<p>Apolipoprotein M could inhibit growth and metastasis of SMMC7721 cells via vitamin D receptor signaling</p>

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 epithelialmesenchymal 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.

Vitamin D promotes the cisplatin sensitivity of oral squamous cell carcinoma by inhibiting LCN2-modulated NF-κB pathway activation through RPS3

“…Vitamin D enters cells by two pathways: the steroid receptor pathway and the direct entry pathway. Vitamin D receptor (VDR) is a membrane receptor for vitamin D. However, whether VDR is a tumour suppressor or an oncogene remains unclear [27][28][29] . The VDR expressions in cisplatin and vitamin D treatments failed to show significant changes (Fig.…”

Apolipoprotein M inhibits proliferation and migration of larynx carcinoma cells

“…Many studies have shown that VDR plays an important role in cell proliferation, differentiation, angiogenesis and apoptosis. Our previous research found that APOM could upregulate the VDR mRNA level in colorectal cancer cells 11 , and APOM could also affect the biological functions of SMMC772I cells via VDR signalling, such as inhibiting proliferation and metastasis 13 . Thus, we examined the VDR mRNA and protein levels in the TU686 cells of the APOM-OE group and NC group.…”

“…In 2018, our research demonstrated that APOM can promote the proliferation and invasion of non-small cell lung cancer cells, which is related to the upregulation of S1P-receptor 1 and activation of the ERK1/2 and PI3K/AKT signalling pathways induced by APOM 12 . Furthermore, we reported that APOM can suppress the proliferation and invasion of SMMC7721 cells, a hepatocellular carcinoma line, through VDR pathways 13 . In the present study, we compared the expression of APOM in different types of laryngeal tissues, analysed the biological effects of APOM overexpression on LC cells, and explored the possible mechanisms of APOM in the development of LC.…”

Revealing the Role of High-Density Lipoprotein in Colorectal Cancer

“…Regardless of its associations with S1P, evidence indicates the beneficial role of apoM in various malignancies [ 88 , 89 ]. Importantly, it was shown that apoM increases the expression of vitamin D receptor in CRC cells [ 90 ].…”