Homeodomain‐interacting protein kinase 2 suppresses proliferation and aerobic glycolysis via ERK/cMyc axis in pancreatic cancer
Objectives To investigate the roles of the homeodomain‐interacting protein kinase (HIPK) family of proteins in pancreatic cancer prognosis and the possible molecular mechanism. Materials and Methods The expression of HIPK family genes and their roles in pancreatic cancer prognosis were analysed by u...
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| Veröffentlicht in: | Cell proliferation 2019-05, Vol.52 (3), p.e12603-n/a |
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| creator | Qin, Yi Hu, Qiangsheng Ji, Shunrong Xu, Jin Dai, Weixing Liu, Wensheng Xu, Wenyan Sun, Qiqing Zhang, Zheng Ni, Quanxing Yu, Xianjun Zhang, Bo Xu, Xiaowu |
| description | Objectives
To investigate the roles of the homeodomain‐interacting protein kinase (HIPK) family of proteins in pancreatic cancer prognosis and the possible molecular mechanism.
Materials and Methods
The expression of HIPK family genes and their roles in pancreatic cancer prognosis were analysed by using The Cancer Genome Atlas (TCGA). The roles of HIPK2 in pancreatic cancer proliferation and glycolysis were tested by overexpression of HIPK2 in pancreatic cancer cells, followed by cell proliferation assay, glucose uptake analysis and Seahorse extracellular flux analysis. The mechanism of action of HIPK2 in pancreatic cancer proliferation and glycolysis was explored by examining its effect on the ERK/cMyc axis.
Results
Decreased HIPK2 expression indicated worse prognosis of pancreatic cancer. Overexpression of HIPK2 in pancreatic cancer cells decreased cell proliferation and attenuated aerobic glycolysis, which sustained proliferation of cancer cells. HIPK2 decreased cMyc protein levels and expression of cMyc‐targeted glycolytic genes. cMyc was a mediator that regulated HIPK2‐induced decrease in aerobic glycolysis. HIPK2 regulated cMyc protein stability via ERK activation, which phosphorylated and controlled cMyc protein stability.
Conclusions
HIPK2 suppressed proliferation of pancreatic cancer in part through inhibiting the ERK/cMyc axis and related aerobic glycolysis. |
| doi_str_mv | 10.1111/cpr.12603 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_24P</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6536454</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2230466127</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4763-cc49e3acc11aff3894ef823f1dd989a663ad79e6c9ce83d7151203bd51e9e0ae3</originalsourceid><addsrcrecordid>eNp1kc9u1DAQh60K1G5LD30BZIlTD-n6T-LEFyS0aimiqFUFZ8s7mSwuWTvY2ZbcyhvwjDwJLlsqOOCLrZnP34z0I-SIsxOezxyGeMKFYnKHzLhUVSF4Uz4jM6YVK-paiD2yn9INY1zyWu2SPcm0FKKqZ-T7eVhjaMPaOv_z_ofzI0YLo_MrOsQwovP0i_M2IRU0bYYhYkqYHnq96zI6uuCp9S21GMPSAV31E4R-Si7RW2fp6fX7OXyYgNpvuZJtg_UQMf8DCvmJ8QV53tk-4eHjfUA-nZ1-XJwXF5dv3y3eXBRQ1koWAKVGaQE4t10nG11i1wjZ8bbVjbZKSdvWGhVowEa2Na-4YHLZVhw1MovygLzeeofNco0toB-j7c0Q3drGyQTrzL8d7z6bVbg1qpKqrMosePUoiOHrBtNobsIm-ryzEUKyUiku6kwdbymIIaWI3dMEzsxDWianZX6nldmXf6_0RP6JJwPzLXDnepz-bzKLq-ut8hfR9qOo</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2230466127</pqid></control><display><type>article</type><title>Homeodomain‐interacting protein kinase 2 suppresses proliferation and aerobic glycolysis via ERK/cMyc axis in pancreatic cancer</title><source>Wiley Online Library</source><creator>Qin, Yi ; Hu, Qiangsheng ; Ji, Shunrong ; Xu, Jin ; Dai, Weixing ; Liu, Wensheng ; Xu, Wenyan ; Sun, Qiqing ; Zhang, Zheng ; Ni, Quanxing ; Yu, Xianjun ; Zhang, Bo ; Xu, Xiaowu</creator><creatorcontrib>Qin, Yi ; Hu, Qiangsheng ; Ji, Shunrong ; Xu, Jin ; Dai, Weixing ; Liu, Wensheng ; Xu, Wenyan ; Sun, Qiqing ; Zhang, Zheng ; Ni, Quanxing ; Yu, Xianjun ; Zhang, Bo ; Xu, Xiaowu</creatorcontrib><description>Objectives
To investigate the roles of the homeodomain‐interacting protein kinase (HIPK) family of proteins in pancreatic cancer prognosis and the possible molecular mechanism.
