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All‐trans‐retinoid acid induces the differentiation of P19 cells into neurons involved in the PI3K/Akt/GSK3β signaling pathway

The pluripotent mouse embryonal carcinoma cell line P19 is widely used as a model for research on all‐trans‐retinoid acid (RA)‐induced neuronal differentiation; however, the signaling pathways involved in this process remain unclear. This study aimed to reveal the molecular mechanism underlying the...

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Published in:Journal of cellular biochemistry 2020-11, Vol.121 (11), p.4386-4396
Main Authors: Fu, Fang, Li, Lu‐Shan, Li, Ru, Deng, Qiong, Yu, Qiu‐Xia, Yang, Xin, Pan, Min, Han, Jin, Zhen, Li, Zhang, Li‐Na, Lei, Ting‐Ying, Li, Dong‐Zhi, Liao, Can
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creator Fu, Fang
Li, Lu‐Shan
Li, Ru
Deng, Qiong
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Yang, Xin
Pan, Min
Han, Jin
Zhen, Li
Zhang, Li‐Na
Lei, Ting‐Ying
Li, Dong‐Zhi
Liao, Can
description The pluripotent mouse embryonal carcinoma cell line P19 is widely used as a model for research on all‐trans‐retinoid acid (RA)‐induced neuronal differentiation; however, the signaling pathways involved in this process remain unclear. This study aimed to reveal the molecular mechanism underlying the RA‐induced neuronal differentiation of P19 cells. Real‐time quantitative polymerase chain reaction and Western blot analysis were used to determine the expression of neuronal‐specific markers, whereas flow cytometry was used to analyze cell cycle and cell apoptosis. The expression profiles of messenger RNAs (mRNAs) in RA‐induced neuronal differentiation of P19 cells were analyzed using high‐throughput sequencing, and the functions of differentially expressed mRNAs (DEMs) were determined by bioinformatics analysis. RA induced an increase in both class III β‐tubulin (TUBB3) and neurofilament medium (NEFM) mRNA expression, indicating that RA successfully induces neuronal differentiation of P19 cells. Cell apoptosis was not affected; however, cell proliferation decreased. We found 4117 DEMs, which were enriched in the phosphoinositide 3‐kinase/protein kinase B (PI3K/Akt) signaling pathway, Wnt signaling pathway, and cell cycle. Particularly, a few DEMs could be identified in the PI3K/Akt signaling pathway networks, such as PI3K, Akt, glycogen synthase kinase‐3β (GSK3β), cyclin‐dependent kinase 4 (CDK4), P21, and Bax. RA significantly increased the protein expression of PI3K, Akt, phosphorylated Akt, GSK3β, phosphorylated GSK3β, CDK4, and P21, but it reduced Bax protein expression. The Akt inhibitor affected the increase of TUBB3 and NEFM mRNA expression in RA‐induced P19 cells. The molecular mechanism underlying the RA‐induced neuronal differentiation of P19 cells is potentially involved in the PI3K/Akt/GSK3β signaling pathway. The decreased cell proliferation ability of neuronally differentiated P19 cells could be associated with the expression of cell cycle proteins. This study aimed to reveal the molecular mechanism underlying all‐trans‐retinoid acid (RA)‐induced neuronal differentiation of P19 cells. The molecular mechanism underlying the RA‐induced neuronal differentiation of P19 cells is potentially involved in the PI3K/Akt/GSK3β signaling pathway. The decreased cell proliferation ability of neuronally differentiated P19 cells could be associated with the expression of cell cycle proteins.
