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Editor’s note iNature is China’s largest academic official account.
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us
.
iNatureERK3, officially called mitogen-activated protein kinase 6 (MAPK6), is an under-researched mitogen-activated protein kinase (MAPK)
.
Recent studies have revealed the up-regulation of ERK3 expression in cancer, and indicated that ERK3 plays an important role in promoting the growth and invasion of certain cancers, especially lung cancer
.
However, whether ERK3 plays a role in spontaneous tumorigenesis in vivo is unclear
.
On October 31, 2021, Wright State University's Long Weiwen research team and researcher Liu Jian from Zhejiang University Edinburgh University Joint College (ZJE) jointly published a titled "Conditional ERK3 overexpression cooperates with PTEN deletion to promotelung adenocarcinoma formation in mice" in Molecular Oncology.
The research paper created a conditional ERK3 transgenic mouse strain, in which the expression of ERK3 transgene is controlled by Cre recombinase.
Through hybridization with lung tissue-specific CCSP-iCre mouse line, it was found that ERK3 overexpression and PTEN deletion Can jointly induce the formation of lung adenocarcinomas (LUADs)
.
In terms of mechanism, ERK3 overexpression stimulates the activation of erb-b2 receptor tyrosine kinase by up-regulating the gene transcription of Sp1 transcription factor (SP1)-mediated neuregulin 1 (NRG1) (effective ligand for ERBB2/ERBB3) Phosphorylation of 2 and 3 (ERBB2 and ERBB3)
.
The study used genetically engineered mouse models to reveal the true tumor-promoting effects of ERK3
.
Together with the results of previous studies showing the role of ERK3 in cultured cells and xenograft lung tumor models, the results of this study confirm that ERK3 is an oncoprotein that promotes the development and progression of LUAD
.
Lung cancer is the type of cancer with the largest number of cancer deaths in the world and in China1.
It is mainly divided into non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC).
NSCLC is the most important type2
.
The occurrence and development of lung cancer are driven by the gradual accumulation of gene mutations, including the inactivation of tumor suppressor genes, such as PTEN, p53 and Smad4, and the mutation and/or amplification of oncogenes, such as Kras, EGFR and ERBB22 that control cell proliferation.
.
Extracellular signal-regulated kinase 3 (ERK3) belongs to atypical mitogen-activated protein kinase (MAPK) subfamily 3.
Compared with the widely studied ERK1 and ERK2 in the MAPK family, we know very little about the cellular and molecular mechanisms of ERK3 Less
.
ERK3 has been shown to promote tumor growth and metastasis in cell tumor models and xenograft mouse models of different human cancers, including lung cancer 4-7, head and neck cancer 8 and breast cancer 9-11
.
However, the underlying mechanism of ERK3 in the development and metastasis of lung cancer is still unclear
.
Figure 1.
Overexpression of ERK3 and deletion of PTEN promote the growth of mouse lung cancer tumors.
This study created an ERK3 transgenic mouse model, which uses Cre recombinase to regulate the expression of ERK3 transgene
.
By crossing with the lung tissue-specific CCSP-iCre mouse line, it was found that ERK3 overexpression and PTEN deletion can jointly induce the formation of lung adenocarcinomas (LUADs) (Figure 1)
.
Mechanistically, the overexpression of ERK3 activates the phosphorylation of ERBB3 and ERBB2 by up-regulating sp1-mediated NRG1 gene transcription (Figure 2)
.
Figure 2.
The molecular mechanism of ERK3 overexpression in PTEN deletion co-promoting lung cancer tumor growth in mice
.
In summary, this study reveals for the first time that ERK3 promotes tumor growth in a mouse model .
In combination with previous studies, ERK3 plays an important role in cultured cell tumor models and xenogeneic lung tumor models.
The findings of this study confirm that ERK3 acts as a tumor regulatory protein to promote the occurrence and progression of lung adenocarcinoma
.
Researcher Liu Jian and Long Weiwen are the co-corresponding authors of the paper.
Dr.
Sreeram Vallabhaneni and Researcher Liu Jian are co-authors of this paper.
Wang Jixin, an undergraduate student majoring in bioinformatics at ZJE2018, participated in the analysis of the student letter of the study
.
Dr.
Marion Morel from Wright State University provided some histochemical data
.
Francesco DeMayo, director of the National Center for Health Research (NIH), provided some genetically modified mouse models
.
In addition, as early as May 2012, the research named "ERK3 signals through SRC-3 coactivator topromote human lung cancer cell invasion" published by Professor Long Weiwen's team and researcher Liu Jian in the internationally renowned journal The Journal of clinical investigation was confirmed for the first time.
ERK3/SRC-3 signaling plays a key role in promoting the invasiveness of lung cancer cells in vivo.
