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°í¼ºÁø (Sungjin Ko) ÀúÀÚ À̸ÞÀÏ º¸±â
University of Pittsburgh School of Medicine
Á¶È¸ 263  ÀμâÇϱâ ÁÖ¼Òº¹»ç Æ®À§ÅÍ °øÀ¯ ÆäÀ̽ººÏ °øÀ¯ 
Inhibiting Glutamine-Dependent mTORC1 Activation Ameliorates Liver Cancers Driven by ¥â-Catenin Mutations
¿­±â Authors and Affiliations

Abstract

Based on their lobule location, hepatocytes display differential gene expression, including pericentral hepatocytes that surround the central vein, which are marked by Wnt-¥â-catenin signaling. Activating ¥â-catenin mutations occur in a variety of liver tumors, including hepatocellular carcinoma (HCC), but no specific therapies are available to treat these tumor subsets. Here, we identify a positive relationship between ¥â-catenin activation, its transcriptional target glutamine synthetase (GS), and p-mTOR-S2448, an indicator of mTORC1 activation. In normal livers of mice and humans, pericentral hepatocytes were simultaneously GS and p-mTOR-S2448 positive, as were ¥â-catenin-mutated liver tumors. Genetic disruption of ¥â-catenin signaling or GS prevented p-mTOR-S2448 expression, while its forced expression in ¥â-catenin-deficient livers led to ectopic p-mTOR-S2448 expression. Further, we found notable therapeutic benefit of mTORC1 inhibition in mutant-¥â-catenin-driven HCC through suppression of cell proliferation and survival. Thus, mTORC1 inhibitors could be highly relevant in the treatment of liver tumors that are ¥â-catenin mutated and GS positive.

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- Çü½Ä: Research article
- °ÔÀçÀÏ: 2019³â 01¿ù (BRIC µî·ÏÀÏ 2019-02-01)
- ¿¬±¸Áø: ±¹¿Ü¿¬±¸Áø
- ºÐ¾ß: Cell_Biology, Medicine
RNF20/40 ÀÇÁ¸Àû eEF1B¥äL ¸ð³ëÀ¯ºñÄûƾȭ¿¡ ÀÇÇÑ ¿­Ãæ°Ý À¯ÀüÀÚ Àü»ç Á¶Àý[Nucleic Acids Res.]
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Cell_Biology

Medicine

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Google (by Sungjin Ko)
Pubmed (by Sungjin Ko)
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Àå¼Ò: Atlanta Marriott Marquis
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´ëÇѰñ´ë»çÇÐȸ The 7th Seoul Symposium on Bone Health & Á¦31Â÷ Ãá°èÇмú´ëȸ
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ÃÊ·ÏÁ¢¼ö: ~2019.02.28
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