doi_str_mv 10.1002/jcb.29659
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This study aimed to reveal the molecular mechanism underlying the RA‐induced neuronal differentiation of P19 cells. Real‐time quantitative polymerase chain reaction and Western blot analysis were used to determine the expression of neuronal‐specific markers, whereas flow cytometry was used to analyze cell cycle and cell apoptosis. The expression profiles of messenger RNAs (mRNAs) in RA‐induced neuronal differentiation of P19 cells were analyzed using high‐throughput sequencing, and the functions of differentially expressed mRNAs (DEMs) were determined by bioinformatics analysis. RA induced an increase in both class III β‐tubulin (TUBB3) and neurofilament medium (NEFM) mRNA expression, indicating that RA successfully induces neuronal differentiation of P19 cells. Cell apoptosis was not affected; however, cell proliferation decreased. We found 4117 DEMs, which were enriched in the phosphoinositide 3‐kinase/protein kinase B (PI3K/Akt) signaling pathway, Wnt signaling pathway, and cell cycle. Particularly, a few DEMs could be identified in the PI3K/Akt signaling pathway networks, such as PI3K, Akt, glycogen synthase kinase‐3β (GSK3β), cyclin‐dependent kinase 4 (CDK4), P21, and Bax. RA significantly increased the protein expression of PI3K, Akt, phosphorylated Akt, GSK3β, phosphorylated GSK3β, CDK4, and P21, but it reduced Bax protein expression. The Akt inhibitor affected the increase of TUBB3 and NEFM mRNA expression in RA‐induced P19 cells. The molecular mechanism underlying the RA‐induced neuronal differentiation of P19 cells is potentially involved in the PI3K/Akt/GSK3β signaling pathway. The decreased cell proliferation ability of neuronally differentiated P19 cells could be associated with the expression of cell cycle proteins. This study aimed to reveal the molecular mechanism underlying all‐trans‐retinoid acid (RA)‐induced neuronal differentiation of P19 cells. The molecular mechanism underlying the RA‐induced neuronal differentiation of P19 cells is potentially involved in the PI3K/Akt/GSK3β signaling pathway. The decreased cell proliferation ability of neuronally differentiated P19 cells could be associated with the expression of cell cycle proteins.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.29659</identifier><identifier>PMID: 31961017</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; Akt ; AKT protein ; all‐trans‐retinoid acid ; Apoptosis ; Bax protein ; Bioinformatics ; Cell cycle ; Cell differentiation ; Cell growth ; Cell proliferation ; Cyclin-dependent kinase 4 ; Cyclin-dependent kinase inhibitor p21 ; Differentiation ; Flow cytometry ; Gene expression ; Glycogen ; Glycogen synthase kinase 3 ; Glycogens ; GSK3β ; GTP-binding protein ; Kinases ; neuronal differentiation ; PI3K ; Pluripotency ; Polymerase chain reaction ; Protein expression ; Proteins ; Signal transduction ; Signaling ; Tubulin ; Wnt protein</subject><ispartof>Journal of cellular biochemistry, 2020-11, Vol.121 (11), p.4386-4396</ispartof><rights>2020 Wiley Periodicals, Inc.</rights><rights>2020 Wiley Periodicals LLC</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3539-544d37d653c349af962f6a74090fd12a6988178e79ce459f3638b8fa3ddd9d633</citedby><cites>FETCH-LOGICAL-c3539-544d37d653c349af962f6a74090fd12a6988178e79ce459f3638b8fa3ddd9d633</cites><orcidid>0000-0002-0056-5453</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31961017$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fu, Fang</creatorcontrib><creatorcontrib>Li, Lu‐Shan</creatorcontrib><creatorcontrib>Li, Ru</creatorcontrib><creatorcontrib>Deng, Qiong</creatorcontrib><creatorcontrib>Yu, Qiu‐Xia</creatorcontrib><creatorcontrib>Yang, Xin</creatorcontrib><creatorcontrib>Pan, Min</creatorcontrib><creatorcontrib>Han, Jin</creatorcontrib><creatorcontrib>Zhen, Li</creatorcontrib><creatorcontrib>Zhang, Li‐Na</creatorcontrib><creatorcontrib>Lei, Ting‐Ying</creatorcontrib><creatorcontrib>Li, Dong‐Zhi</creatorcontrib><creatorcontrib>Liao, Can</creatorcontrib><title>All‐trans‐retinoid acid induces the differentiation of P19 cells into neurons involved in the PI3K/Akt/GSK3β signaling pathway</title><title>Journal of cellular biochemistry</title><addtitle>J Cell Biochem</addtitle><description>The pluripotent mouse embryonal carcinoma cell line P19 is widely used as a model for research on all‐trans‐retinoid acid (RA)‐induced neuronal differentiation; however, the signaling pathways involved in this process remain unclear. 