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MiR-196a promotes pancreatic cancer progression by targeting nuclear factor kappa-B-inhibitor alpha
Aberrant expression of miR-196a has been frequently reported in different cancers including pancreatic cancer. However, its function in pancreatic cancer has not been fully elucidated. Here, we investigated the expression pattern and the biological role of miR-196a in pancreatic cancer cell lines, a...
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Published in: | PloS one 2014-02, Vol.9 (2), p.e87897-e87897 |
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description | Aberrant expression of miR-196a has been frequently reported in different cancers including pancreatic cancer. However, its function in pancreatic cancer has not been fully elucidated. Here, we investigated the expression pattern and the biological role of miR-196a in pancreatic cancer cell lines, as well as its interaction with a metastasis-related gene, nuclear factor-kappa-B-inhibitor alpha (NFKBIA). We demonstrated that miR-196a was up-regulated in human pancreatic cancer cell lines compared with immortalized pancreatic ductal epithelial cells by means of microRNAs microarray and qRT-PCR. Furthermore, down-regulation of miR-196a in PANC-1 suppressed its proliferation and migration with an increase in G0/G1 transition and decreased expression of Cyclin D1 and CDK4/6. Meanwhile, an increased expression in E-cadherin and decreased expression in N-cadherin and Vimentin were also observed. We identified a novel miR-196a target, NFKBIA, and down-regulation of miR-196a enhanced the expression of NFKBIA protein. Luciferase assay confirmed that NFKBIA was a direct and specific target of miR-196a. Silencing NFKBIA in PANC-1 cells enhanced its proliferation and migration. Taken together, our findings indicate that miR-196a is highly expressed in pancreatic cancer cell lines, and may play a crucial role in pancreatic cancer proliferation and migration, possibly through its downstream target, NFKBIA. Thus, miR-196a may serve as a potential therapeutic target for pancreatic cancer. |
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However, its function in pancreatic cancer has not been fully elucidated. Here, we investigated the expression pattern and the biological role of miR-196a in pancreatic cancer cell lines, as well as its interaction with a metastasis-related gene, nuclear factor-kappa-B-inhibitor alpha (NFKBIA). We demonstrated that miR-196a was up-regulated in human pancreatic cancer cell lines compared with immortalized pancreatic ductal epithelial cells by means of microRNAs microarray and qRT-PCR. Furthermore, down-regulation of miR-196a in PANC-1 suppressed its proliferation and migration with an increase in G0/G1 transition and decreased expression of Cyclin D1 and CDK4/6. Meanwhile, an increased expression in E-cadherin and decreased expression in N-cadherin and Vimentin were also observed. We identified a novel miR-196a target, NFKBIA, and down-regulation of miR-196a enhanced the expression of NFKBIA protein. Luciferase assay confirmed that NFKBIA was a direct and specific target of miR-196a. Silencing NFKBIA in PANC-1 cells enhanced its proliferation and migration. Taken together, our findings indicate that miR-196a is highly expressed in pancreatic cancer cell lines, and may play a crucial role in pancreatic cancer proliferation and migration, possibly through its downstream target, NFKBIA. Thus, miR-196a may serve as a potential therapeutic target for pancreatic cancer.