Abstract
Protein arginine methyltransferase 5 (PRMT5), a type II PRMT, is highly expressed in several types of tumors including cervical cancer. Arginine methyltransferase inhibitor 1 (AMI-1) inhibits solid tumors by targeting PRMT5. However, the effect of AMI-1 on cervical cancer is still unknown. In this study, we provided the first evidence that AMI-1 reduced cervical cancer cell proliferation, colony formation and promoted cell apoptosis in vitro. Suppression of tumorigenicity was also confirmed in vivo. Mechanistic studies revealed that AMI-1 significantly reduced PRMT5 level in cells and mice xenografts model of cervical cancer. These results suggest that AMI-1 inhibits cervical cancer by type II PRMT5.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antineoplastic Agents / pharmacology*
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Apoptosis / drug effects
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Cell Line, Tumor
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Cell Proliferation / drug effects
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Eukaryotic Initiation Factor-4E / metabolism
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Female
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HeLa Cells
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Humans
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Mice
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Mice, Inbred BALB C
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Mice, Nude
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Naphthalenesulfonates / pharmacology*
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Protein-Arginine N-Methyltransferases / antagonists & inhibitors*
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Protein-Arginine N-Methyltransferases / metabolism
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Urea / analogs & derivatives*
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Urea / pharmacology
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Uterine Cervical Neoplasms / drug therapy*
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Uterine Cervical Neoplasms / enzymology
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Uterine Cervical Neoplasms / pathology
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Xenograft Model Antitumor Assays
Substances
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7,7'-carbonylbis(azanediyl) bis(4-hydroxynaphthalene-2-sulfonic acid
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Antineoplastic Agents
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Eukaryotic Initiation Factor-4E
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Naphthalenesulfonates
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Urea
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PRMT5 protein, human
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Protein-Arginine N-Methyltransferases