Targeting PLA2G16, a lipid metabolism gene, by Ginsenoside Compound K to suppress the malignant progression of colorectal cancer

[Display omitted] •PLA2G16 is up-regulated in CRC, and high expression of PLA2G16 is associated with the advanced stages.•PLA2G16 promotes the malignant progression of CRC through the Hippo signaling pathway.•GCK exerts its anti-CRC effects by inhibiting the protein expression of PLA2G16.•Provide a...

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Published in:	Journal of advanced research Vol. 36; pp. 265 - 276
Main Authors:	Yang, Li, Zheng, Lingjie, Xie, Xiaonv, Luo, Junjia, Yu, Jing, Zhang, Lihua, Meng, Wenhui, Zhou, Yingen, Chen, Ling, Ouyang, Dongsheng, Zhou, Honghao, Tan, Zhirong
Format:	Journal Article
Language:	English
Published:	Egypt Elsevier B.V 01-02-2022 Elsevier
Subjects:	Animals Cell Line, Tumor Colorectal cancer Colorectal Neoplasms - drug therapy Colorectal Neoplasms - genetics Colorectal Neoplasms - metabolism Ginsenoside Compound K Ginsenosides Hippo signaling pathway Humans Lipid Metabolism Lipid metabolism gene Lipidomics Mice Mice, Nude Pharmaceutical Science PLA2G16 PLA2G16 Lipid metabolism gene Lipidomics Ginsenoside Compound K Hippo signaling pathway Colorectal cancer
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Summary:	[Display omitted] •PLA2G16 is up-regulated in CRC, and high expression of PLA2G16 is associated with the advanced stages.•PLA2G16 promotes the malignant progression of CRC through the Hippo signaling pathway.•GCK exerts its anti-CRC effects by inhibiting the protein expression of PLA2G16.•Provide a new insights towards the development of effective therapeutic strategies for CRC treatment by targeting PLA2G16. Colorectal cancer (CRC) is a common malignant tumor with a high global incidence, metastasis rate and low cure rate. Changes in lipid metabolism-related genes can affect the occurrence and development of CRC, and may be a potential therapeutic target for CRC. Therefore, starting from lipid metabolism-related genes to find natural medicines for tumor treatment may become a new direction in CRC research. This study aimed to investigate the effect of PLA2G16, a key gene involved in lipid metabolism, on the biological function of CRC, and whether the anti-CRC effect of GCK is related to PLA2G16. To explore the role of PLA2G16 in CRC in vitro and in vivo, we performed cell proliferation, migration, invasion and nude mice tumorigenesis assays. As for the mechanism, we designed RNA-seq analysis and verified by western blotting and immunofluorescence experiments. Subsequently, we found the anti-CRC effect of GCK is related to PLA2G16 through western blotting and rescue experiments. We showed that PLA2G16 was significantly higher in CRC tissues than the adjacent normal appearing tissues, and high PLA2G16 expression correlates with unfavorable prognosis of CRC patients. Further, PLA2G16 promoted the malignant progression of CRC by inhibiting the Hippo signaling pathway determined by RNA-seq analysis, and GCK exerted anti-CRC effects by inhibiting the protein expression of PLA2G16 in vitro and in vivo. Our results suggested that PLA2G16 promote the malignant progression of CRC by inhibiting the Hippo signaling pathway and the anti-CRC effect of GCK is through inhibiting the protein expression of PLA2G16.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Li Yang, Lingjie Zheng and Xiaonv Xie contributed equally to this article.
ISSN:	2090-1232 2090-1224
DOI:	10.1016/j.jare.2021.06.009