Materials and Methods
The expression of HIPK family genes and their roles in pancreatic cancer prognosis were analysed by using The Cancer Genome Atlas (TCGA). The roles of HIPK2 in pancreatic cancer proliferation and glycolysis were tested by overexpression of HIPK2 in pancreatic cancer cells, followed by cell proliferation assay, glucose uptake analysis and Seahorse extracellular flux analysis. The mechanism of action of HIPK2 in pancreatic cancer proliferation and glycolysis was explored by examining its effect on the ERK/cMyc axis.
Results
Decreased HIPK2 expression indicated worse prognosis of pancreatic cancer. Overexpression of HIPK2 in pancreatic cancer cells decreased cell proliferation and attenuated aerobic glycolysis, which sustained proliferation of cancer cells. HIPK2 decreased cMyc protein levels and expression of cMyc‐targeted glycolytic genes. cMyc was a mediator that regulated HIPK2‐induced decrease in aerobic glycolysis. HIPK2 regulated cMyc protein stability via ERK activation, which phosphorylated and controlled cMyc protein stability.
Conclusions
HIPK2 suppressed proliferation of pancreatic cancer in part through inhibiting the ERK/cMyc axis and related aerobic glycolysis.</description><identifier>ISSN: 0960-7722</identifier><identifier>EISSN: 1365-2184</identifier><identifier>DOI: 10.1111/cpr.12603</identifier><identifier>PMID: 30932257</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Aerobiosis ; Cancer ; Carrier Proteins - genetics ; Carrier Proteins - metabolism ; Cell growth ; Cell Line, Tumor ; Cell proliferation ; Cell Proliferation - genetics ; Cell Proliferation - physiology ; cMyc ; Control stability ; ERK ; Extracellular signal-regulated kinase ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genes ; Genomes ; Glycolysis ; Glycolysis - genetics ; HIPK2 ; HIPK2 protein ; Homeobox ; Humans ; Kinases ; MAP Kinase Signaling System ; Medical prognosis ; Original ; Pancreatic cancer ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - metabolism ; Pancreatic Neoplasms - pathology ; Prognosis ; proliferation ; Protein kinase ; Protein Stability ; Protein-Serine-Threonine Kinases - genetics ; Protein-Serine-Threonine Kinases - metabolism ; Proteins ; Proto-Oncogene Proteins c-myc - metabolism</subject><ispartof>Cell proliferation, 2019-05, Vol.52 (3), p.e12603-n/a</ispartof><rights>2019 John Wiley & Sons Ltd</rights><rights>2019 John Wiley & Sons Ltd.</rights><rights>2019. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4763-cc49e3acc11aff3894ef823f1dd989a663ad79e6c9ce83d7151203bd51e9e0ae3</citedby><cites>FETCH-LOGICAL-c4763-cc49e3acc11aff3894ef823f1dd989a663ad79e6c9ce83d7151203bd51e9e0ae3</cites><orcidid>0000-0002-6697-7143</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6536454/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6536454/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fcpr.12603$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30932257$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qin, Yi</creatorcontrib><creatorcontrib>Hu, Qiangsheng</creatorcontrib><creatorcontrib>Ji, Shunrong</creatorcontrib><creatorcontrib>Xu, Jin</creatorcontrib><creatorcontrib>Dai, Weixing</creatorcontrib><creatorcontrib>Liu, Wensheng</creatorcontrib><creatorcontrib>Xu, Wenyan</creatorcontrib><creatorcontrib>Sun, Qiqing</creatorcontrib><creatorcontrib>Zhang, Zheng</creatorcontrib><creatorcontrib>Ni, Quanxing</creatorcontrib><creatorcontrib>Yu, Xianjun</creatorcontrib><creatorcontrib>Zhang, Bo</creatorcontrib><creatorcontrib>Xu, Xiaowu</creatorcontrib><title>Homeodomain‐interacting protein kinase 2 suppresses proliferation and aerobic glycolysis via ERK/cMyc axis in pancreatic cancer</title><title>Cell proliferation</title><addtitle>Cell Prolif</addtitle><description>Objectives
To investigate the roles of the homeodomain‐interacting protein kinase (HIPK) family of proteins in pancreatic cancer prognosis and the possible molecular mechanism.
Materials and Methods
The expression of HIPK family genes and their roles in pancreatic cancer prognosis were analysed by using The Cancer Genome Atlas (TCGA). The roles of HIPK2 in pancreatic cancer proliferation and glycolysis were tested by overexpression of HIPK2 in pancreatic cancer cells, followed by cell proliferation assay, glucose uptake analysis and Seahorse extracellular flux analysis. The mechanism of action of HIPK2 in pancreatic cancer proliferation and glycolysis was explored by examining its effect on the ERK/cMyc axis.
