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Silencing PROK2 Inhibits Invasion of Human Cervical Cancer Cells by Targeting MMP15 Expression
Cervical cancer is the second most frequent type of gynecologic cancer worldwide. Prokineticin 2 (PROK2) is reported to be involved in tumor progression in some malignant tumors. However, the role of PROK2 in the development of cervical cancer remains unknown. Our results indicate that PROK2 is over...
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| Published in: | International journal of molecular sciences 2020-09, Vol.21 (17), p.6391 |
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| description | Cervical cancer is the second most frequent type of gynecologic cancer worldwide. Prokineticin 2 (PROK2) is reported to be involved in tumor progression in some malignant tumors. However, the role of PROK2 in the development of cervical cancer remains unknown. Our results indicate that PROK2 is overexpressed in the human cervical cancer. Cervical cancer patients with high PROK2 expression have a shorter overall survival rate (OS) and disease-free survival rate (DFS). PROK2 acts as a potential biomarker for predicting OS and DFS of cervical cancer patients. We further show that PROK2 is important factor for oncogenic migration and invasion in human cervical cancer cells. Knockdown PROK2 significantly inhibited cell migration, invasion, and MMP15 protein expression in HeLa cells. High expression of MMP15 is confirmed in the human cervical cancer, is significantly associated with the shorter overall survival rate (OS) and is correlated with PROK2 expression. Overexpression of PROK2 using PROK2 plasmid significantly reverses the function of knockdown PROK2, and further upregulates MMP15 expression, migration and invasion of human cervical cancer cells. In conclusion, our findings are the first to demonstrate the role of PROK2 as a novel and potential biomarker for clinical use, and reveal the oncogenic functions of PROK2 as therapeutic target for cervical cancer. |
| doi_str_mv | 10.3390/ijms21176391 |
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Prokineticin 2 (PROK2) is reported to be involved in tumor progression in some malignant tumors. However, the role of PROK2 in the development of cervical cancer remains unknown. Our results indicate that PROK2 is overexpressed in the human cervical cancer. Cervical cancer patients with high PROK2 expression have a shorter overall survival rate (OS) and disease-free survival rate (DFS). PROK2 acts as a potential biomarker for predicting OS and DFS of cervical cancer patients. We further show that PROK2 is important factor for oncogenic migration and invasion in human cervical cancer cells. Knockdown PROK2 significantly inhibited cell migration, invasion, and MMP15 protein expression in HeLa cells. High expression of MMP15 is confirmed in the human cervical cancer, is significantly associated with the shorter overall survival rate (OS) and is correlated with PROK2 expression. Overexpression of PROK2 using PROK2 plasmid significantly reverses the function of knockdown PROK2, and further upregulates MMP15 expression, migration and invasion of human cervical cancer cells. In conclusion, our findings are the first to demonstrate the role of PROK2 as a novel and potential biomarker for clinical use, and reveal the oncogenic functions of PROK2 as therapeutic target for cervical cancer.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms21176391</identifier><identifier>PMID: 32887509</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Apoptosis ; Biomarkers ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Breast cancer ; Cancer therapies ; Cell adhesion & migration ; Cell Cycle ; Cell growth ; Cell Movement ; Cell Proliferation ; Cervical cancer ; Cervix ; Chemotherapy ; Colorectal cancer ; Female ; Gastrointestinal Hormones - antagonists & inhibitors ; Gastrointestinal Hormones - genetics ; Gastrointestinal Hormones - metabolism ; Gene Expression Regulation, Neoplastic ; Human papillomavirus ; Humans ; invasion ; Liver cancer ; Matrix Metalloproteinase 15 - chemistry ; Matrix Metalloproteinase 15 - genetics ; Matrix Metalloproteinase 15 - metabolism ; Medical prognosis ; Metastasis ; migration ; MMP15 ; Neoplasm Invasiveness ; Neuroblastoma ; Neuropeptides - antagonists & inhibitors ; Neuropeptides - genetics ; Neuropeptides - metabolism ; Prognosis ; PROK2 ; Prostate ; Protein expression ; Proteins ; Radiation therapy ; Survival ; Tumor Cells, Cultured ; Tumors ; Uterine Cervical Neoplasms - genetics ; Uterine Cervical Neoplasms - metabolism ; Uterine Cervical Neoplasms - pathology ; Womens health</subject><ispartof>International journal of molecular sciences, 2020-09, Vol.21 (17), p.6391</ispartof><rights>2020. This work is licensed under http://creativecommons.org/licenses/by/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2020 by the authors. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-86ca7389e531cc07e2b86e5a533e8fef014d61e9a9edac4a52ed083ec84522cd3</citedby><cites>FETCH-LOGICAL-c478t-86ca7389e531cc07e2b86e5a533e8fef014d61e9a9edac4a52ed083ec84522cd3</cites><orcidid>0000-0003-4942-1888 ; 0000-0002-2657-565X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2440538550/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2440538550?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32887509$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Min-Hua</creatorcontrib><creatorcontrib>Wu, Pei-Ru</creatorcontrib><creatorcontrib>Hsieh, Yi-Hsien</creatorcontrib><creatorcontrib>Lin, Chia-Liang</creatorcontrib><creatorcontrib>Liu, Chung-Jung</creatorcontrib><creatorcontrib>Ying, Tsung-Ho</creatorcontrib><title>Silencing PROK2 Inhibits Invasion of Human Cervical Cancer Cells by Targeting MMP15 Expression</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Cervical cancer is the second most frequent type of gynecologic cancer worldwide. Prokineticin 2 (PROK2) is reported to be involved in tumor progression in some malignant tumors. However, the role of PROK2 in the development of cervical cancer remains unknown. Our results indicate that PROK2 is overexpressed in the human cervical cancer. Cervical cancer patients with high PROK2 expression have a shorter overall survival rate (OS) and disease-free survival rate (DFS). PROK2 acts as a potential biomarker for predicting OS and DFS of cervical cancer patients. We further show that PROK2 is important factor for oncogenic migration and invasion in human cervical cancer cells. Knockdown PROK2 significantly inhibited cell migration, invasion, and MMP15 protein expression in HeLa cells. High expression of MMP15 is confirmed in the human cervical cancer, is significantly associated with the shorter overall survival rate (OS) and is correlated with PROK2 expression. Overexpression of PROK2 using PROK2 plasmid significantly reverses the function of knockdown PROK2, and further upregulates MMP15 expression, migration and invasion of human cervical cancer cells. In conclusion, our findings are the first to demonstrate the role of PROK2 as a novel and potential biomarker for clinical use, and reveal the oncogenic functions of PROK2 as therapeutic target for cervical cancer.</description><subject>Apoptosis</subject><subject>Biomarkers</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Breast cancer</subject><subject>Cancer therapies</subject><subject>Cell adhesion & migration</subject><subject>Cell Cycle</subject><subject>Cell growth</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cervical cancer</subject><subject>Cervix</subject><subject>Chemotherapy</subject><subject>Colorectal cancer</subject><subject>Female</subject><subject>Gastrointestinal Hormones - antagonists & inhibitors</subject><subject>Gastrointestinal Hormones - genetics</subject><subject>Gastrointestinal Hormones - metabolism</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Human papillomavirus</subject><subject>Humans</subject><subject>invasion</subject><subject>Liver cancer</subject><subject>Matrix Metalloproteinase 15 - 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genetics</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Breast cancer</topic><topic>Cancer therapies</topic><topic>Cell adhesion & migration</topic><topic>Cell Cycle</topic><topic>Cell growth</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cervical cancer</topic><topic>Cervix</topic><topic>Chemotherapy</topic><topic>Colorectal cancer</topic><topic>Female</topic><topic>Gastrointestinal Hormones - antagonists & inhibitors</topic><topic>Gastrointestinal Hormones - genetics</topic><topic>Gastrointestinal Hormones - metabolism</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Human papillomavirus</topic><topic>Humans</topic><topic>invasion</topic><topic>Liver cancer</topic><topic>Matrix