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A preliminary study: is fibulin 1 a friend or an enemy that needs to be silenced with siRNAs for mesothelioma?

INTRODUCTION: The impaired balance between cell proliferation and cell death, followed the inability to receive the death signals, cells push towards the neoplasia pathway. Fibulin 1 (FBLN1) plays a role as a co-factor in the mechanism of action of a protease such as a disintegrin and metalloprotein...

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Autores principales: Aksoy, Asude, Tektemur, Ahmet, Melek, Elif, Kayfeci, Mustafa, Uslu, Muhammed F., Cosar, Ugurcan, Onalan, Ebru
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7836276/
https://www.ncbi.nlm.nih.gov/pubmed/33531871
http://dx.doi.org/10.5114/wo.2020.102826
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author Aksoy, Asude
Tektemur, Ahmet
Melek, Elif
Kayfeci, Mustafa
Uslu, Muhammed F.
Cosar, Ugurcan
Onalan, Ebru
author_facet Aksoy, Asude
Tektemur, Ahmet
Melek, Elif
Kayfeci, Mustafa
Uslu, Muhammed F.
Cosar, Ugurcan
Onalan, Ebru
author_sort Aksoy, Asude
collection PubMed
description INTRODUCTION: The impaired balance between cell proliferation and cell death, followed the inability to receive the death signals, cells push towards the neoplasia pathway. Fibulin 1 (FBLN1) plays a role as a co-factor in the mechanism of action of a protease such as a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS-1), which has important roles in angiogenesis, can also act as both tumor suppressor gene (TSG) and an oncogene in the main constituent of the extra-cellular matrix. This preliminary study has investigated the effects of silencing FBLN1 with siRNA on autophagy, proliferation, apoptosis pathways in the MSM cell line. MATERIAL AND METHODS: It was transfected siRNA specific to FBLN1 incubated MSM SPC212 cells, and compared with negative control siRNAs by a real-time polymerase chain reaction. It was determined apoptosis, proliferation, autophagy-related genes in mRNA levels. RESULTS: It was observed that increased anti-apoptosis genes, such as CASP2, CASP7, DDFA, and BCL2, anti-apoptotic gene, reduced APAF1, CASP8. Proliferation induced through while increased ADAMTS1, CDH1, CDH6, CLDN7, CSF3, MMP7, MMP13 genes. Autophagy increased via increasing MAP1LC3B, ATG-16L1 genes while decreased via suppressed ULK1, and ATG7 genes by silencing FBLN1 with siRNAs (p < 0.05). CONCLUSIONS: Proliferation can be induction with silencing of FBLN1 with siRNA in processing mechanism MSM. It was concluded that FBLN1 could be act as pleiotropic on autophagy, and apoptosis pathways in proliferation processing for MSM. Therefore we think that FBLN1 acts like a TSG. FBLN1 can be considered as a targeted treatment option in advanced stage MSM.
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spelling pubmed-78362762021-02-01 A preliminary study: is fibulin 1 a friend or an enemy that needs to be silenced with siRNAs for mesothelioma? Aksoy, Asude Tektemur, Ahmet Melek, Elif Kayfeci, Mustafa Uslu, Muhammed F. Cosar, Ugurcan Onalan, Ebru Contemp Oncol (Pozn) Original Paper INTRODUCTION: The impaired balance between cell proliferation and cell death, followed the inability to receive the death signals, cells push towards the neoplasia pathway. Fibulin 1 (FBLN1) plays a role as a co-factor in the mechanism of action of a protease such as a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS-1), which has important roles in angiogenesis, can also act as both tumor suppressor gene (TSG) and an oncogene in the main constituent of the extra-cellular matrix. This preliminary study has investigated the effects of silencing FBLN1 with siRNA on autophagy, proliferation, apoptosis pathways in the MSM cell line. MATERIAL AND METHODS: It was transfected siRNA specific to FBLN1 incubated MSM SPC212 cells, and compared with negative control siRNAs by a real-time polymerase chain reaction. It was determined apoptosis, proliferation, autophagy-related genes in mRNA levels. RESULTS: It was observed that increased anti-apoptosis genes, such as CASP2, CASP7, DDFA, and BCL2, anti-apoptotic gene, reduced APAF1, CASP8. Proliferation induced through while increased ADAMTS1, CDH1, CDH6, CLDN7, CSF3, MMP7, MMP13 genes. Autophagy increased via increasing MAP1LC3B, ATG-16L1 genes while decreased via suppressed ULK1, and ATG7 genes by silencing FBLN1 with siRNAs (p < 0.05). CONCLUSIONS: Proliferation can be induction with silencing of FBLN1 with siRNA in processing mechanism MSM. It was concluded that FBLN1 could be act as pleiotropic on autophagy, and apoptosis pathways in proliferation processing for MSM. Therefore we think that FBLN1 acts like a TSG. FBLN1 can be considered as a targeted treatment option in advanced stage MSM. Termedia Publishing House 2021-01-04 2020 /pmc/articles/PMC7836276/ /pubmed/33531871 http://dx.doi.org/10.5114/wo.2020.102826 Text en Copyright © 2020 Termedia http://creativecommons.org/licenses/by-nc-sa/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0). License (http://creativecommons.org/licenses/by-nc-sa/4.0/)
spellingShingle Original Paper
Aksoy, Asude
Tektemur, Ahmet
Melek, Elif
Kayfeci, Mustafa
Uslu, Muhammed F.
Cosar, Ugurcan
Onalan, Ebru
A preliminary study: is fibulin 1 a friend or an enemy that needs to be silenced with siRNAs for mesothelioma?
title A preliminary study: is fibulin 1 a friend or an enemy that needs to be silenced with siRNAs for mesothelioma?
title_full A preliminary study: is fibulin 1 a friend or an enemy that needs to be silenced with siRNAs for mesothelioma?
title_fullStr A preliminary study: is fibulin 1 a friend or an enemy that needs to be silenced with siRNAs for mesothelioma?
title_full_unstemmed A preliminary study: is fibulin 1 a friend or an enemy that needs to be silenced with siRNAs for mesothelioma?
title_short A preliminary study: is fibulin 1 a friend or an enemy that needs to be silenced with siRNAs for mesothelioma?
title_sort preliminary study: is fibulin 1 a friend or an enemy that needs to be silenced with sirnas for mesothelioma?
topic Original Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7836276/
https://www.ncbi.nlm.nih.gov/pubmed/33531871
http://dx.doi.org/10.5114/wo.2020.102826
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