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LncRNA LOC285194 modulates gastric carcinoma progression through activating Wnt/β‐catenin signaling pathway

Emerging evidences have revealed long noncoding RNAs (lncRNAs’) critical roles in diverse human carcinoma. Among these cancers, lncRNA LOC285194 has been extensively investigated in several types of carcinomas in the recent years. Nevertheless, the biological function, clinical relevance, and the in...

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Autores principales: Zhong, Bingzheng, Wang, Qiang, He, Jiali, Xiong, Yi, Cao, Jie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7064030/
https://www.ncbi.nlm.nih.gov/pubmed/31991056
http://dx.doi.org/10.1002/cam4.2844
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author Zhong, Bingzheng
Wang, Qiang
He, Jiali
Xiong, Yi
Cao, Jie
author_facet Zhong, Bingzheng
Wang, Qiang
He, Jiali
Xiong, Yi
Cao, Jie
author_sort Zhong, Bingzheng
collection PubMed
description Emerging evidences have revealed long noncoding RNAs (lncRNAs’) critical roles in diverse human carcinoma. Among these cancers, lncRNA LOC285194 has been extensively investigated in several types of carcinomas in the recent years. Nevertheless, the biological function, clinical relevance, and the influence of LOC285194 in gastric cancer (GC) are not fully understood. The present study aims to explore the biological function of LOC285194 in the progression and development of GC. First, LOC285194 expressions were detected in GC tissues and cell lines. The functional role of LOC285194 in GC was evaluated both in vitro and in vivo. Our data found that LOC285194 was lowly expressed both in human GC tissues and GC cell lines compared with corresponding normal controls. Moreover, LOC285194 was mitigated by transfection with LV‐LOC285194 in both HGC‐27 and MKN45 cell lines. Silencing of LOC285194 remarkably induced GC cell livability and cell proliferation. On the contrary, the LOC285194 overexpression suppressed MKN45 and HGC‐27 cell proliferation and promoted cell apoptosis. Additionally, silencing of LOC285194 increased the ability of colony formation, cell migration, and invasive capacities, together with blocking the apoptotic rates of GC cells. Correspondently, LOC285194 overexpression exerted the opposite effects. Mechanistically, silencing of LOC285194 promoted GC progression via inducing Wnt signaling activity. Moreover, in vivo xenografts nude mice model results showed that LOC285194 inhibited GC progression through targeting Wnt signaling. Taken together, LOC285194 is associated with GC progression by regulating the Wnt signaling transduction, potentiating LOC285194's promising role as a novel treatment biomarker in GC.
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spelling pubmed-70640302020-03-16 LncRNA LOC285194 modulates gastric carcinoma progression through activating Wnt/β‐catenin signaling pathway Zhong, Bingzheng Wang, Qiang He, Jiali Xiong, Yi Cao, Jie Cancer Med Cancer Biology Emerging evidences have revealed long noncoding RNAs (lncRNAs’) critical roles in diverse human carcinoma. Among these cancers, lncRNA LOC285194 has been extensively investigated in several types of carcinomas in the recent years. Nevertheless, the biological function, clinical relevance, and the influence of LOC285194 in gastric cancer (GC) are not fully understood. The present study aims to explore the biological function of LOC285194 in the progression and development of GC. First, LOC285194 expressions were detected in GC tissues and cell lines. The functional role of LOC285194 in GC was evaluated both in vitro and in vivo. Our data found that LOC285194 was lowly expressed both in human GC tissues and GC cell lines compared with corresponding normal controls. Moreover, LOC285194 was mitigated by transfection with LV‐LOC285194 in both HGC‐27 and MKN45 cell lines. Silencing of LOC285194 remarkably induced GC cell livability and cell proliferation. On the contrary, the LOC285194 overexpression suppressed MKN45 and HGC‐27 cell proliferation and promoted cell apoptosis. Additionally, silencing of LOC285194 increased the ability of colony formation, cell migration, and invasive capacities, together with blocking the apoptotic rates of GC cells. Correspondently, LOC285194 overexpression exerted the opposite effects. Mechanistically, silencing of LOC285194 promoted GC progression via inducing Wnt signaling activity. Moreover, in vivo xenografts nude mice model results showed that LOC285194 inhibited GC progression through targeting Wnt signaling. Taken together, LOC285194 is associated with GC progression by regulating the Wnt signaling transduction, potentiating LOC285194's promising role as a novel treatment biomarker in GC. John Wiley and Sons Inc. 2020-01-28 /pmc/articles/PMC7064030/ /pubmed/31991056 http://dx.doi.org/10.1002/cam4.2844 Text en © 2020 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. 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.
spellingShingle Cancer Biology
Zhong, Bingzheng
Wang, Qiang
He, Jiali
Xiong, Yi
Cao, Jie
LncRNA LOC285194 modulates gastric carcinoma progression through activating Wnt/β‐catenin signaling pathway
title LncRNA LOC285194 modulates gastric carcinoma progression through activating Wnt/β‐catenin signaling pathway
title_full LncRNA LOC285194 modulates gastric carcinoma progression through activating Wnt/β‐catenin signaling pathway
title_fullStr LncRNA LOC285194 modulates gastric carcinoma progression through activating Wnt/β‐catenin signaling pathway
title_full_unstemmed LncRNA LOC285194 modulates gastric carcinoma progression through activating Wnt/β‐catenin signaling pathway
title_short LncRNA LOC285194 modulates gastric carcinoma progression through activating Wnt/β‐catenin signaling pathway
title_sort lncrna loc285194 modulates gastric carcinoma progression through activating wnt/β‐catenin signaling pathway
topic Cancer Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7064030/
https://www.ncbi.nlm.nih.gov/pubmed/31991056
http://dx.doi.org/10.1002/cam4.2844
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