Let-7 prevents early cancer progression by suppressing expression of the embryonic gene HMGA2

Sun Mi Park; Scott Shell; Amir Reza Radjabi; Robert Schickel; Christine Feig; Ben Boyerinas; Daniela M. Dinulescu; Ernst Lengyel; Marcus E. Peter

doi:10.4161/cc.6.21.4845

Let-7 prevents early cancer progression by suppressing expression of the embryonic gene HMGA2

Sun Mi Park, Scott Shell, Amir Reza Radjabi, Robert Schickel, Christine Feig, Ben Boyerinas, Daniela M. Dinulescu, Ernst Lengyel, Marcus E. Peter^*

^*Corresponding author for this work

Medicine, Hematology Oncology Division

Research output: Contribution to journal › Article › peer-review

210 Scopus citations

Abstract

The microRNA let-7 regulates late embryonic development by suppressing expression of a number of genes such as c-myc and RAS as well as the embryonic gene high mobility group, A2 (HMGA2). We now demonstrate that HMGA2 is more efficiently targeted by let-7 than RAS. Its expression inversely correlates with the expression of let-7 in the NCI60 cells lines, and the expression of RAS does not change when amounts of let-7 that efficiently silence expression of HMGA2 are introduced into tumor cells. We did not find a difference in the expression of HMGA2 between primary ovarian cancer samples and matching metastases, suggesting that the expression of HMGA2 represents an early event during cancer progression. The late repression of HMGA2 by let-7 during embryonic development, and the early reexpression of HMGA2 during cancer development, is in line with the hypothesis that cancer development represents a case of reverse embryogenesis.

Original language	English (US)
Pages (from-to)	2585-2590
Number of pages	6
Journal	Cell Cycle
Volume	6
Issue number	21
DOIs	https://doi.org/10.4161/cc.6.21.4845
State	Published - Nov 1 2007

Keywords

Metastasis
Ovarian cancer
Reverse embryogenesis
Supercluster
microRNA

ASJC Scopus subject areas

Molecular Biology
Developmental Biology
Cell Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.4161/cc.6.21.4845

Cite this

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title = "Let-7 prevents early cancer progression by suppressing expression of the embryonic gene HMGA2",

abstract = "The microRNA let-7 regulates late embryonic development by suppressing expression of a number of genes such as c-myc and RAS as well as the embryonic gene high mobility group, A2 (HMGA2). We now demonstrate that HMGA2 is more efficiently targeted by let-7 than RAS. Its expression inversely correlates with the expression of let-7 in the NCI60 cells lines, and the expression of RAS does not change when amounts of let-7 that efficiently silence expression of HMGA2 are introduced into tumor cells. We did not find a difference in the expression of HMGA2 between primary ovarian cancer samples and matching metastases, suggesting that the expression of HMGA2 represents an early event during cancer progression. The late repression of HMGA2 by let-7 during embryonic development, and the early reexpression of HMGA2 during cancer development, is in line with the hypothesis that cancer development represents a case of reverse embryogenesis.",

keywords = "Metastasis, Ovarian cancer, Reverse embryogenesis, Supercluster, microRNA",

author = "Park, {Sun Mi} and Scott Shell and Radjabi, {Amir Reza} and Robert Schickel and Christine Feig and Ben Boyerinas and Dinulescu, {Daniela M.} and Ernst Lengyel and Peter, {Marcus E.}",

note = "Funding Information: supported by the Ovarian Cancer Research Members of the let-7/miR-98 family10-15 are induced late in mammalian embryonic Fund (Liz Tilberis Scholars Program) and development suppressing expression of embryonic genes that are not expressed in the NIH grants R01 CA111882 (to E.L.) and adult organism. Reported let-7 targets include RAS, c-myc and HMGA2.15-20Let-7 is R01 GM61712 {\textcopyright}2007 LANDES BIOSCIENCE(to M.E.P). 12-15,17 frequently downregulated in human neoplasms, suggesting that embryonic target genes of let-7 may be upregulated in cancer. We have recently provided the first direct link in a human cancer between downregulation of let-7 and upregulation of HMGA2.17",

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language = "English (US)",

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T1 - Let-7 prevents early cancer progression by suppressing expression of the embryonic gene HMGA2

AU - Park, Sun Mi

AU - Shell, Scott

AU - Radjabi, Amir Reza

AU - Schickel, Robert

AU - Feig, Christine

AU - Boyerinas, Ben

AU - Dinulescu, Daniela M.

AU - Lengyel, Ernst

AU - Peter, Marcus E.

N1 - Funding Information: supported by the Ovarian Cancer Research Members of the let-7/miR-98 family10-15 are induced late in mammalian embryonic Fund (Liz Tilberis Scholars Program) and development suppressing expression of embryonic genes that are not expressed in the NIH grants R01 CA111882 (to E.L.) and adult organism. Reported let-7 targets include RAS, c-myc and HMGA2.15-20Let-7 is R01 GM61712 ©2007 LANDES BIOSCIENCE(to M.E.P). 12-15,17 frequently downregulated in human neoplasms, suggesting that embryonic target genes of let-7 may be upregulated in cancer. We have recently provided the first direct link in a human cancer between downregulation of let-7 and upregulation of HMGA2.17

PY - 2007/11/1

Y1 - 2007/11/1

N2 - The microRNA let-7 regulates late embryonic development by suppressing expression of a number of genes such as c-myc and RAS as well as the embryonic gene high mobility group, A2 (HMGA2). We now demonstrate that HMGA2 is more efficiently targeted by let-7 than RAS. Its expression inversely correlates with the expression of let-7 in the NCI60 cells lines, and the expression of RAS does not change when amounts of let-7 that efficiently silence expression of HMGA2 are introduced into tumor cells. We did not find a difference in the expression of HMGA2 between primary ovarian cancer samples and matching metastases, suggesting that the expression of HMGA2 represents an early event during cancer progression. The late repression of HMGA2 by let-7 during embryonic development, and the early reexpression of HMGA2 during cancer development, is in line with the hypothesis that cancer development represents a case of reverse embryogenesis.

AB - The microRNA let-7 regulates late embryonic development by suppressing expression of a number of genes such as c-myc and RAS as well as the embryonic gene high mobility group, A2 (HMGA2). We now demonstrate that HMGA2 is more efficiently targeted by let-7 than RAS. Its expression inversely correlates with the expression of let-7 in the NCI60 cells lines, and the expression of RAS does not change when amounts of let-7 that efficiently silence expression of HMGA2 are introduced into tumor cells. We did not find a difference in the expression of HMGA2 between primary ovarian cancer samples and matching metastases, suggesting that the expression of HMGA2 represents an early event during cancer progression. The late repression of HMGA2 by let-7 during embryonic development, and the early reexpression of HMGA2 during cancer development, is in line with the hypothesis that cancer development represents a case of reverse embryogenesis.

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KW - Ovarian cancer

KW - Reverse embryogenesis

KW - Supercluster

KW - microRNA

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Let-7 prevents early cancer progression by suppressing expression of the embryonic gene HMGA2

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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