Results
Decreased HIPK2 expression indicated worse prognosis of pancreatic cancer. Overexpression of HIPK2 in pancreatic cancer cells decreased cell proliferation and attenuated aerobic glycolysis, which sustained proliferation of cancer cells. HIPK2 decreased cMyc protein levels and expression of cMyc‐targeted glycolytic genes. cMyc was a mediator that regulated HIPK2‐induced decrease in aerobic glycolysis. HIPK2 regulated cMyc protein stability via ERK activation, which phosphorylated and controlled cMyc protein stability.
Conclusions
HIPK2 suppressed proliferation of pancreatic cancer in part through inhibiting the ERK/cMyc axis and related aerobic glycolysis.</description><subject>Aerobiosis</subject><subject>Cancer</subject><subject>Carrier Proteins - genetics</subject><subject>Carrier Proteins - metabolism</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Cell Proliferation - physiology</subject><subject>cMyc</subject><subject>Control stability</subject><subject>ERK</subject><subject>Extracellular signal-regulated kinase</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Genomes</subject><subject>Glycolysis</subject><subject>Glycolysis - genetics</subject><subject>HIPK2</subject><subject>HIPK2 protein</subject><subject>Homeobox</subject><subject>Humans</subject><subject>Kinases</subject><subject>MAP Kinase Signaling System</subject><subject>Medical prognosis</subject><subject>Original</subject><subject>Pancreatic cancer</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Prognosis</subject><subject>proliferation</subject><subject>Protein kinase</subject><subject>Protein Stability</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-myc - metabolism</subject><issn>0960-7722</issn><issn>1365-2184</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kc9u1DAQh60K1G5LD30BZIlTD-n6T-LEFyS0aimiqFUFZ8s7mSwuWTvY2ZbcyhvwjDwJLlsqOOCLrZnP34z0I-SIsxOezxyGeMKFYnKHzLhUVSF4Uz4jM6YVK-paiD2yn9INY1zyWu2SPcm0FKKqZ-T7eVhjaMPaOv_z_ofzI0YLo_MrOsQwovP0i_M2IRU0bYYhYkqYHnq96zI6uuCp9S21GMPSAV31E4R-Si7RW2fp6fX7OXyYgNpvuZJtg_UQMf8DCvmJ8QV53tk-4eHjfUA-nZ1-XJwXF5dv3y3eXBRQ1koWAKVGaQE4t10nG11i1wjZ8bbVjbZKSdvWGhVowEa2Na-4YHLZVhw1MovygLzeeofNco0toB-j7c0Q3drGyQTrzL8d7z6bVbg1qpKqrMosePUoiOHrBtNobsIm-ryzEUKyUiku6kwdbymIIaWI3dMEzsxDWianZX6nldmXf6_0RP6JJwPzLXDnepz-bzKLq-ut8hfR9qOo</recordid><startdate>201905</startdate><enddate>201905</enddate><creator>Qin, Yi</creator><creator>Hu, Qiangsheng</creator><creator>Ji, Shunrong</creator><creator>Xu, Jin</creator><creator>Dai, Weixing</creator><creator>Liu, Wensheng</creator><creator>Xu, Wenyan</creator><creator>Sun, Qiqing</creator><creator>Zhang, Zheng</creator><creator>Ni, Quanxing</creator><creator>Yu, Xianjun</creator><creator>Zhang, Bo</creator><creator>Xu, Xiaowu</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6697-7143</orcidid></search><sort><creationdate>201905</creationdate><title>Homeodomain‐interacting protein kinase 2 suppresses proliferation and aerobic glycolysis via ERK/cMyc axis in pancreatic cancer</title><author>Qin, Yi ; Hu, Qiangsheng ; Ji, Shunrong ; Xu, Jin ; Dai, Weixing ; Liu, Wensheng ; Xu, Wenyan ; Sun, Qiqing ; Zhang, Zheng ; Ni, Quanxing ; Yu, Xianjun ; Zhang, Bo ; Xu, Xiaowu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4763-cc49e3acc11aff3894ef823f1dd989a663ad79e6c9ce83d7151203bd51e9e0ae3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Aerobiosis</topic><topic>Cancer</topic><topic>Carrier Proteins - genetics</topic><topic>Carrier Proteins - metabolism</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>Cell Proliferation - physiology</topic><topic>cMyc</topic><topic>Control stability</topic><topic>ERK</topic><topic>Extracellular signal-regulated kinase</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>Genomes</topic><topic>Glycolysis</topic><topic>Glycolysis - genetics</topic><topic>HIPK2</topic><topic>HIPK2 protein</topic><topic>Homeobox</topic><topic>Humans</topic><topic>Kinases</topic><topic>MAP Kinase Signaling System</topic><topic>Medical prognosis</topic><topic>Original</topic><topic>Pancreatic cancer</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Prognosis</topic><topic>proliferation</topic><topic>Protein