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0087897</identifier><identifier>PMID: 24504166</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>3' Untranslated Regions ; Aberration ; Apoptosis ; Apoptosis - genetics ; Base Sequence ; Biology ; Biotechnology ; Cancer ; Cancer metastasis ; Cell Cycle - genetics ; Cell growth ; Cell Line, Tumor ; Cell Movement - genetics ; Cell Proliferation ; Cluster Analysis ; Colorectal cancer ; Comparative analysis ; Cyclin D1 ; Cyclin-dependent kinase 4 ; Disease Progression ; DNA microarrays ; E-cadherin ; Epithelial cells ; Gastroenterology ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Growth factors ; Humans ; I-kappa B Proteins - chemistry ; I-kappa B Proteins - genetics ; Inhibitors ; Luciferase ; Lymphoma ; Medical prognosis ; Medicine ; Melanoma ; Metastases ; Metastasis ; MicroRNA ; MicroRNAs ; MicroRNAs - chemistry ; MicroRNAs - genetics ; miRNA ; N-Cadherin ; NF-KappaB Inhibitor alpha ; Pancreatic cancer ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - pathology ; Penicillin ; RNA Interference ; Skin cancer ; Target recognition ; Tumor cell lines ; Vimentin</subject><ispartof>PloS one, 2014-02, Vol.9 (2), p.e87897-e87897</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Huang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Huang et al 2014 Huang et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-cb037d81236bb00c1db9b62a00adfaf39fd862e879427735a0af56c4f4b8500c3</citedby><cites>FETCH-LOGICAL-c758t-cb037d81236bb00c1db9b62a00adfaf39fd862e879427735a0af56c4f4b8500c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1494405620/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1494405620?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,25732,27903,27904,36991,36992,44569,53769,53771,74872</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24504166$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Cheng, Jin Q.</contributor><creatorcontrib>Huang, Fengting</creatorcontrib><creatorcontrib>Tang, Jian</creatorcontrib><creatorcontrib>Zhuang, Xiaohong</creatorcontrib><creatorcontrib>Zhuang, Yanyan</creatorcontrib><creatorcontrib>Cheng, Wenjie</creatorcontrib><creatorcontrib>Chen, Wenbo</creatorcontrib><creatorcontrib>Yao, Herui</creatorcontrib><creatorcontrib>Zhang, Shineng</creatorcontrib><title>MiR-196a promotes pancreatic cancer progression by targeting nuclear factor kappa-B-inhibitor alpha</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Aberrant expression of miR-196a has been frequently reported in different cancers including pancreatic cancer. However, its function in pancreatic cancer has not been fully elucidated. Here, we investigated the expression pattern and the biological role of miR-196a in pancreatic cancer cell lines, as well as its interaction with a metastasis-related gene, nuclear factor-kappa-B-inhibitor alpha (NFKBIA). We demonstrated that miR-196a was up-regulated in human pancreatic cancer cell lines compared with immortalized pancreatic ductal epithelial cells by means of microRNAs microarray and qRT-PCR. Furthermore, down-regulation of miR-196a in PANC-1 suppressed its proliferation and migration with an increase in G0/G1 transition and decreased expression of Cyclin D1 and CDK4/6. Meanwhile, an increased expression in E-cadherin and decreased expression in N-cadherin and Vimentin were also observed. We identified a novel miR-196a target, NFKBIA, and down-regulation of miR-196a enhanced the expression of NFKBIA protein. Luciferase assay confirmed that NFKBIA was a direct and specific target of miR-196a. Silencing NFKBIA in PANC-1 cells enhanced its proliferation and migration. Taken together, our findings indicate that miR-196a is highly expressed in pancreatic cancer cell lines, and may play a crucial role in pancreatic cancer proliferation and migration, possibly through its downstream target, NFKBIA. Thus, miR-196a may serve as a potential therapeutic target for pancreatic cancer.