CNBP controls tumor cell biology by regulating tumor-promoting gene expression

Eunhye Lee; Taeyun A. Lee; Hye Jin Yoo; Sungwook Lee; Boyoun Park

doi:10.1002/mc.23030

CNBP controls tumor cell biology by regulating tumor-promoting gene expression

Eunhye Lee, Taeyun A. Lee, Hye Jin Yoo, Sungwook Lee, Boyoun Park

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

8 Citations (Scopus)

Abstract

Cellular nucleic acid-binding protein (CNBP) is associated with cell proliferation, and its expression is elevated in human tumors, but the molecular mechanisms of CNBP in tumor cell biology have not been fully elucidated. In this study, we report that CNBP is a transcription factor essential for regulating matrix metalloproteinases mmp-2, mmp-14, and transcription factor e2f2 gene expression by binding to their promoter regions via a sequence-specific manner. Importantly, epidermal growth factor stimulation is required to induce CNBP phosphorylation and nuclear transport, thereby promoting the expression of mmp-2, mmp-14, and e2f2 genes. As a consequence, loss of cnbp attenuates the ability of tumor cell growth, invasion, and migration. Conversely, overexpression of cnbp is associated with tumor cell biology. Collectively, our findings reveal CNBP as a key transcriptional regulator of tumor-promoting target genes to control tumor cell biology.

Original language	English
Pages (from-to)	1492-1501
Number of pages	10
Journal	Molecular Carcinogenesis
Volume	58
Issue number	8
DOIs	https://doi.org/10.1002/mc.23030
Publication status	Published - 2019 Aug

Bibliographical note

Funding Information:
This study was supported by grants from the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT, and future planning (2016R1A5A1010764 and 2017R1E1A1A01074135). SL was supported by a research grant from the National Cancer Center of Korea (NCC-1710210) and NRF (2018R1D1A1B07048930). EL and TAL were supported by the Brain Korea (BK21) PLUS Program, and EL was partially supported by the Graduate School of YONSEI University Research Scholarship Grants in 2017.

Funding Information:
This study was supported by grants from the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT, and future planning (2016R1A5A1010764 and 2017R1E1A1A01074135). SL was supported by a research grant from the National Cancer Center of Korea (NCC‐1710210) and NRF (2018R1D1A1B07048930). EL and TAL were supported by the Brain Korea (BK21) PLUS Program, and EL was partially supported by the Graduate School of YONSEI University Research Scholarship Grants in 2017.

Publisher Copyright:
© 2019 Wiley Periodicals, Inc.

All Science Journal Classification (ASJC) codes

Molecular Biology
Cancer Research

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10.1002/mc.23030

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title = "CNBP controls tumor cell biology by regulating tumor-promoting gene expression",

abstract = "Cellular nucleic acid-binding protein (CNBP) is associated with cell proliferation, and its expression is elevated in human tumors, but the molecular mechanisms of CNBP in tumor cell biology have not been fully elucidated. In this study, we report that CNBP is a transcription factor essential for regulating matrix metalloproteinases mmp-2, mmp-14, and transcription factor e2f2 gene expression by binding to their promoter regions via a sequence-specific manner. Importantly, epidermal growth factor stimulation is required to induce CNBP phosphorylation and nuclear transport, thereby promoting the expression of mmp-2, mmp-14, and e2f2 genes. As a consequence, loss of cnbp attenuates the ability of tumor cell growth, invasion, and migration. Conversely, overexpression of cnbp is associated with tumor cell biology. Collectively, our findings reveal CNBP as a key transcriptional regulator of tumor-promoting target genes to control tumor cell biology.",

author = "Eunhye Lee and Lee, {Taeyun A.} and Yoo, {Hye Jin} and Sungwook Lee and Boyoun Park",

note = "Funding Information: This study was supported by grants from the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT, and future planning (2016R1A5A1010764 and 2017R1E1A1A01074135). SL was supported by a research grant from the National Cancer Center of Korea (NCC-1710210) and NRF (2018R1D1A1B07048930). EL and TAL were supported by the Brain Korea (BK21) PLUS Program, and EL was partially supported by the Graduate School of YONSEI University Research Scholarship Grants in 2017. Funding Information: This study was supported by grants from the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT, and future planning (2016R1A5A1010764 and 2017R1E1A1A01074135). SL was supported by a research grant from the National Cancer Center of Korea (NCC‐1710210) and NRF (2018R1D1A1B07048930). EL and TAL were supported by the Brain Korea (BK21) PLUS Program, and EL was partially supported by the Graduate School of YONSEI University Research Scholarship Grants in 2017. Publisher Copyright: {\textcopyright} 2019 Wiley Periodicals, Inc.",

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AU - Park, Boyoun

N1 - Funding Information: This study was supported by grants from the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT, and future planning (2016R1A5A1010764 and 2017R1E1A1A01074135). SL was supported by a research grant from the National Cancer Center of Korea (NCC-1710210) and NRF (2018R1D1A1B07048930). EL and TAL were supported by the Brain Korea (BK21) PLUS Program, and EL was partially supported by the Graduate School of YONSEI University Research Scholarship Grants in 2017. Funding Information: This study was supported by grants from the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT, and future planning (2016R1A5A1010764 and 2017R1E1A1A01074135). SL was supported by a research grant from the National Cancer Center of Korea (NCC‐1710210) and NRF (2018R1D1A1B07048930). EL and TAL were supported by the Brain Korea (BK21) PLUS Program, and EL was partially supported by the Graduate School of YONSEI University Research Scholarship Grants in 2017. Publisher Copyright: © 2019 Wiley Periodicals, Inc.

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N2 - Cellular nucleic acid-binding protein (CNBP) is associated with cell proliferation, and its expression is elevated in human tumors, but the molecular mechanisms of CNBP in tumor cell biology have not been fully elucidated. In this study, we report that CNBP is a transcription factor essential for regulating matrix metalloproteinases mmp-2, mmp-14, and transcription factor e2f2 gene expression by binding to their promoter regions via a sequence-specific manner. Importantly, epidermal growth factor stimulation is required to induce CNBP phosphorylation and nuclear transport, thereby promoting the expression of mmp-2, mmp-14, and e2f2 genes. As a consequence, loss of cnbp attenuates the ability of tumor cell growth, invasion, and migration. Conversely, overexpression of cnbp is associated with tumor cell biology. Collectively, our findings reveal CNBP as a key transcriptional regulator of tumor-promoting target genes to control tumor cell biology.

AB - Cellular nucleic acid-binding protein (CNBP) is associated with cell proliferation, and its expression is elevated in human tumors, but the molecular mechanisms of CNBP in tumor cell biology have not been fully elucidated. In this study, we report that CNBP is a transcription factor essential for regulating matrix metalloproteinases mmp-2, mmp-14, and transcription factor e2f2 gene expression by binding to their promoter regions via a sequence-specific manner. Importantly, epidermal growth factor stimulation is required to induce CNBP phosphorylation and nuclear transport, thereby promoting the expression of mmp-2, mmp-14, and e2f2 genes. As a consequence, loss of cnbp attenuates the ability of tumor cell growth, invasion, and migration. Conversely, overexpression of cnbp is associated with tumor cell biology. Collectively, our findings reveal CNBP as a key transcriptional regulator of tumor-promoting target genes to control tumor cell biology.

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CNBP controls tumor cell biology by regulating tumor-promoting gene expression

Abstract

Bibliographical note

All Science Journal Classification (ASJC) codes

UN SDGs

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