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We found 4117 DEMs, which were enriched in the phosphoinositide 3‐kinase/protein kinase B (PI3K/Akt) signaling pathway, Wnt signaling pathway, and cell cycle. Particularly, a few DEMs could be identified in the PI3K/Akt signaling pathway networks, such as PI3K, Akt, glycogen synthase kinase‐3β (GSK3β), cyclin‐dependent kinase 4 (CDK4), P21, and Bax. RA significantly increased the protein expression of PI3K, Akt, phosphorylated Akt, GSK3β, phosphorylated GSK3β, CDK4, and P21, but it reduced Bax protein expression. The Akt inhibitor affected the increase of TUBB3 and NEFM mRNA expression in RA‐induced P19 cells. The molecular mechanism underlying the RA‐induced neuronal differentiation of P19 cells is potentially involved in the PI3K/Akt/GSK3β signaling pathway. The decreased cell proliferation ability of neuronally differentiated P19 cells could be associated with the expression of cell cycle proteins. This study aimed to reveal the molecular mechanism underlying all‐trans‐retinoid acid (RA)‐induced neuronal differentiation of P19 cells. The molecular mechanism underlying the RA‐induced neuronal differentiation of P19 cells is potentially involved in the PI3K/Akt/GSK3β signaling pathway. 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however, the signaling pathways involved in this process remain unclear. This study aimed to reveal the molecular mechanism underlying the RA‐induced neuronal differentiation of P19 cells. Real‐time quantitative polymerase chain reaction and Western blot analysis were used to determine the expression of neuronal‐specific markers, whereas flow cytometry was used to analyze cell cycle and cell apoptosis. The expression profiles of messenger RNAs (mRNAs) in RA‐induced neuronal differentiation of P19 cells were analyzed using high‐throughput sequencing, and the functions of differentially expressed mRNAs (DEMs) were determined by bioinformatics analysis. RA induced an increase in both class III β‐tubulin (TUBB3) and neurofilament medium (NEFM) mRNA expression, indicating that RA successfully induces neuronal differentiation of P19 cells. Cell apoptosis was not affected; however, cell proliferation decreased. We found 4117 DEMs, which were enriched in the phosphoinositide 3‐kinase/protein kinase B (PI3K/Akt) signaling pathway, Wnt signaling pathway, and cell cycle. Particularly, a few DEMs could be identified in the PI3K/Akt signaling pathway networks, such as PI3K, Akt, glycogen synthase kinase‐3β (GSK3β), cyclin‐dependent kinase 4 (CDK4), P21, and Bax. RA significantly increased the protein expression of PI3K, Akt, phosphorylated Akt, GSK3β, phosphorylated GSK3β, CDK4, and P21, but it reduced Bax protein expression. The Akt inhibitor affected the increase of TUBB3 and NEFM mRNA expression in RA‐induced P19 cells. The molecular mechanism underlying the RA‐induced neuronal differentiation of P19 cells is potentially involved in the PI3K/Akt/GSK3β signaling pathway. The decreased cell proliferation ability of neuronally differentiated P19 cells could be associated with the expression of cell cycle proteins. This study aimed to reveal the molecular mechanism underlying all‐trans‐retinoid acid (RA)‐induced neuronal differentiation of P19 cells. The molecular mechanism underlying the RA‐induced neuronal differentiation of P19 cells is potentially involved in the PI3K/Akt/GSK3β signaling pathway. The decreased cell proliferation ability of neuronally differentiated P19 cells could be associated with the expression of cell cycle proteins.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>31961017</pmid><doi>10.1002/jcb.29659</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-0056-5453</orcidid></addata></record>
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subjects 1-Phosphatidylinositol 3-kinase
Akt
AKT protein
all‐trans‐retinoid acid
Apoptosis
Bax protein
Bioinformatics
Cell cycle
Cell differentiation
Cell growth
Cell proliferation
Cyclin-dependent kinase 4
Cyclin-dependent kinase inhibitor p21
Differentiation
Flow cytometry
Gene expression
Glycogen
Glycogen synthase kinase 3
Glycogens
GSK3β
GTP-binding protein
Kinases
neuronal differentiation
PI3K
Pluripotency
Polymerase chain reaction
Protein expression
Proteins
Signal transduction
Signaling
Tubulin
Wnt protein
title All‐trans‐retinoid acid induces the differentiation of P19 cells into neurons involved in the PI3K/Akt/GSK3β signaling pathway
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