kinase</topic><topic>Protein Stability</topic><topic>Protein-Serine-Threonine Kinases - genetics</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-myc - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Qin, Yi</creatorcontrib><creatorcontrib>Hu, Qiangsheng</creatorcontrib><creatorcontrib>Ji, Shunrong</creatorcontrib><creatorcontrib>Xu, Jin</creatorcontrib><creatorcontrib>Dai, Weixing</creatorcontrib><creatorcontrib>Liu, Wensheng</creatorcontrib><creatorcontrib>Xu, Wenyan</creatorcontrib><creatorcontrib>Sun, Qiqing</creatorcontrib><creatorcontrib>Zhang, Zheng</creatorcontrib><creatorcontrib>Ni, Quanxing</creatorcontrib><creatorcontrib>Yu, Xianjun</creatorcontrib><creatorcontrib>Zhang, Bo</creatorcontrib><creatorcontrib>Xu, Xiaowu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>ProQuest Biological Science Journals</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell proliferation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Qin, Yi</au><au>Hu, Qiangsheng</au><au>Ji, Shunrong</au><au>Xu, Jin</au><au>Dai, Weixing</au><au>Liu, Wensheng</au><au>Xu, Wenyan</au><au>Sun, Qiqing</au><au>Zhang, Zheng</au><au>Ni, Quanxing</au><au>Yu, Xianjun</au><au>Zhang, Bo</au><au>Xu, Xiaowu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Homeodomain‐interacting protein kinase 2 suppresses proliferation and aerobic glycolysis via ERK/cMyc axis in pancreatic cancer</atitle><jtitle>Cell proliferation</jtitle><addtitle>Cell Prolif</addtitle><date>2019-05</date><risdate>2019</risdate><volume>52</volume><issue>3</issue><spage>e12603</spage><epage>n/a</epage><pages>e12603-n/a</pages><issn>0960-7722</issn><eissn>1365-2184</eissn><abstract>Objectives
To investigate the roles of the homeodomain‐interacting protein kinase (HIPK) family of proteins in pancreatic cancer prognosis and the possible molecular mechanism.
Materials and Methods
The expression of HIPK family genes and their roles in pancreatic cancer prognosis were analysed by using The Cancer Genome Atlas (TCGA). The roles of HIPK2 in pancreatic cancer proliferation and glycolysis were tested by overexpression of HIPK2 in pancreatic cancer cells, followed by cell proliferation assay, glucose uptake analysis and Seahorse extracellular flux analysis. The mechanism of action of HIPK2 in pancreatic cancer proliferation and glycolysis was explored by examining its effect on the ERK/cMyc axis.
Results
Decreased HIPK2 expression indicated worse prognosis of pancreatic cancer. Overexpression of HIPK2 in pancreatic cancer cells decreased cell proliferation and attenuated aerobic glycolysis, which sustained proliferation of cancer cells. HIPK2 decreased cMyc protein levels and expression of cMyc‐targeted glycolytic genes. cMyc was a mediator that regulated HIPK2‐induced decrease in aerobic glycolysis. HIPK2 regulated cMyc protein stability via ERK activation, which phosphorylated and controlled cMyc protein stability.
Conclusions
HIPK2 suppressed proliferation of pancreatic cancer in part through inhibiting the ERK/cMyc axis and related aerobic glycolysis.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>30932257</pmid><doi>10.1111/cpr.12603</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-6697-7143</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Aerobiosis Cancer Carrier Proteins - genetics Carrier Proteins - metabolism Cell growth Cell Line, Tumor Cell proliferation Cell Proliferation - genetics Cell Proliferation - physiology cMyc Control stability ERK Extracellular signal-regulated kinase Gene expression Gene Expression Regulation, Neoplastic Genes Genomes Glycolysis Glycolysis - genetics HIPK2 HIPK2 protein Homeobox Humans Kinases MAP Kinase Signaling System Medical prognosis Original Pancreatic cancer Pancreatic Neoplasms - genetics Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Prognosis proliferation Protein kinase Protein Stability Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism Proteins Proto-Oncogene Proteins c-myc - metabolism |
| title | Homeodomain‐interacting protein kinase 2 suppresses proliferation and aerobic glycolysis via ERK/cMyc axis in pancreatic cancer |
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