It is proposed that ERK3 protein kinase may be an attractive target for the treatment of invasive lung cancer
.
Zhejiang University-Postdoctoral Recruitment for Liu Jian's Research Group Liu Jian: Researcher, Ph.
D.
Supervisor of Zhejiang University, Adjunct Professor of Zhejiang University, Honorary PI of the University of Edinburgh, Winner of Zhejiang Outstanding Youth Fund; the research group was established in the International Campus of Zhejiang University in early November 2020 ; Has published 40 SCI papers (including 16 newsletters or one work (including common)); laboratory website https://person.
zju.
edu.
cn/liujian
.
The
main research direction of the research group is tumor biology, epigenetics And gene editing
.
At present, the main focus is to combine clinical databases, genetically modified mouse models and multiple sequencing methods to study the molecular mechanism of lung squamous cell carcinoma, aiming to promote the targeted therapy of lung squamous cell carcinoma
.
Now I am recruiting the first author to develop Postdoctoral fellows with high-level research papers and strong subjective initiative
.
Postdoctoral treatment: 1) High-level research platform; 2) Annual salary of 300,000-500,000; 3) Living in an apartment with a bag; 4) Zhejiang University unified postdoctoral treatment (children's study, medical insurance, etc.
); 5) Support application for independent PI position
.
Contact email: JianL@intl.
zju.
edu.
cn
.
References: 1.
Sung, H.
et al.
CA: a cancer journal for clinicians (2021) 2.
Herbst, RS, et al.
Nature (2018) 3.
Coulombe, P.
& Meloche, S.
Biochim Biophys Acta (2007).
4.
Long, W.
et al.
Journal of Clinical Investigation (2012) 5.
Bian, K.
et al.
Oncotarget (2016).
6.
Bogucka, K.
et al.
Cancer Gene Therapy (2021) .
7.
Elkhadragy, L.
et al.
Molecular Oncology (2017).
8.
Al-Mahdi, R.
et al.
Cell Adhesion & Migration (2015).
9.
Bogucka, K.
et al.
Elife (2020).
10 Elkhadragy, L.
et al.
International Journal of Molecular Sciences (2020).
11.
Chen, M.
et al.
Journal of Cellular Physiology (2019).
Reference news: https://febs.
onlinelibrary.
wiley.
com/doi /10.
1002/1878-0261.
13132
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us
.
iNatureERK3, officially called mitogen-activated protein kinase 6 (MAPK6), is an under-researched mitogen-activated protein kinase (MAPK)
.
Recent studies have revealed the up-regulation of ERK3 expression in cancer, and indicated that ERK3 plays an important role in promoting the growth and invasion of certain cancers, especially lung cancer
.
However, whether ERK3 plays a role in spontaneous tumorigenesis in vivo is unclear
.
On October 31, 2021, Wright State University's Long Weiwen research team and researcher Liu Jian from Zhejiang University Edinburgh University Joint College (ZJE) jointly published a titled "Conditional ERK3 overexpression cooperates with PTEN deletion to promotelung adenocarcinoma formation in mice" in Molecular Oncology.
The research paper created a conditional ERK3 transgenic mouse strain, in which the expression of ERK3 transgene is controlled by Cre recombinase.
Through hybridization with lung tissue-specific CCSP-iCre mouse line, it was found that ERK3 overexpression and PTEN deletion Can jointly induce the formation of lung adenocarcinomas (LUADs)
.
In terms of mechanism, ERK3 overexpression stimulates the activation of erb-b2 receptor tyrosine kinase by up-regulating the gene transcription of Sp1 transcription factor (SP1)-mediated neuregulin 1 (NRG1) (effective ligand for ERBB2/ERBB3) Phosphorylation of 2 and 3 (ERBB2 and ERBB3)
.
The study used genetically engineered mouse models to reveal the true tumor-promoting effects of ERK3
.
Together with the results of previous studies showing the role of ERK3 in cultured cells and xenograft lung tumor models, the results of this study confirm that ERK3 is an oncoprotein that promotes the development and progression of LUAD
.
Lung cancer is the type of cancer with the largest number of cancer deaths in the world and in China1.
It is mainly divided into non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC).
NSCLC is the most important type2
.
The occurrence and development of lung cancer are driven by the gradual accumulation of gene mutations, including the inactivation of tumor suppressor genes, such as PTEN, p53 and Smad4, and the mutation and/or amplification of oncogenes, such as Kras, EGFR and ERBB22 that control cell proliferation.
.
Extracellular signal-regulated kinase 3 (ERK3) belongs to atypical mitogen-activated protein kinase (MAPK) subfamily 3.
