LncRNA UCA1 promotes vasculogenic mimicry by targeting miR-1-3p in gastric cancer

Abstract Long noncoding RNA urothelial carcinoma-associated 1 (UCA1) has been implicated in several tumors. UCA1 promotes cell proliferation, migration, and invasion of gastric cancer (GC) cells, but the molecular mechanism has not been fully elucidated. This study revealed the oncogenic effects of...

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Veröffentlicht in:Carcinogenesis (New York) 2024-09, Vol.45 (9), p.658-672
Hauptverfasser: Lu, Yida, Yang, Bo, Shen, Aolin, Yu, Kexun, Ma, MengDi, Li, Yongxiang, Wang, Huizhen
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container_issue 9
container_start_page 658
container_title Carcinogenesis (New York)
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creator Lu, Yida
Yang, Bo
Shen, Aolin
Yu, Kexun
Ma, MengDi
Li, Yongxiang
Wang, Huizhen
description Abstract Long noncoding RNA urothelial carcinoma-associated 1 (UCA1) has been implicated in several tumors. UCA1 promotes cell proliferation, migration, and invasion of gastric cancer (GC) cells, but the molecular mechanism has not been fully elucidated. This study revealed the oncogenic effects of UCA1 on cell growth and invasion. Furthermore, UCA1 expression was significantly correlated with the overall survival of GC patients, and the clinicopathological indicators, including tumor size, depth of invasion, lymph node metastasis, and TNM stage. Additionally, miR-1-3p was identified as a downstream target of UCA1, which was negatively regulated by UCA1. MiR-1-3p inhibited cell proliferation and vasculogenic mimicry (VM), and induced cell apoptosis by upregulating BAX, BAD, and tumor suppressor TP53 expression levels. Moreover, miR-1-3p almost completely reversed the oncogenic effect caused by UCA1, including cell growth, migration, and VM formation. This study also confirmed that UCA1 promoted tumor growth in vivo. In this study, we also revealed the correlation between UCA1 and VM formation, which is potentially crucial for tumor metastasis. Meanwhile, its downstream target miR-1-3p inhibited VM formation in GC cells. In summary, these findings indicate that the UCA1/miR-1-3p axis is a potential target for GC treatment. Graphical Abstract Graphical Abstract
doi_str_mv 10.1093/carcin/bgae031
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UCA1 promotes cell proliferation, migration, and invasion of gastric cancer (GC) cells, but the molecular mechanism has not been fully elucidated. This study revealed the oncogenic effects of UCA1 on cell growth and invasion. Furthermore, UCA1 expression was significantly correlated with the overall survival of GC patients, and the clinicopathological indicators, including tumor size, depth of invasion, lymph node metastasis, and TNM stage. Additionally, miR-1-3p was identified as a downstream target of UCA1, which was negatively regulated by UCA1. MiR-1-3p inhibited cell proliferation and vasculogenic mimicry (VM), and induced cell apoptosis by upregulating BAX, BAD, and tumor suppressor TP53 expression levels. Moreover, miR-1-3p almost completely reversed the oncogenic effect caused by UCA1, including cell growth, migration, and VM formation. This study also confirmed that UCA1 promoted tumor growth in vivo. In this study, we also revealed the correlation between UCA1 and VM formation, which is potentially crucial for tumor metastasis. Meanwhile, its downstream target miR-1-3p inhibited VM formation in GC cells. In summary, these findings indicate that the UCA1/miR-1-3p axis is a potential target for GC treatment. Graphical Abstract Graphical Abstract</description><identifier>ISSN: 0143-3334</identifier><identifier>ISSN: 1460-2180</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/bgae031</identifier><identifier>PMID: 38742453</identifier><language>eng</language><publisher>UK: Oxford University Press</publisher><subject>Animals ; Apoptosis - genetics ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Cell Line, Tumor ; Cell Movement - genetics ; Cell Proliferation - genetics ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNAs - genetics ; Middle Aged ; Neovascularization, Pathologic - genetics ; Neovascularization, Pathologic - pathology ; Prognosis ; RNA, Long Noncoding - genetics ; Stomach Neoplasms - genetics ; Stomach Neoplasms - pathology ; Xenograft Model Antitumor Assays</subject><ispartof>Carcinogenesis (New York), 2024-09, Vol.45 (9), p.658-672</ispartof><rights>The Author(s) 2024. Published by Oxford University Press. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com. 2024</rights><rights>The Author(s) 2024. Published by Oxford University Press. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. 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UCA1 promotes cell proliferation, migration, and invasion of gastric cancer (GC) cells, but the molecular mechanism has not been fully elucidated. This study revealed the oncogenic effects of UCA1 on cell growth and invasion. Furthermore, UCA1 expression was significantly correlated with the overall survival of GC patients, and the clinicopathological indicators, including tumor size, depth of invasion, lymph node metastasis, and TNM stage. Additionally, miR-1-3p was identified as a downstream target of UCA1, which was negatively regulated by UCA1. MiR-1-3p inhibited cell proliferation and vasculogenic mimicry (VM), and induced cell apoptosis by upregulating BAX, BAD, and tumor suppressor TP53 expression levels. Moreover, miR-1-3p almost completely reversed the oncogenic effect caused by UCA1, including cell growth, migration, and VM formation. This study also confirmed that UCA1 promoted tumor growth in vivo. In this study, we also revealed the correlation between UCA1 and VM formation, which is potentially crucial for tumor metastasis. Meanwhile, its downstream target miR-1-3p inhibited VM formation in GC cells. In summary, these findings indicate that the UCA1/miR-1-3p axis is a potential target for GC treatment. 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In this study, we also revealed the correlation between UCA1 and VM formation, which is potentially crucial for tumor metastasis. Meanwhile, its downstream target miR-1-3p inhibited VM formation in GC cells. In summary, these findings indicate that the UCA1/miR-1-3p axis is a potential target for GC treatment. Graphical Abstract Graphical Abstract</abstract><cop>UK</cop><pub>Oxford University Press</pub><pmid>38742453</pmid><doi>10.1093/carcin/bgae031</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0001-7183-9485</orcidid></addata></record>
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source MEDLINE; Oxford University Press Journals All Titles (1996-Current)
subjects Animals
Apoptosis - genetics
Biomarkers, Tumor - genetics
Biomarkers, Tumor - metabolism
Cell Line, Tumor
Cell Movement - genetics
Cell Proliferation - genetics
Female
Gene Expression Regulation, Neoplastic
Humans
Male
Mice
Mice, Inbred BALB C
Mice, Nude
MicroRNAs - genetics
Middle Aged
Neovascularization, Pathologic - genetics
Neovascularization, Pathologic - pathology
Prognosis
RNA, Long Noncoding - genetics
Stomach Neoplasms - genetics
Stomach Neoplasms - pathology
Xenograft Model Antitumor Assays
title LncRNA UCA1 promotes vasculogenic mimicry by targeting miR-1-3p in gastric cancer
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