The Expression Levels of IL-4/IL-13/STAT6 Signaling Pathway Genes and SOCS3 Could Help to Differentiate the Histopathological Subtypes of Non-Small Cell Lung Carcinoma
Background The interleukin (IL)-4/IL-13/signal transducer and activator of transcription (STAT) 6 signaling pathway and the SOCS3 gene, one of its main regulators, constitute an important link between the inflammation process in the epithelial cells and inflammatory-related tumorigenesis. The presen...
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creator | Pastuszak-Lewandoska, Dorota Domańska-Senderowska, Daria Antczak, Adam Kordiak, Jacek Górski, Paweł Czarnecka, Karolina H. Migdalska-Sęk, Monika Nawrot, Ewa Kiszałkiewicz, Justyna M. Brzeziańska-Lasota, Ewa |
description | Background
The interleukin (IL)-4/IL-13/signal transducer and activator of transcription (STAT) 6 signaling pathway and the
SOCS3
gene, one of its main regulators, constitute an important link between the inflammation process in the epithelial cells and inflammatory-related tumorigenesis. The present study is the first to evaluate
IL-4, IL-13, STAT6
, and
SOCS3
mRNA expression in non-small cell lung carcinoma (NSCLC) histopathological subtypes.
Methods
Gene expression levels were assessed using TaqMan
®
probes by quantitative reverse transcription PCR (qRT-PCR) in lung tumor samples and unchanged lung tissue samples.
Results
Increased expression of
IL-4
,
IL-13
, and
STAT6
was observed in all histopathological NSCLC subtypes (squamous cell carcinoma [SCC], adenocarcinoma [AC], and large cell carcinoma [LCC]). Significantly higher expression of
IL-13
and
STAT6
(
p
= 0.019 and
p
= 0.008, respectively) was found in SCC than in LCC. No statistically significant differences were found for
IL-4
. Significantly higher
SOCS3
expression was found in LCC than in AC (
p
= 0.027). A negative correlation (rho = –0.519) was observed for the
STAT6
and
SOCS3
genes in SCC (
p
= 0.005). No associations were found between gene expression and tumor staging (post-operative Tumor Node Metastasis [pTNM], American Joint Committee on Cancer [AJCC]), patients’ age, sex, or history of smoking.
Conclusions
As the number of LCC cases in our study was quite low, the statistically significant results obtained should be confirmed in a larger group of patients, particularly as the relationships identified between increased
IL-4, IL-13,
and
STAT6 mRNA
expression and decreased
SOCS3
expression suggest that these genes may serve as potential diagnostic markers for differentiating between NSCLC histopathological subtypes. |
doi_str_mv | 10.1007/s40291-018-0355-7 |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6132440</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2193094241</sourcerecordid><originalsourceid>FETCH-LOGICAL-c470t-db2acc984e6a6e120b08acd416437e4bf58b99fe2cfb53d91b2d6fd08c8adadb3</originalsourceid><addsrcrecordid>eNp1UUtv1DAQjhCIlsIP4IIscQ47fuR1QarS0q0UUaQsZ8txJruuvHGwk8L-Iv4mbrcUOHCZGWm-x2i-JHlL4QMFKFZBAKtoCrRMgWdZWjxLTiktqpQBwPOHuUgp5OwkeRXCLYDI8oq9TE44UMgKnp0mPzc7JJc_Jo8hGDeSBu_QBuIGct2kYhUL5at2c77JSWu2o7Jm3JIvat59VwdyhSMGosaetDd1y0ntFtuTNdqJzI5cmGFAj-Ns1Ixkjj5rE2Y3RbKzbmu0sqRduvkw4YPhZzem7V5ZS2qMpVmiU628NqPbq9fJi0HZgG8e-1ny9dPlpl6nzc3VdX3epFoUMKd9x5TWVSkwVzlSBh2USveC5oIXKLohK7uqGpDpoct4X9GO9fnQQ6lL1au-42fJx6PutHR77HU83ysrJ2_2yh-kU0b-uxnNTm7dncwpZ0JAFHj_KODdtwXDLG_d4uPjgmS04lAJJmhE0SNKexeCx-HJgYK8z1Yes5UxW3mfrSwi593fpz0xfocZAewICHE1btH_sf6_6i-pZ7D7</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2193094241</pqid></control><display><type>article</type><title>The