<i>Retracted:</i> Overexpression HERG K⁺ channel gene mediates cell‐growth signals on activation of oncoproteins SP1 and NF‐κB and inactivation of tumor suppressor Nkx3.1

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Post-publication record

Nature

Retraction

Reason

Breach of Policy by Author;Duplication of Data;Duplication of/in Image;Falsification/Fabrication of Data;Investigation by Company/Institution;

Date

11/25/2011 0:00

Flagged by OpenAlex?

Yes

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Abstract

The long QT syndrome gene human ether-a-go-go related gene (HERG) encodes a K(+) channel critical to cardiac repolarization. It peculiarly overexpresses in cancer cells of different histogenesis and promotes tumorigenesis. To decipher the molecular mechanisms for HERG overexpression, we identified and characterized the promoter region of the HERG gene, which contains cis-elements for multiple oncoproteins and tumor suppressors. Oncoprotein Sp1 was found to be essential to driving the HERG promoter thereby transcription. Another oncoprotein NF-kappaB transactivated, while tumor suppressor Nkx3.1 repressed HERG promoter activity and endogenous HERG transcription. Loss-of-function mutations in the corresponding cis-elements rendered a loss of the ability of the oncoproteins Sp1 and NF-kappaB to transactivate, and of the tumor repressor Nkx3.1 to repress, HERG transcription. Either activation of Sp1 and NF-kappaB or silencing of Nkx3.1 promoted tumor cell growth, and the effects were abrogated by HERG inhibition or knockdown, but facilitated by overexpression of HERG, indicating that HERG mediates the cell growth signals generated by activation of oncoproteins or inactivation of tumor suppressors. Binding of Sp1, NF-kappaB, and Nkx3.1 to their respective cis-elements in the HERG promoter in vitro and their presence on the HERG promoter in vivo were confirmed. Therefore, the HERG promoter region is characterized by multiple Sp1 binding sites that are responsible for transcription initiation of the HERG gene and by binding sites for multiple other oncogenes and tumor suppressor genes being important for regulating HERG expression. The HERG K(+) channel is likely a mediator of growth-promoting processes induced by oncoproteins and/or by silencing of tumor suppressors.

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The record

Venue

Journal of Cellular Physiology

Topic

RNA Research and Splicing

Field

Biochemistry, Genetics and Molecular Biology

Canadian institutions

Université de MontréalMontreal Heart Institute

Funders

National Natural Science Foundation of China

Keywords

hERGTranscription factorGene knockdownCarcinogenesisBiologySp1 transcription factorPromoterSuppressorTranscription (linguistics)Molecular biologyTumor suppressor geneCell biologyCancer researchChemistryGenePotassium channelGene expressionGenetics

Has abstract in OpenAlex

yes

API

/api/v1/works/W2027868820