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MedChemExpress - Model 1-Methyladenosine - 15763-06-1

1-Methyladenosine is an RNA modification that can serve as a tumor marker, with elevated levels in the body associated with cancer development. Following 1-methyladenosine methylation, upregulation of PPARδ expression regulates cholesterol metabolism and activates Hedgehog signaling pathway, driving liver tumorigenesis[1][2][3].

1-Methyladenosine

MCE China：1-Methyladenosine

Brand：MedChemExpress (MCE)

Cat. No.HY-113081

CAS：15763-06-1

Purity：99.21%

Storage：Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month

Shipping：Room temperature in continental US; may vary elsewhere.

Description：1-Methyladenosine is an RNA modification that can serve as a tumor marker, with elevated levels in the body associated with cancer development. Following 1-methyladenosine methylation, upregulation of PPARδ expression regulates cholesterol metabolism and activates Hedgehog signaling pathway, driving liver tumorigenesis.

In Vitro：Compared to surrounding tumor tissues, 1-methyladenosine methylation in RNA is aberrantly elevated in hepatocellular carcinoma (HCC) cell lines and liver cancer stem cells (CSCs). Methylated 1-methyladenosine can promote cholesterol synthesis and activate the Hedgehog signaling pathway by enhancing the translation of PPARδ in liver CSCs, ultimately driving the self-renewal and tumorigenesis of liver cancer stem cells[3].

IC50 & Target：Human Endogenous Metabolite PPAR-γ

References：

[1]. Hauenschild R, et al. The reverse transcription signature of N-1-methyladenosine in RNA-Seq is sequence dependent. Nucleic Acids Res. 2015 Nov 16;43(20):9950-64. [Content Brief]

[2]. Banys K, et al. Effect of Genistein Supplementation on the Progression of Neoplasms and the Level of the Modified Nucleosides in Rats With Mammary Cancer. In Vivo. 2021 Jul-Aug;35(4):2059-2072. [Content Brief]

[3]. Wang Y, et al. N 1-methyladenosine methylation in tRNA drives liver tumourigenesis by regulating cholesterol metabolism[J]. Nature communications, 2021, 12(1): 6314. [Content Brief]

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