IL-24 inhibits lung cancer cell migration and invasion by disrupting the SDF-1/CXCR4 signaling axis
The stromal cell derived factor (SDF)-1/chemokine receptor (CXCR)-4 signaling pathway plays a key role in lung cancer metastasis and is molecular target for therapy. In the present study we investigated whether interleukin (IL)-24 can inhibit the SDF-1/CXCR4 axis and suppress lung cancer cell migrat...
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| Veröffentlicht in: | PloS one 2015-03, Vol.10 (3), p.e0122439 |
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| creator | Panneerselvam, Janani Jin, Jiankang Shanker, Manish Lauderdale, Jason Bates, Jonathan Wang, Qi Zhao, Yan D Archibald, Stephen J Hubin, Timothy J Ramesh, Rajagopal |
| description | The stromal cell derived factor (SDF)-1/chemokine receptor (CXCR)-4 signaling pathway plays a key role in lung cancer metastasis and is molecular target for therapy. In the present study we investigated whether interleukin (IL)-24 can inhibit the SDF-1/CXCR4 axis and suppress lung cancer cell migration and invasion in vitro. Further, the efficacy of IL-24 in combination with CXCR4 antagonists was investigated.
Human H1299, A549, H460 and HCC827 lung cancer cell lines were used in the present study. The H1299 lung cancer cell line was stably transfected with doxycycline-inducible plasmid expression vector carrying the human IL-24 cDNA and used in the present study to determine the inhibitory effects of IL-24 on SDF-1/CXCR4 axis. H1299 and A549 cell lines were used in transient transfection studies. The inhibitory effects of IL-24 on SDF1/CXCR4 and its downstream targets were analyzed by quantitative RT-PCR, western blot, luciferase reporter assay, flow cytometry and immunocytochemistry. Functional studies included cell migration and invasion assays.
Endogenous CXCR4 protein expression levels varied among the four human lung cancer cell lines. Doxycycline-induced IL-24 expression in the H1299-IL24 cell line resulted in reduced CXCR4 mRNA and protein expression. IL-24 post-transcriptionally regulated CXCR4 mRNA expression by decreasing the half-life of CXCR4 mRNA (>40%). Functional studies showed IL-24 inhibited tumor cell migration and invasion concomitant with reduction in CXCR4 and its downstream targets (pAKTS473, pmTORS2448, pPRAS40T246 and HIF-1α). Additionally, IL-24 inhibited tumor cell migration both in the presence and absence of the CXCR4 agonist, SDF-1. Finally, IL-24 when combined with CXCR4 inhibitors (AMD3100, SJA5) or with CXCR4 siRNA demonstrated enhanced inhibitory activity on tumor cell migration.
IL-24 disrupts the SDF-1/CXCR4 signaling pathway and inhibits lung tumor cell migration and invasion. Additionally, IL-24, when combined with CXCR4 inhibitors exhibited enhanced anti-metastatic activity and is an attractive therapeutic strategy for lung metastasis. |
| doi_str_mv | 10.1371/journal.pone.0122439 |
| format | Article |
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Human H1299, A549, H460 and HCC827 lung cancer cell lines were used in the present study. The H1299 lung cancer cell line was stably transfected with doxycycline-inducible plasmid expression vector carrying the human IL-24 cDNA and used in the present study to determine the inhibitory effects of IL-24 on SDF-1/CXCR4 axis. H1299 and A549 cell lines were used in transient transfection studies. The inhibitory effects of IL-24 on SDF1/CXCR4 and its downstream targets were analyzed by quantitative RT-PCR, western blot, luciferase reporter assay, flow cytometry and immunocytochemistry. Functional studies included cell migration and invasion assays.
Endogenous CXCR4 protein expression levels varied among the four human lung cancer cell lines. Doxycycline-induced IL-24 expression in the H1299-IL24 cell line resulted in reduced CXCR4 mRNA and protein expression. IL-24 post-transcriptionally regulated CXCR4 mRNA expression by decreasing the half-life of CXCR4 mRNA (>40%). Functional studies showed IL-24 inhibited tumor cell migration and invasion concomitant with reduction in CXCR4 and its downstream targets (pAKTS473, pmTORS2448, pPRAS40T246 and HIF-1α). Additionally, IL-24 inhibited tumor cell migration both in the presence and absence of the CXCR4 agonist, SDF-1. Finally, IL-24 when combined with CXCR4 inhibitors (AMD3100, SJA5) or with CXCR4 siRNA demonstrated enhanced inhibitory activity on tumor cell migration.
