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Apolipoprotein M could inhibit growth and metastasis of SMMC7721 cells via vitamin D receptor signaling

Objective: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors with high mortality-to-incidence ratios. Apolipoprotein M (ApoM), a member of the apolipoprotein family, is mainly synthesized in the liver, whereas its role in HCC has not been elucidated. Here, we examined the eff...

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Autores principales: Yu, Miaomei, Pan, Lili, Sang, Chen, Mu, Qinfeng, Zheng, Lu, Luo, Guanghua, Xu, Ning
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6525829/
https://www.ncbi.nlm.nih.gov/pubmed/31190977
http://dx.doi.org/10.2147/CMAR.S202799
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author Yu, Miaomei
Pan, Lili
Sang, Chen
Mu, Qinfeng
Zheng, Lu
Luo, Guanghua
Xu, Ning
author_facet Yu, Miaomei
Pan, Lili
Sang, Chen
Mu, Qinfeng
Zheng, Lu
Luo, Guanghua
Xu, Ning
author_sort Yu, Miaomei
collection PubMed
description Objective: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors with high mortality-to-incidence ratios. Apolipoprotein M (ApoM), a member of the apolipoprotein family, is mainly synthesized in the liver, whereas its role in HCC has not been elucidated. Here, we examined the effect of ApoM on the biological behavior of HCC cells and the possible mechanisms. Methods: We used CRISPR/Cas9 technology to knock out ApoM in SMMC7721 cells. Differentially expressed genes before and after ApoM knockout (KO) were analyzed by GeneChip microarrays and confirmed by qRT-PCR. Cell assays of proliferation, apoptosis, migration and invasion were performed in SMMC7721 cells, and the expression of epithelial–mesenchymal transition (EMT) markers was performed by western blot. And we performed functional recovery experiments by overexpressing vitamin D receptor (VDR) in SMMC7721. Results: The ApoM-KO SMMC7721 cell line was successfully constructed using the CRISPR/Cas9 technology. Our results showed that silencing ApoM suppressed apoptosis and promoted proliferation, migration, invasion and EMT of SMMC7721 cells. The microarray data revealed that a total of 1,868 differentially expressed genes were identified, including VDR. The qRT-PCR and western blot verification results demonstrated that knocking out ApoM could significantly reduce the expression of VDR. The functional recovery experiments indicated that VDR overexpression could offset the inhibition of cell apoptosis and the promotion of cell proliferation, migration, invasion and EMT caused by knocking out ApoM in SMMC7721 cells. Conclusion: ApoM could function as a tumor suppressor to inhibit the growth and metastasis of SMMC7721 cells via VDR signaling in HCC.
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spelling pubmed-65258292019-06-12 Apolipoprotein M could inhibit growth and metastasis of SMMC7721 cells via vitamin D receptor signaling Yu, Miaomei Pan, Lili Sang, Chen Mu, Qinfeng Zheng, Lu Luo, Guanghua Xu, Ning Cancer Manag Res Original Research Objective: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors with high mortality-to-incidence ratios. Apolipoprotein M (ApoM), a member of the apolipoprotein family, is mainly synthesized in the liver, whereas its role in HCC has not been elucidated. Here, we examined the effect of ApoM on the biological behavior of HCC cells and the possible mechanisms. Methods: We used CRISPR/Cas9 technology to knock out ApoM in SMMC7721 cells. Differentially expressed genes before and after ApoM knockout (KO) were analyzed by GeneChip microarrays and confirmed by qRT-PCR. Cell assays of proliferation, apoptosis, migration and invasion were performed in SMMC7721 cells, and the expression of epithelial–mesenchymal transition (EMT) markers was performed by western blot. And we performed functional recovery experiments by overexpressing vitamin D receptor (VDR) in SMMC7721. Results: The ApoM-KO SMMC7721 cell line was successfully constructed using the CRISPR/Cas9 technology. Our results showed that silencing ApoM suppressed apoptosis and promoted proliferation, migration, invasion and EMT of SMMC7721 cells. The microarray data revealed that a total of 1,868 differentially expressed genes were identified, including VDR. The qRT-PCR and western blot verification results demonstrated that knocking out ApoM could significantly reduce the expression of VDR. The functional recovery experiments indicated that VDR overexpression could offset the inhibition of cell apoptosis and the promotion of cell proliferation, migration, invasion and EMT caused by knocking out ApoM in SMMC7721 cells. Conclusion: ApoM could function as a tumor suppressor to inhibit the growth and metastasis of SMMC7721 cells via VDR signaling in HCC. Dove 2019-04-30 /pmc/articles/PMC6525829/ /pubmed/31190977 http://dx.doi.org/10.2147/CMAR.S202799 Text en © 2019 Yu et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Yu, Miaomei
Pan, Lili
Sang, Chen
Mu, Qinfeng
Zheng, Lu
Luo, Guanghua
Xu, Ning
Apolipoprotein M could inhibit growth and metastasis of SMMC7721 cells via vitamin D receptor signaling
title Apolipoprotein M could inhibit growth and metastasis of SMMC7721 cells via vitamin D receptor signaling
title_full Apolipoprotein M could inhibit growth and metastasis of SMMC7721 cells via vitamin D receptor signaling
title_fullStr Apolipoprotein M could inhibit growth and metastasis of SMMC7721 cells via vitamin D receptor signaling
title_full_unstemmed Apolipoprotein M could inhibit growth and metastasis of SMMC7721 cells via vitamin D receptor signaling
title_short Apolipoprotein M could inhibit growth and metastasis of SMMC7721 cells via vitamin D receptor signaling
title_sort apolipoprotein m could inhibit growth and metastasis of smmc7721 cells via vitamin d receptor signaling
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6525829/
https://www.ncbi.nlm.nih.gov/pubmed/31190977
http://dx.doi.org/10.2147/CMAR.S202799
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