</description><subject>3' Untranslated Regions</subject><subject>Aberration</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Base Sequence</subject><subject>Biology</subject><subject>Biotechnology</subject><subject>Cancer</subject><subject>Cancer metastasis</subject><subject>Cell Cycle - genetics</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation</subject><subject>Cluster Analysis</subject><subject>Colorectal cancer</subject><subject>Comparative analysis</subject><subject>Cyclin D1</subject><subject>Cyclin-dependent kinase 4</subject><subject>Disease Progression</subject><subject>DNA microarrays</subject><subject>E-cadherin</subject><subject>Epithelial cells</subject><subject>Gastroenterology</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Silencing</subject><subject>Growth factors</subject><subject>Humans</subject><subject>I-kappa B Proteins - chemistry</subject><subject>I-kappa B Proteins - genetics</subject><subject>Inhibitors</subject><subject>Luciferase</subject><subject>Lymphoma</subject><subject>Medical prognosis</subject><subject>Medicine</subject><subject>Melanoma</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - chemistry</subject><subject>MicroRNAs - genetics</subject><subject>miRNA</subject><subject>N-Cadherin</subject><subject>NF-KappaB Inhibitor alpha</subject><subject>Pancreatic cancer</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Penicillin</subject><subject>RNA Interference</subject><subject>Skin cancer</subject><subject>Target recognition</subject><subject>Tumor cell lines</subject><subject>Vimentin</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNqNk01v1DAQhiMEomXhHyCIhITgkMWOHce5IJWKj5WKKpWPqzVxnKxL1k5tB9F_j9NNqw3qAflga_zMO57xTJI8x2iNSYnfXdrRGejXgzVqjRAveVU-SI5xRfKM5Yg8PDgfJU-8v0SoIJyxx8lRTgtEMWPHifyqLzJcMUgHZ3c2KJ8OYKRTELRMZTwqN111TnmvrUnr6zSA61TQpkvNKHsFLm1BBuvSXzAMkH3ItNnqWk8W6IctPE0etdB79WzeV8mPTx-_n37Jzs4_b05PzjJZFjxkskakbDjOCatrhCRu6qpmOSAETQstqdqGs1zxsqJ5WZICELQFk7SlNS8iT1bJy73u0Fsv5vp4gWlFKSqmOqySzZ5oLFyKwekduGthQYsbg3WdABcT75VgEktS4IYrVlBghBeVVMAJZnmR84ZGrfdztLHeqUYqExz0C9HljdFb0dnfglSYMDYJvJkFnL0alQ9ip71UfQ9G2fHm3VUsBiVlRF_9g96f3Ux1EBPQprUxrpxExQkteXw7plPY9T1UXI3aaRmbqdXRvnB4u3CITFB_Qgej92Lz7eL_2fOfS_b1AbtV0Iett_0YYpv5JUj3oHTWe6fauyJjJKZZuK2GmGZBzLMQ3V4cftCd023zk7_vcQNi</recordid><startdate>20140204</startdate><enddate>20140204</enddate><creator>Huang, Fengting</creator><creator>Tang, Jian</creator><creator>Zhuang, Xiaohong</creator><creator>Zhuang, Yanyan</creator><creator>Cheng, Wenjie</creator><creator>Chen, Wenbo</creator><creator>Yao, Herui</creator><creator>Zhang, Shineng</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140204</creationdate><title>MiR-196a promotes pancreatic cancer progression by targeting nuclear factor kappa-B-inhibitor alpha</title><author>Huang, Fengting ; Tang, Jian ; Zhuang, Xiaohong ; Zhuang, Yanyan ; Cheng, Wenjie ; Chen, Wenbo ; Yao, Herui ; Zhang, Shineng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-cb037d81236bb00c1db9b62a00adfaf39fd862e879427735a0af56c4f4b8500c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>3' Untranslated Regions</topic><topic>Aberration</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Base Sequence</topic><topic>Biology</topic><topic>Biotechnology</topic><topic>Cancer</topic><topic>Cancer metastasis</topic><topic>Cell Cycle - genetics</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation</topic><topic>Cluster Analysis</topic><topic>Colorectal cancer</topic><topic>Comparative analysis</topic><topic>Cyclin D1</topic><topic>Cyclin-dependent kinase 4</topic><topic>Disease Progression</topic><topic>DNA microarrays</topic><topic>E-cadherin</topic><topic>Epithelial cells</topic><topic>Gastroenterology</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Silencing</topic><topic>Growth factors</topic><topic>Humans</topic><topic>I-kappa B Proteins - chemistry</topic><topic>I-kappa B Proteins - genetics</topic><topic>Inhibitors</topic><topic>Luciferase</topic><topic>Lymphoma</topic><topic>Medical prognosis</topic><topic>Medicine</topic><topic>Melanoma</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - chemistry</topic><topic>MicroRNAs - genetics</topic><topic>miRNA</topic><topic>N-Cadherin</topic><topic>NF-KappaB Inhibitor alpha</topic><topic>Pancreatic cancer</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Penicillin</topic><topic>RNA Interference</topic><topic>Skin cancer</topic><topic>Target recognition</topic><topic>Tumor cell