IL-24 disrupts the SDF-1/CXCR4 signaling pathway and inhibits lung tumor cell migration and invasion. Additionally, IL-24, when combined with CXCR4 inhibitors exhibited enhanced anti-metastatic activity and is an attractive therapeutic strategy for lung metastasis.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0122439</identifier><identifier>PMID: 25775124</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Biotechnology ; Cancer ; Cancer metastasis ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - metabolism ; Carcinoma, Non-Small-Cell Lung - pathology ; Cell adhesion & migration ; Cell Line, Tumor ; Cell migration ; Cell Movement - drug effects ; Cell Movement - genetics ; Chemokine CXCL12 - metabolism ; Chemokines ; CXCR4 protein ; Cytokines ; Cytometry ; Downstream ; Doxycycline ; Drug Synergism ; Flow cytometry ; Gene Expression ; Gene Expression Regulation, Neoplastic ; Gene therapy ; Genetic vectors ; Health aspects ; Health sciences ; Heart surgery ; Heterocyclic Compounds - pharmacology ; Humans ; Immunocytochemistry ; Inhibitors ; Interleukin 24 ; Interleukins ; Interleukins - genetics ; Interleukins - pharmacology ; Leukemia ; Ligands ; Luciferase ; Lung cancer ; Lung diseases ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; Melanoma ; Metastases ; Metastasis ; Pathology ; Polymerase chain reaction ; Post-transcription ; Protein expression ; Proteins ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; Receptors, CXCR4 - antagonists & inhibitors ; Receptors, CXCR4 - genetics ; Receptors, CXCR4 - metabolism ; RNA ; RNA, Small Interfering ; SDF-1 protein ; Signal transduction ; Signal Transduction - drug effects ; Signaling ; siRNA ; Studies ; TOR Serine-Threonine Kinases - metabolism ; Transfection ; Tumor cell lines ; Tumors</subject><ispartof>PloS one, 2015-03, Vol.10 (3), p.e0122439</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Panneerselvam 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>2015 Panneerselvam et al 2015 Panneerselvam et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-a09689654492790b6f61b9350da0690de2fd24f76427938248a835eab97d64223</citedby><cites>FETCH-LOGICAL-c692t-a09689654492790b6f61b9350da0690de2fd24f76427938248a835eab97d64223</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4361489/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4361489/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,2914,23846,27903,27904,53769,53771,79346,79347</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25775124$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Singh, Ajay Pratap</contributor><creatorcontrib>Panneerselvam, Janani</creatorcontrib><creatorcontrib>Jin, Jiankang</creatorcontrib><creatorcontrib>Shanker, Manish</creatorcontrib><creatorcontrib>Lauderdale, Jason</creatorcontrib><creatorcontrib>Bates, Jonathan</creatorcontrib><creatorcontrib>Wang, Qi</creatorcontrib><creatorcontrib>Zhao, Yan D</creatorcontrib><creatorcontrib>Archibald, Stephen J</creatorcontrib><creatorcontrib>Hubin, Timothy J</creatorcontrib><creatorcontrib>Ramesh, Rajagopal</creatorcontrib><title>IL-24 inhibits lung cancer cell migration and invasion by disrupting the SDF-1/CXCR4 signaling axis</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The stromal cell derived factor (SDF)-1/chemokine receptor (CXCR)-4 signaling pathway plays a key role in lung cancer metastasis and is molecular target for therapy. In the present study we investigated whether interleukin (IL)-24 can inhibit the SDF-1/CXCR4 axis and suppress lung cancer cell migration and invasion in vitro. Further, the efficacy of IL-24 in combination with CXCR4 antagonists was investigated.
Human H1299, A549, H460 and HCC827 lung cancer cell lines were used in the present study. The H1299 lung cancer cell line was stably transfected with doxycycline-inducible plasmid expression vector carrying the human IL-24 cDNA and used in the present study to determine the inhibitory effects of IL-24 on SDF-1/CXCR4 axis. H1299 and A549 cell lines were used in transient transfection studies. The inhibitory effects of IL-24 on SDF1/CXCR4 and its downstream targets were analyzed by quantitative RT-PCR, western blot, luciferase reporter assay, flow cytometry and immunocytochemistry. Functional studies included cell migration and invasion assays.
