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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 and Xu, Ning LU (2019) In Cancer Management and Research 11. p.3691-3701
Abstract

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... (More)

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, includingVDR. 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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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Apolipoprotein M, CRISPR/Cas9, Genechip microarrays, Hepatocellular carcinoma cells, Vitamin D receptor
in
Cancer Management and Research
volume
11
pages
11 pages
publisher
Dove Medical Press Ltd.
external identifiers
  • scopus:85067043454
ISSN
1179-1322
DOI
10.2147/CMAR.S202799
language
English
LU publication?
yes
id
1183f199-35f7-4896-9c8d-c13157213760
date added to LUP
2019-07-01 13:12:26
date last changed
2019-07-16 04:13:44
@article{1183f199-35f7-4896-9c8d-c13157213760,
  abstract     = {<p>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, includingVDR. 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.</p>},
  author       = {Yu, Miaomei and Pan, Lili and Sang, Chen and Mu, Qinfeng and Zheng, Lu and Luo, Guanghua and Xu, Ning},
  issn         = {1179-1322},
  keyword      = {Apolipoprotein M,CRISPR/Cas9,Genechip microarrays,Hepatocellular carcinoma cells,Vitamin D receptor},
  language     = {eng},
  pages        = {3691--3701},
  publisher    = {Dove Medical Press Ltd.},
  series       = {Cancer Management and Research},
  title        = {Apolipoprotein M could inhibit growth and metastasis of SMMC7721 cells via vitamin D receptor signaling},
  url          = {http://dx.doi.org/10.2147/CMAR.S202799},
  volume       = {11},
  year         = {2019},
}