Expression Levels of IL-4/IL-13/STAT6 Signaling Pathway Genes and SOCS3 Could Help to Differentiate the Histopathological Subtypes of Non-Small Cell Lung Carcinoma</title><source>MEDLINE</source><source>Springer Online Journals</source><creator>Pastuszak-Lewandoska, Dorota ; Domańska-Senderowska, Daria ; Antczak, Adam ; Kordiak, Jacek ; Górski, Paweł ; Czarnecka, Karolina H. ; Migdalska-Sęk, Monika ; Nawrot, Ewa ; Kiszałkiewicz, Justyna M. ; Brzeziańska-Lasota, Ewa</creator><creatorcontrib>Pastuszak-Lewandoska, Dorota ; Domańska-Senderowska, Daria ; Antczak, Adam ; Kordiak, Jacek ; Górski, Paweł ; Czarnecka, Karolina H. ; Migdalska-Sęk, Monika ; Nawrot, Ewa ; Kiszałkiewicz, Justyna M. ; Brzeziańska-Lasota, Ewa</creatorcontrib><description>Background
The interleukin (IL)-4/IL-13/signal transducer and activator of transcription (STAT) 6 signaling pathway and the
SOCS3
gene, one of its main regulators, constitute an important link between the inflammation process in the epithelial cells and inflammatory-related tumorigenesis. The present study is the first to evaluate
IL-4, IL-13, STAT6
, and
SOCS3
mRNA expression in non-small cell lung carcinoma (NSCLC) histopathological subtypes.
Methods
Gene expression levels were assessed using TaqMan
®
probes by quantitative reverse transcription PCR (qRT-PCR) in lung tumor samples and unchanged lung tissue samples.
Results
Increased expression of
IL-4
,
IL-13
, and
STAT6
was observed in all histopathological NSCLC subtypes (squamous cell carcinoma [SCC], adenocarcinoma [AC], and large cell carcinoma [LCC]). Significantly higher expression of
IL-13
and
STAT6
(
p
= 0.019 and
p
= 0.008, respectively) was found in SCC than in LCC. No statistically significant differences were found for
IL-4
. Significantly higher
SOCS3
expression was found in LCC than in AC (
p
= 0.027). A negative correlation (rho = –0.519) was observed for the
STAT6
and
SOCS3
genes in SCC (
p
= 0.005). No associations were found between gene expression and tumor staging (post-operative Tumor Node Metastasis [pTNM], American Joint Committee on Cancer [AJCC]), patients’ age, sex, or history of smoking.
Conclusions
As the number of LCC cases in our study was quite low, the statistically significant results obtained should be confirmed in a larger group of patients, particularly as the relationships identified between increased
IL-4, IL-13,
and
STAT6 mRNA
expression and decreased
SOCS3
expression suggest that these genes may serve as potential diagnostic markers for differentiating between NSCLC histopathological subtypes.</description><identifier>ISSN: 1177-1062</identifier><identifier>EISSN: 1179-2000</identifier><identifier>DOI: 10.1007/s40291-018-0355-7</identifier><identifier>PMID: 30105735</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Adenocarcinoma ; Aged ; Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Breast cancer ; Cancer Research ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - metabolism ; Carcinoma, Non-Small-Cell Lung - pathology ; Cell Line, Tumor ; Cytokines ; Diagnostic systems ; Epithelial cells ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genes ; Growth factors ; Human Genetics ; Humans ; Inflammation ; Inflammatory diseases ; Interleukin 13 ; Interleukin 4 ; Interleukin-13 - genetics ; Interleukin-4 - genetics ; Kinases ; Laboratory Medicine ; Lung cancer ; Lung carcinoma ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; Male ; Metastases ; Middle Aged ; Molecular Medicine ; Neoplasm Grading ; Neoplasm Staging ; Non-small cell lung carcinoma ; Original ; Original Research Article ; Patients ; Pharmacotherapy ; Prostate cancer ; Proteins ; Regulators ; Reverse transcription ; Samples ; Signal Transduction ; Signaling ; Small cell lung carcinoma ; Smoking ; Squamous cell carcinoma ; Stat6 protein ; STAT6 Transcription Factor - metabolism ; Statistical analysis ; Statistical methods ; Statistical significance ; Studies ; Suppressor of Cytokine Signaling 3 Protein - genetics ; Thoracic surgery ; Tumorigenesis ; Tumors</subject><ispartof>Molecular diagnosis & therapy, 2018-10, Vol.22 (5), p.621-629</ispartof><rights>The Author(s) 2018</rights><rights>Copyright Springer Nature B.V. Oct 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-db2acc984e6a6e120b08acd416437e4bf58b99fe2cfb53d91b2d6fd08c8adadb3</citedby><cites>FETCH-LOGICAL-c470t-db2acc984e6a6e120b08acd416437e4bf58b99fe2cfb53d91b2d6fd08c8adadb3</cites><orcidid>0000-0001-7602-9203</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s40291-018-0355-7$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s40291-018-0355-7$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30105735$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pastuszak-Lewandoska, Dorota</creatorcontrib><creatorcontrib>Domańska-Senderowska, Daria</creatorcontrib><creatorcontrib>Antczak, Adam</creatorcontrib><creatorcontrib>Kordiak, Jacek</creatorcontrib><creatorcontrib>Górski, Paweł</creatorcontrib><creatorcontrib>Czarnecka, Karolina H.</creatorcontrib><creatorcontrib>Migdalska-Sęk, Monika</creatorcontrib><creatorcontrib>Nawrot, Ewa</creatorcontrib><creatorcontrib>Kiszałkiewicz, Justyna M.</creatorcontrib><creatorcontrib>Brzeziańska-Lasota, Ewa</creatorcontrib><title>The Expression Levels of IL-4/IL-13/STAT6 Signaling Pathway Genes and SOCS3 Could Help to Differentiate the Histopathological Subtypes of Non-Small Cell Lung Carcinoma</title><title>Molecular diagnosis & therapy</title><addtitle>Mol Diagn Ther</addtitle><addtitle>Mol Diagn Ther</addtitle><description>Background
The interleukin (IL)-4/IL-13/signal transducer and activator of transcription (STAT) 6 signaling pathway and the
SOCS3
gene, one of its main regulators, constitute an important link between the inflammation process in the epithelial cells and inflammatory-related tumorigenesis. The present study is the first to evaluate
IL-4, IL-13, STAT6
, and
SOCS3
mRNA expression in non-small cell lung carcinoma (NSCLC) histopathological subtypes.
Methods
Gene expression levels were assessed using TaqMan
®
probes by quantitative reverse transcription PCR (qRT-PCR) in lung tumor samples and unchanged lung tissue samples.
Results
Increased expression of
IL-4
,
IL-13
, and
STAT6
was observed in all histopathological NSCLC subtypes (squamous cell carcinoma [SCC], adenocarcinoma [AC], and large cell carcinoma [LCC]). Significantly higher expression of
IL-13
and
STAT6
(
p
= 0.019 and
p
= 0.008, respectively) was found in SCC than in LCC. No statistically significant differences were found for
IL-4
. Significantly higher
SOCS3
expression was found in LCC than in AC (
p
= 0.027). A negative correlation (rho = –0.519) was observed for the
STAT6
and
SOCS3
genes in SCC (
p
= 0.005). No associations were found between gene expression and tumor staging (post-operative Tumor Node Metastasis [pTNM], American Joint Committee on Cancer [AJCC]), patients’ age, sex, or history of smoking.