lines</topic><topic>Vimentin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Fengting</creatorcontrib><creatorcontrib>Tang, Jian</creatorcontrib><creatorcontrib>Zhuang, Xiaohong</creatorcontrib><creatorcontrib>Zhuang, Yanyan</creatorcontrib><creatorcontrib>Cheng, Wenjie</creatorcontrib><creatorcontrib>Chen, Wenbo</creatorcontrib><creatorcontrib>Yao, Herui</creatorcontrib><creatorcontrib>Zhang, Shineng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Opposing Viewpoints In Context</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>ProQuest Nursing and Allied Health Journals</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Complete (ProQuest Database)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Fengting</au><au>Tang, Jian</au><au>Zhuang, Xiaohong</au><au>Zhuang, Yanyan</au><au>Cheng, Wenjie</au><au>Chen, Wenbo</au><au>Yao, Herui</au><au>Zhang, Shineng</au><au>Cheng, Jin Q.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MiR-196a promotes pancreatic cancer progression by targeting nuclear factor kappa-B-inhibitor alpha</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-02-04</date><risdate>2014</risdate><volume>9</volume><issue>2</issue><spage>e87897</spage><epage>e87897</epage><pages>e87897-e87897</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Aberrant expression of miR-196a has been frequently reported in different cancers including pancreatic cancer. However, its function in pancreatic cancer has not been fully elucidated. Here, we investigated the expression pattern and the biological role of miR-196a in pancreatic cancer cell lines, as well as its interaction with a metastasis-related gene, nuclear factor-kappa-B-inhibitor alpha (NFKBIA). We demonstrated that miR-196a was up-regulated in human pancreatic cancer cell lines compared with immortalized pancreatic ductal epithelial cells by means of microRNAs microarray and qRT-PCR. Furthermore, down-regulation of miR-196a in PANC-1 suppressed its proliferation and migration with an increase in G0/G1 transition and decreased expression of Cyclin D1 and CDK4/6. Meanwhile, an increased expression in E-cadherin and decreased expression in N-cadherin and Vimentin were also observed. We identified a novel miR-196a target, NFKBIA, and down-regulation of miR-196a enhanced the expression of NFKBIA protein. Luciferase assay confirmed that NFKBIA was a direct and specific target of miR-196a. Silencing NFKBIA in PANC-1 cells enhanced its proliferation and migration. Taken together, our findings indicate that miR-196a is highly expressed in pancreatic cancer cell lines, and may play a crucial role in pancreatic cancer proliferation and migration, possibly through its downstream target, NFKBIA. Thus, miR-196a may serve as a potential therapeutic target for pancreatic cancer.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24504166</pmid><doi>10.1371/journal.pone.0087897</doi><tpages>e87897</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 3' Untranslated Regions Aberration Apoptosis Apoptosis - genetics Base Sequence Biology Biotechnology Cancer Cancer metastasis Cell Cycle - genetics Cell growth Cell Line, Tumor Cell Movement - genetics Cell Proliferation Cluster Analysis Colorectal cancer Comparative analysis Cyclin D1 Cyclin-dependent kinase 4 Disease Progression DNA microarrays E-cadherin Epithelial cells Gastroenterology Gene expression Gene Expression Profiling Gene Expression Regulation, Neoplastic Gene Silencing Growth factors Humans I-kappa B Proteins - chemistry I-kappa B Proteins - genetics Inhibitors Luciferase Lymphoma Medical prognosis Medicine Melanoma Metastases Metastasis MicroRNA MicroRNAs MicroRNAs - chemistry MicroRNAs - genetics miRNA N-Cadherin NF-KappaB Inhibitor alpha Pancreatic cancer Pancreatic Neoplasms - genetics Pancreatic Neoplasms - pathology Penicillin RNA Interference Skin cancer Target recognition Tumor cell lines Vimentin |
title | MiR-196a promotes pancreatic cancer progression by targeting nuclear factor kappa-B-inhibitor alpha |
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