Metalloproteinase 15 - chemistry</topic><topic>Matrix Metalloproteinase 15 - genetics</topic><topic>Matrix Metalloproteinase 15 - metabolism</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>migration</topic><topic>MMP15</topic><topic>Neoplasm Invasiveness</topic><topic>Neuroblastoma</topic><topic>Neuropeptides - antagonists & inhibitors</topic><topic>Neuropeptides - genetics</topic><topic>Neuropeptides - metabolism</topic><topic>Prognosis</topic><topic>PROK2</topic><topic>Prostate</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Radiation therapy</topic><topic>Survival</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><topic>Uterine Cervical Neoplasms - genetics</topic><topic>Uterine Cervical Neoplasms - metabolism</topic><topic>Uterine Cervical Neoplasms - pathology</topic><topic>Womens health</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Min-Hua</creatorcontrib><creatorcontrib>Wu, Pei-Ru</creatorcontrib><creatorcontrib>Hsieh, Yi-Hsien</creatorcontrib><creatorcontrib>Lin, Chia-Liang</creatorcontrib><creatorcontrib>Liu, Chung-Jung</creatorcontrib><creatorcontrib>Ying, Tsung-Ho</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Min-Hua</au><au>Wu, Pei-Ru</au><au>Hsieh, Yi-Hsien</au><au>Lin, Chia-Liang</au><au>Liu, Chung-Jung</au><au>Ying, Tsung-Ho</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Silencing PROK2 Inhibits Invasion of Human Cervical Cancer Cells by Targeting MMP15 Expression</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2020-09-02</date><risdate>2020</risdate><volume>21</volume><issue>17</issue><spage>6391</spage><pages>6391-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Cervical cancer is the second most frequent type of gynecologic cancer worldwide. Prokineticin 2 (PROK2) is reported to be involved in tumor progression in some malignant tumors. However, the role of PROK2 in the development of cervical cancer remains unknown. Our results indicate that PROK2 is overexpressed in the human cervical cancer. Cervical cancer patients with high PROK2 expression have a shorter overall survival rate (OS) and disease-free survival rate (DFS). PROK2 acts as a potential biomarker for predicting OS and DFS of cervical cancer patients. We further show that PROK2 is important factor for oncogenic migration and invasion in human cervical cancer cells. Knockdown PROK2 significantly inhibited cell migration, invasion, and MMP15 protein expression in HeLa cells. High expression of MMP15 is confirmed in the human cervical cancer, is significantly associated with the shorter overall survival rate (OS) and is correlated with PROK2 expression. Overexpression of PROK2 using PROK2 plasmid significantly reverses the function of knockdown PROK2, and further upregulates MMP15 expression, migration and invasion of human cervical cancer cells. In conclusion, our findings are the first to demonstrate the role of PROK2 as a novel and potential biomarker for clinical use, and reveal the oncogenic functions of PROK2 as therapeutic target for cervical cancer.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>32887509</pmid><doi>10.3390/ijms21176391</doi><orcidid>https://orcid.org/0000-0003-4942-1888</orcidid><orcidid>https://orcid.org/0000-0002-2657-565X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis Biomarkers Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Breast cancer Cancer therapies Cell adhesion & migration Cell Cycle Cell growth Cell Movement Cell Proliferation Cervical cancer Cervix Chemotherapy Colorectal cancer Female Gastrointestinal Hormones - antagonists & inhibitors Gastrointestinal Hormones - genetics Gastrointestinal Hormones - metabolism Gene Expression Regulation, Neoplastic Human papillomavirus Humans invasion Liver cancer Matrix Metalloproteinase 15 - chemistry Matrix Metalloproteinase 15 - genetics Matrix Metalloproteinase 15 - metabolism Medical prognosis Metastasis migration MMP15 Neoplasm Invasiveness Neuroblastoma Neuropeptides - antagonists & inhibitors Neuropeptides - genetics Neuropeptides - metabolism Prognosis PROK2 Prostate Protein expression Proteins Radiation therapy Survival Tumor Cells, Cultured Tumors Uterine Cervical Neoplasms - genetics Uterine Cervical Neoplasms - metabolism Uterine Cervical Neoplasms - pathology Womens health |
| title | Silencing PROK2 Inhibits Invasion of Human Cervical Cancer Cells by Targeting MMP15 Expression |
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