Endogenous CXCR4 protein expression levels varied among the four human lung cancer cell lines. Doxycycline-induced IL-24 expression in the H1299-IL24 cell line resulted in reduced CXCR4 mRNA and protein expression. IL-24 post-transcriptionally regulated CXCR4 mRNA expression by decreasing the half-life of CXCR4 mRNA (>40%). Functional studies showed IL-24 inhibited tumor cell migration and invasion concomitant with reduction in CXCR4 and its downstream targets (pAKTS473, pmTORS2448, pPRAS40T246 and HIF-1α). Additionally, IL-24 inhibited tumor cell migration both in the presence and absence of the CXCR4 agonist, SDF-1. Finally, IL-24 when combined with CXCR4 inhibitors (AMD3100, SJA5) or with CXCR4 siRNA demonstrated enhanced inhibitory activity on tumor cell migration.
IL-24 disrupts the SDF-1/CXCR4 signaling pathway and inhibits lung tumor cell migration and invasion. Additionally, IL-24, when combined with CXCR4 inhibitors exhibited enhanced anti-metastatic activity and is an attractive therapeutic strategy for lung metastasis.</description><subject>Biotechnology</subject><subject>Cancer</subject><subject>Cancer metastasis</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - metabolism</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Cell adhesion & migration</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - drug effects</subject><subject>Cell Movement - genetics</subject><subject>Chemokine CXCL12 - metabolism</subject><subject>Chemokines</subject><subject>CXCR4 protein</subject><subject>Cytokines</subject><subject>Cytometry</subject><subject>Downstream</subject><subject>Doxycycline</subject><subject>Drug Synergism</subject><subject>Flow cytometry</subject><subject>Gene Expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene therapy</subject><subject>Genetic vectors</subject><subject>Health aspects</subject><subject>Health sciences</subject><subject>Heart surgery</subject><subject>Heterocyclic Compounds - pharmacology</subject><subject>Humans</subject><subject>Immunocytochemistry</subject><subject>Inhibitors</subject><subject>Interleukin 24</subject><subject>Interleukins</subject><subject>Interleukins - genetics</subject><subject>Interleukins - pharmacology</subject><subject>Leukemia</subject><subject>Ligands</subject><subject>Luciferase</subject><subject>Lung cancer</subject><subject>Lung diseases</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>Melanoma</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Pathology</subject><subject>Polymerase chain reaction</subject><subject>Post-transcription</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Receptors, CXCR4 - antagonists & inhibitors</subject><subject>Receptors, CXCR4 - 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genetics</topic><topic>Interleukins - pharmacology</topic><topic>Leukemia</topic><topic>Ligands</topic><topic>Luciferase</topic><topic>Lung cancer</topic><topic>Lung diseases</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>Melanoma</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Pathology</topic><topic>Polymerase chain reaction</topic><topic>Post-transcription</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Receptors, CXCR4 - antagonists & inhibitors</topic><topic>Receptors, CXCR4 - genetics</topic><topic>Receptors, CXCR4 - metabolism</topic><topic>RNA</topic><topic>RNA, Small Interfering</topic><topic>SDF-1 protein</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Signaling</topic><topic>siRNA</topic><topic>Studies</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><topic>Transfection</topic><topic>Tumor cell lines</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Panneerselvam, Janani</creatorcontrib><creatorcontrib>Jin, Jiankang</creatorcontrib><creatorcontrib>Shanker, Manish</creatorcontrib><creatorcontrib>Lauderdale, Jason</creatorcontrib><creatorcontrib>Bates, Jonathan</creatorcontrib><creatorcontrib>Wang, Qi</creatorcontrib><creatorcontrib>Zhao, Yan D</creatorcontrib><creatorcontrib>Archibald, Stephen J</creatorcontrib><creatorcontrib>Hubin, Timothy J</creatorcontrib><creatorcontrib>Ramesh, Rajagopal</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</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>Nursing & Allied Health Database</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 Collection</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 Edition)</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>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 Korea</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>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</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>Panneerselvam, Janani</au><au>Jin, Jiankang</au><au>Shanker, Manish</au><au>Lauderdale, Jason</au><au>Bates, Jonathan</au><au>Wang, Qi</au><au>Zhao, Yan D</au><au>Archibald, Stephen J</au><au>Hubin, Timothy J</au><au>Ramesh, Rajagopal</au><au>Singh, Ajay Pratap</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IL-24 inhibits lung cancer cell migration and invasion by disrupting the SDF-1/CXCR4 signaling axis</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-03-16</date><risdate>2015</risdate><volume>10</volume><issue>3</issue><spage>e0122439</spage><pages>e0122439-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The stromal cell derived factor (SDF)-1/chemokine receptor (CXCR)-4 signaling pathway plays a key role in lung cancer metastasis and is molecular target for therapy. In the present study we investigated whether interleukin (IL)-24 can inhibit the SDF-1/CXCR4 axis and suppress lung cancer cell migration and invasion in vitro. Further, the efficacy of IL-24 in combination with CXCR4 antagonists was investigated.
