PELI3 mediates pro-tumor actions of down-regulated miR-365a-5p in non-small cell lung cancer

Abstract Background: To analyze the relative expression of PELI3 and its mechanistic involvement in the non-small cell lung cancer (NSCLC). Methods: PELI3 expression in NSCLC tissue samples was determined by the immunohistochemistry. The transcripts abundance of PELI3 was measured with real-time P...

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Autores principales: He,Yuzheng, Shi,Yantao, Liu,Ruilin, Wang,Zhichao, Wang,Baohua, Li,Shujun, Zhang,Helin
Lenguaje:English
Publicado: Sociedad de Biología de Chile 2019
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Acceso en línea:http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602019000100222
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spelling oai:scielo:S0716-976020190001002222019-10-10PELI3 mediates pro-tumor actions of down-regulated miR-365a-5p in non-small cell lung cancerHe,YuzhengShi,YantaoLiu,RuilinWang,ZhichaoWang,BaohuaLi,ShujunZhang,Helin PELI3 miR-365a-5p Non-small cell lung cancer Cell viability Abstract Background: To analyze the relative expression of PELI3 and its mechanistic involvement in the non-small cell lung cancer (NSCLC). Methods: PELI3 expression in NSCLC tissue samples was determined by the immunohistochemistry. The transcripts abundance of PELI3 was measured with real-time PCR. The protein intensity was analyzed by western blot. The overall survival in respect to PELI3 or miR-365a-5p expression was plotted by the Kaplan–Meier's analysis. Cell growth was determined by colony formation assay. Cell viability was measured by MTT assay. The migration and invasion were evaluated by wound healing and transwell assay respectively. The regulatory effect of miR-365a-5p on PELI3 was interrogated with luciferase reporter assay. The direct binding between miR-365a-5p and PELI3 was analyzed by pulldown assay. Results: PELI3 was aberrantly up-regulated in NSCLC both in vivo and in vitro. High level of PELI3 associated with poor prognosis. PELI3-deficiency significantly inhibited cell viability, colony formation, migration and invasion. We further identified that miR-365a-5p negatively regulated PELI3 in this disease. Ectopic expression of miR-365a-5p in both A549 and H1299 phenocopied PELI3-deficiency. Meanwhile, PELI3-silencing significantly abolished the pro-tumoral effect elicited by miR-365a-5p inhibition. Conclusion: Our results highlighted the importance of dysregulated miR-365a-5p-PELI3 signaling axis in NSCLC.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.52 20192019-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602019000100222en10.1186/s40659-019-0230-y
institution Scielo Chile
collection Scielo Chile
language English
topic PELI3
miR-365a-5p
Non-small cell lung cancer
Cell viability
spellingShingle PELI3
miR-365a-5p
Non-small cell lung cancer
Cell viability
He,Yuzheng
Shi,Yantao
Liu,Ruilin
Wang,Zhichao
Wang,Baohua
Li,Shujun
Zhang,Helin
PELI3 mediates pro-tumor actions of down-regulated miR-365a-5p in non-small cell lung cancer
description Abstract Background: To analyze the relative expression of PELI3 and its mechanistic involvement in the non-small cell lung cancer (NSCLC). Methods: PELI3 expression in NSCLC tissue samples was determined by the immunohistochemistry. The transcripts abundance of PELI3 was measured with real-time PCR. The protein intensity was analyzed by western blot. The overall survival in respect to PELI3 or miR-365a-5p expression was plotted by the Kaplan–Meier's analysis. Cell growth was determined by colony formation assay. Cell viability was measured by MTT assay. The migration and invasion were evaluated by wound healing and transwell assay respectively. The regulatory effect of miR-365a-5p on PELI3 was interrogated with luciferase reporter assay. The direct binding between miR-365a-5p and PELI3 was analyzed by pulldown assay. Results: PELI3 was aberrantly up-regulated in NSCLC both in vivo and in vitro. High level of PELI3 associated with poor prognosis. PELI3-deficiency significantly inhibited cell viability, colony formation, migration and invasion. We further identified that miR-365a-5p negatively regulated PELI3 in this disease. Ectopic expression of miR-365a-5p in both A549 and H1299 phenocopied PELI3-deficiency. Meanwhile, PELI3-silencing significantly abolished the pro-tumoral effect elicited by miR-365a-5p inhibition. Conclusion: Our results highlighted the importance of dysregulated miR-365a-5p-PELI3 signaling axis in NSCLC.
author He,Yuzheng
Shi,Yantao
Liu,Ruilin
Wang,Zhichao
Wang,Baohua
Li,Shujun
Zhang,Helin
author_facet He,Yuzheng
Shi,Yantao
Liu,Ruilin
Wang,Zhichao
Wang,Baohua
Li,Shujun
Zhang,Helin
author_sort He,Yuzheng
title PELI3 mediates pro-tumor actions of down-regulated miR-365a-5p in non-small cell lung cancer
title_short PELI3 mediates pro-tumor actions of down-regulated miR-365a-5p in non-small cell lung cancer
title_full PELI3 mediates pro-tumor actions of down-regulated miR-365a-5p in non-small cell lung cancer
title_fullStr PELI3 mediates pro-tumor actions of down-regulated miR-365a-5p in non-small cell lung cancer
title_full_unstemmed PELI3 mediates pro-tumor actions of down-regulated miR-365a-5p in non-small cell lung cancer
title_sort peli3 mediates pro-tumor actions of down-regulated mir-365a-5p in non-small cell lung cancer
publisher Sociedad de Biología de Chile
publishDate 2019
url http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602019000100222
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