast cancer heterogeneity publication-title: Nat. Rev. Clin. Oncol. doi: 10.1038/nrclinonc.2015.73 – volume: 7 start-page: 605623 year: 2020 ident: B4 article-title: Long non-coding RNA BTG3-7:1 and JUND Co-regulate C21ORF91 to promote triple-negative breast cancer progress publication-title: Front. Mol. Biosci. doi: 10.3389/fmolb.2020.605623 – volume: 22 start-page: 61 year: 2020 ident: B34 article-title: Triple-negative breast cancer molecular subtyping and treatment progress publication-title: Breast Cancer Res. doi: 10.1186/s13058-020-01296-5 – volume: 1846 start-page: 297 year: 2014 ident: B27 article-title: NFAT as cancer target: mission possible? publication-title: Biochim. Biophys. Acta doi: 10.1016/j.bbcan.2014.07.009 – volume: 179 start-page: 169 year: 2020 ident: B21 article-title: EPHA2 antisense RNA modulates EPHA2 mRNA levels in basal-like/triple-negative breast cancer cells publication-title: Biochimie doi: 10.1016/j.biochi.2020.10.002 – volume: 1 start-page: a000034 year: 2009 ident: B20 article-title: The NF-kappaB family of transcription factors and its regulation publication-title: Cold Spring Harb. Perspect. Biol. doi: 10.1101/cshperspect.a000034 – volume: 8 start-page: 111 year: 2005 ident: B15 article-title: A conditional feedback loop regulates Ras activity through EphA2 publication-title: Cancer Cell doi: 10.1016/j.ccr.2005.07.005 – volume: 22 start-page: 2941 year: 2020 ident: B32 article-title: EphA2-enriched exosomes promote cell migration and are a potential diagnostic serum marker in pancreatic cancer publication-title: Mol. Med. Rep. doi: 10.3892/mmr.2020.11384 – volume: 105 start-page: 2415 year: 2008 ident: B28 article-title: A chemical method for fast and sensitive detection of DNA synthesis in vivo publication-title: Proc. Natl. Acad. Sci. U. S. A. doi: 10.1073/pnas.0712168105 – volume: 13 start-page: 114 year: 2020 ident: B33 article-title: Targeting EphA2 in cancer publication-title: J. Hematol. Oncol. doi: 10.1186/s13045-020-00944-9 – volume: 70 start-page: 1451 year: 2013 ident: B9 article-title: Stabilization of human interferon-α1 mRNA by its antisense RNA publication-title: Cell Mol. Life Sci. doi: 10.1007/s00018-012-1216-x – volume: 7 year: 2018 ident: B39 article-title: RalB directly triggers invasion downstream Ras by mobilizing the Wave complex publication-title: Elife. doi: 10.7554/eLife.40474 – volume: 11 start-page: 315 year: 2023 ident: B1 article-title: Eph receptors in cancer publication-title: Biomedicines doi: 10.3390/biomedicines11020315 – volume: 72 start-page: 2749 year: 2015 ident: B10 article-title: Interferon-alpha competing endogenous RNA network antagonizes microRNA-1270 publication-title: Cell Mol. Life Sci. doi: 10.1007/s00018-015-1875-5 – volume: 65 start-page: 6910 year: 2005 ident: B12 article-title: Therapeutic EphA2 gene targeting in vivo using neutral liposomal small interfering RNA delivery publication-title: Cancer Res. doi: 10.1158/0008-5472.Can-05-0530 – volume: 14 start-page: e1007802 year: 2018 ident: B8 article-title: A natural antisense lncRNA controls breast cancer progression by promoting tumor suppressor gene mRNA stability publication-title: PLoS Genet. doi: 10.1371/journal.pgen.1007802 – volume: 18 start-page: 6694 year: 1999 ident: B26 article-title: NF-kappaB activation by a signaling complex containing TRAF2, TANK and TBK1, a novel IKK-related kinase publication-title: Embo J. doi: 10.1093/emboj/18.23.6694 |
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| Snippet | Ephrin type-A receptor 2 (EPHA2) is a receptor tyrosine kinase that is overexpressed in a variety of cancers, including breast cancer. EPHA2 expression may be... |
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| SubjectTerms | EPHA2 EPHA2-AS1/2 JUND MAPK8/JNK1 MAPK9/JNK2 Molecular Biosciences NFATC2/NFAT1 |
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| Title | Ephrin type-A receptor 2-antisense RNA1/2 promote proliferation and migration of MDA-MB-231 cells through EPHA2-dependent Ras signaling pathway mediated by MAPK8/JNK1, MAPK9/JNK2-NFATC2/NFAT1 and JUND |
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