Compared with the widely studied ERK1 and ERK2 in the MAPK family, we know very little about the cellular and molecular mechanisms of ERK3 Less
.
ERK3 has been shown to promote tumor growth and metastasis in cell tumor models and xenograft mouse models of different human cancers, including lung cancer 4-7, head and neck cancer 8 and breast cancer 9-11
.
However, the underlying mechanism of ERK3 in the development and metastasis of lung cancer is still unclear
.
Figure 1.
Overexpression of ERK3 and deletion of PTEN promote the growth of mouse lung cancer tumors.
This study created an ERK3 transgenic mouse model, which uses Cre recombinase to regulate the expression of ERK3 transgene
.
By crossing with the lung tissue-specific CCSP-iCre mouse line, it was found that ERK3 overexpression and PTEN deletion can jointly induce the formation of lung adenocarcinomas (LUADs) (Figure 1)
.
Mechanistically, the overexpression of ERK3 activates the phosphorylation of ERBB3 and ERBB2 by up-regulating sp1-mediated NRG1 gene transcription (Figure 2)
.
Figure 2.
The molecular mechanism of ERK3 overexpression in PTEN deletion co-promoting lung cancer tumor growth in mice
.
In summary, this study reveals for the first time that ERK3 promotes tumor growth in a mouse model .
In combination with previous studies, ERK3 plays an important role in cultured cell tumor models and xenogeneic lung tumor models.
The findings of this study confirm that ERK3 acts as a tumor regulatory protein to promote the occurrence and progression of lung adenocarcinoma
.
Researcher Liu Jian and Long Weiwen are the co-corresponding authors of the paper.
Dr.
Sreeram Vallabhaneni and Researcher Liu Jian are co-authors of this paper.
Wang Jixin, an undergraduate student majoring in bioinformatics at ZJE2018, participated in the analysis of the student letter of the study
.
Dr.
Marion Morel from Wright State University provided some histochemical data
.
Francesco DeMayo, director of the National Center for Health Research (NIH), provided some genetically modified mouse models
.
In addition, as early as May 2012, the research named "ERK3 signals through SRC-3 coactivator topromote human lung cancer cell invasion" published by Professor Long Weiwen's team and researcher Liu Jian in the internationally renowned journal The Journal of clinical investigation was confirmed for the first time.
ERK3/SRC-3 signaling plays a key role in promoting the invasiveness of lung cancer cells in vivo.
It is proposed that ERK3 protein kinase may be an attractive target for the treatment of invasive lung cancer
.
Zhejiang University-Postdoctoral Recruitment for Liu Jian's Research Group Liu Jian: Researcher, Ph.
D.
Supervisor of Zhejiang University, Adjunct Professor of Zhejiang University, Honorary PI of the University of Edinburgh, Winner of Zhejiang Outstanding Youth Fund; the research group was established in the International Campus of Zhejiang University in early November 2020 ; Has published 40 SCI papers (including 16 newsletters or one work (including common)); laboratory website https://person.
zju.
edu.
cn/liujian
.
The
main research direction of the research group is tumor biology, epigenetics And gene editing
.
At present, the main focus is to combine clinical databases, genetically modified mouse models and multiple sequencing methods to study the molecular mechanism of lung squamous cell carcinoma, aiming to promote the targeted therapy of lung squamous cell carcinoma
.
Now I am recruiting the first author to develop Postdoctoral fellows with high-level research papers and strong subjective initiative
.
Postdoctoral treatment: 1) High-level research platform; 2) Annual salary of 300,000-500,000; 3) Living in an apartment with a bag; 4) Zhejiang University unified postdoctoral treatment (children's study, medical insurance, etc.
); 5) Support application for independent PI position
.
Contact email: JianL@intl.
zju.
edu.
cn
.
References: 1.
Sung, H.
et al.
CA: a cancer journal for clinicians (2021) 2.
Herbst, RS, et al.
Nature (2018) 3.
Coulombe, P.
& Meloche, S.
Biochim Biophys Acta (2007).
4.
Long, W.
et al.
Journal of Clinical Investigation (2012) 5.
Bian, K.
et al.
Oncotarget (2016).
6.
Bogucka, K.
et al.
Cancer Gene Therapy (2021) .
7.
Elkhadragy, L.
et al.
Molecular Oncology (2017).
8.
Al-Mahdi, R.
et al.
Cell Adhesion & Migration (2015).
9.
Bogucka, K.
et al.
Elife (2020).
10 Elkhadragy, L.
et al.
International Journal of Molecular Sciences (2020).
11.
Chen, M.
et al.
Journal of Cellular Physiology (2019).
Reference news: https://febs.
onlinelibrary.
wiley.
com/doi /10.
1002/1878-0261.
13132
