Why the study?
The functions of layilin, which is highly expressed in malignant glioma cells, are not completely understood, prompting investigation into its functional relationship to the low-density lipoprotein receptor (LDLR).
Does layilin knockdown affect LDLR expression and LDL uptake in malignant glioma cells?
Does layilin knockdown affect LDLR expression and LDL uptake in malignant glioma cells?
Layilin down-regulates LDLR at the protein level in malignant glioma cells, suggesting a novel regulatory mechanism for LDL uptake in these cells.
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Layilin downregulates LDLR protein in glioma cells; hypothesis-generating for lipid metabolism targeting, needs validation before clinical consideration.
Objective: Layilin is a type I transmembrane protein that possesses a C-type lectin motif in its extracellular domain, and whose functions have not yet been completely understood. Previously, we reported that layilin was highly expressed in malignant glioma cells. In this study, we investigated whether layilin was functionally related to low-density lipoprotein receptor (LDLR) in malignant glioma cells because one of the characteristics of malignant glioma cells is the high expression of LDLR.Methods: Under layilin-knockdown (KD) conditions in A172 cells, a malignant glioma cell line, we measured LDLR mRNA and protein levels by quantitative polymerase chain reaction and western blotting, respectively. Furthermore, we measured LDL uptake in layilin-KD cells by LDL uptake assay.Results: Even though the amounts of mRNA for LDLR were unaffected by layilin-KD, the amounts of LDLR protein were significantly increased by layilin-KD 48 h after transfection with small interfering RNAs for layilin (p<0.05). Accordingly, LDL uptake was increased by layilin-KD (p<0.05).Conclusion: Our data suggest a novel function of layilin, that is, down-regulation of LDLR at the protein level.
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Ushimaru et al. (2020) studied this question.
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