Human H1299, A549, H460 and HCC827 lung cancer cell lines were used in the present study. The H1299 lung cancer cell line was stably transfected with doxycycline-inducible plasmid expression vector carrying the human IL-24 cDNA and used in the present study to determine the inhibitory effects of IL-24 on SDF-1/CXCR4 axis. H1299 and A549 cell lines were used in transient transfection studies. The inhibitory effects of IL-24 on SDF1/CXCR4 and its downstream targets were analyzed by quantitative RT-PCR, western blot, luciferase reporter assay, flow cytometry and immunocytochemistry. Functional studies included cell migration and invasion assays.
Endogenous CXCR4 protein expression levels varied among the four human lung cancer cell lines. Doxycycline-induced IL-24 expression in the H1299-IL24 cell line resulted in reduced CXCR4 mRNA and protein expression. IL-24 post-transcriptionally regulated CXCR4 mRNA expression by decreasing the half-life of CXCR4 mRNA (>40%). Functional studies showed IL-24 inhibited tumor cell migration and invasion concomitant with reduction in CXCR4 and its downstream targets (pAKTS473, pmTORS2448, pPRAS40T246 and HIF-1α). Additionally, IL-24 inhibited tumor cell migration both in the presence and absence of the CXCR4 agonist, SDF-1. Finally, IL-24 when combined with CXCR4 inhibitors (AMD3100, SJA5) or with CXCR4 siRNA demonstrated enhanced inhibitory activity on tumor cell migration.
IL-24 disrupts the SDF-1/CXCR4 signaling pathway and inhibits lung tumor cell migration and invasion. Additionally, IL-24, when combined with CXCR4 inhibitors exhibited enhanced anti-metastatic activity and is an attractive therapeutic strategy for lung metastasis.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25775124</pmid><doi>10.1371/journal.pone.0122439</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2015-03, Vol.10 (3), p.e0122439 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1663911897 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Biotechnology Cancer Cancer metastasis Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - metabolism Carcinoma, Non-Small-Cell Lung - pathology Cell adhesion & migration Cell Line, Tumor Cell migration Cell Movement - drug effects Cell Movement - genetics Chemokine CXCL12 - metabolism Chemokines CXCR4 protein Cytokines Cytometry Downstream Doxycycline Drug Synergism Flow cytometry Gene Expression Gene Expression Regulation, Neoplastic Gene therapy Genetic vectors Health aspects Health sciences Heart surgery Heterocyclic Compounds - pharmacology Humans Immunocytochemistry Inhibitors Interleukin 24 Interleukins Interleukins - genetics Interleukins - pharmacology Leukemia Ligands Luciferase Lung cancer Lung diseases Lung Neoplasms - genetics Lung Neoplasms - metabolism Lung Neoplasms - pathology Melanoma Metastases Metastasis Pathology Polymerase chain reaction Post-transcription Protein expression Proteins Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Receptors, CXCR4 - antagonists & inhibitors Receptors, CXCR4 - genetics Receptors, CXCR4 - metabolism RNA RNA, Small Interfering SDF-1 protein Signal transduction Signal Transduction - drug effects Signaling siRNA Studies TOR Serine-Threonine Kinases - metabolism Transfection Tumor cell lines Tumors |
| title | IL-24 inhibits lung cancer cell migration and invasion by disrupting the SDF-1/CXCR4 signaling axis |
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