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Lipogenesis by regulating ERK2/PPARY signaling in a non-canonical manner

ABSTRACT: To delve deeper into the underlying mechanism of Argl’s involvement in lipid metabolism, weconducted co-immunoprecipitation (Co-IP) and mass spectrometry analysis to identify proteins thinteract with Argl.

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ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Hepatocyte, Liver

DISEASE(S): Disease Free

SUBMITTER: Yujun Shi

LAB HEAD: shi yujun

PROVIDER: PXD059821 | Pride | 2026-02-03

REPOSITORIES: Pride

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Project description:Amongst varied cancers, colorectal cancer (CRC) is the second highest cause for mortality worldwide, suggesting inefficacy of existing medications. Thereby, justifying the need for extensive research to delineate the molecular mechanisms, and evolve new therapies. It has been well established that one of the major pathways responsible for adenoma formation in CRC is the aberrant Wnt/β-catenin signaling. The constant unearthing of it’s molecular players has contributed to a deeper understanding of tumor progression and prognosis, increasing the horizon for targeted therapeutics. One of the methodologies adopted is the repurposing of drugs that target a physiological pathway, known to be dysregulated in tumorigenesis. Hypercholesterolemia has been associated with high-risk CRC patients exclusively, making statins a potential drug for trials in human subjects. Statins are a well-established family of drugs that selectively inhibit de novo cholesterol biosynthesis causing a reduction in systemic cholesterol levels in dyslipidemia. We have contributed to building evidence of statin's anti-tumor activity in both in vitro and in vivo. Our multi-pronged approach provides a holistic view of statin treatment at the lipid, transcript, and protein levels. Interestingly, we observe the Wnt/ β-catenin signaling players getting targeted, one of the most important being SATB (Special AT-rich Binding protein) proteins. Previously, we established the role of SATB1 in tumorigenesis, regulated by β-catenin in Wnt “ON” conditions. On the other hand, SATB2, belonging to the same family, has been reported playing an opposite role. We show that Statins target the physiological balance between the two proteins by downregulating SATB1 and upregulating SATB2. Our phase II trial study in CRC patients further strengthens our hypothesis regarding the differential expression of SATB proteins as a key in determining the tumorigenic outcome. Collectively, these results establish that this molecular switch could provide new therapeutic possibilities in the future, by repurposing statins.

			Action	DRS
	201631wtsmallkd.zip	Other
	201631wtsmallkdIPIgG.zip	Other
	201632wtbigkd.zip	Other
	201632wtbigkdIgG.zip	Other
	checksum.txt	Txt

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Lipogenesis by regulating ERK2/PPARY signaling in a non-canonical manner

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