Conclusions
As the number of LCC cases in our study was quite low, the statistically significant results obtained should be confirmed in a larger group of patients, particularly as the relationships identified between increased
IL-4, IL-13,
and
STAT6 mRNA
expression and decreased
SOCS3
expression suggest that these genes may serve as potential diagnostic markers for differentiating between NSCLC histopathological subtypes.</description><subject>Adenocarcinoma</subject><subject>Aged</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Breast cancer</subject><subject>Cancer Research</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 Line, Tumor</subject><subject>Cytokines</subject><subject>Diagnostic systems</subject><subject>Epithelial cells</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Growth factors</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammatory diseases</subject><subject>Interleukin 13</subject><subject>Interleukin 4</subject><subject>Interleukin-13 - genetics</subject><subject>Interleukin-4 - genetics</subject><subject>Kinases</subject><subject>Laboratory Medicine</subject><subject>Lung cancer</subject><subject>Lung carcinoma</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>Male</subject><subject>Metastases</subject><subject>Middle Aged</subject><subject>Molecular Medicine</subject><subject>Neoplasm Grading</subject><subject>Neoplasm Staging</subject><subject>Non-small cell lung carcinoma</subject><subject>Original</subject><subject>Original Research Article</subject><subject>Patients</subject><subject>Pharmacotherapy</subject><subject>Prostate cancer</subject><subject>Proteins</subject><subject>Regulators</subject><subject>Reverse transcription</subject><subject>Samples</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Small cell lung carcinoma</subject><subject>Smoking</subject><subject>Squamous cell carcinoma</subject><subject>Stat6 protein</subject><subject>STAT6 Transcription Factor - metabolism</subject><subject>Statistical analysis</subject><subject>Statistical methods</subject><subject>Statistical significance</subject><subject>Studies</subject><subject>Suppressor of Cytokine Signaling 3 Protein - genetics</subject><subject>Thoracic surgery</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><issn>1177-1062</issn><issn>1179-2000</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1UUtv1DAQjhCIlsIP4IIscQ47fuR1QarS0q0UUaQsZ8txJruuvHGwk8L-Iv4mbrcUOHCZGWm-x2i-JHlL4QMFKFZBAKtoCrRMgWdZWjxLTiktqpQBwPOHuUgp5OwkeRXCLYDI8oq9TE44UMgKnp0mPzc7JJc_Jo8hGDeSBu_QBuIGct2kYhUL5at2c77JSWu2o7Jm3JIvat59VwdyhSMGosaetDd1y0ntFtuTNdqJzI5cmGFAj-Ns1Ixkjj5rE2Y3RbKzbmu0sqRduvkw4YPhZzem7V5ZS2qMpVmiU628NqPbq9fJi0HZgG8e-1ny9dPlpl6nzc3VdX3epFoUMKd9x5TWVSkwVzlSBh2USveC5oIXKLohK7uqGpDpoct4X9GO9fnQQ6lL1au-42fJx6PutHR77HU83ysrJ2_2yh-kU0b-uxnNTm7dncwpZ0JAFHj_KODdtwXDLG_d4uPjgmS04lAJJmhE0SNKexeCx-HJgYK8z1Yes5UxW3mfrSwi593fpz0xfocZAewICHE1btH_sf6_6i-pZ7D7</recordid><startdate>20181001</startdate><enddate>20181001</enddate><creator>Pastuszak-Lewandoska, Dorota</creator><creator>Domańska-Senderowska, Daria</creator><creator>Antczak, Adam</creator><creator>Kordiak, Jacek</creator><creator>Górski, Paweł</creator><creator>Czarnecka, Karolina H.</creator><creator>Migdalska-Sęk, Monika</creator><creator>Nawrot, Ewa</creator><creator>Kiszałkiewicz, Justyna M.</creator><creator>Brzeziańska-Lasota, Ewa</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>C6C</scope><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>3V.</scope><scope>4T-</scope><scope>7QO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7602-9203</orcidid></search><sort><creationdate>20181001</creationdate><title>The Expression Levels of IL-4/IL-13/STAT6 Signaling Pathway Genes and SOCS3 Could Help to Differentiate the Histopathological Subtypes of Non-Small Cell Lung Carcinoma</title><author>Pastuszak-Lewandoska, Dorota ; Domańska-Senderowska, Daria ; Antczak, Adam ; Kordiak, Jacek ; Górski, Paweł ; Czarnecka, Karolina H. ; Migdalska-Sęk, Monika ; Nawrot, Ewa ; Kiszałkiewicz, Justyna M. ; Brzeziańska-Lasota, Ewa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-db2acc984e6a6e120b08acd416437e4bf58b99fe2cfb53d91b2d6fd08c8adadb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adenocarcinoma</topic><topic>Aged</topic><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Breast cancer</topic><topic>Cancer Research</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - metabolism</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cytokines</topic><topic>Diagnostic systems</topic><topic>Epithelial cells</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>Growth factors</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammatory diseases</topic><topic>Interleukin 13</topic><topic>Interleukin 4</topic><topic>Interleukin-13 - genetics</topic><topic>Interleukin-4 - genetics</topic><topic>Kinases</topic><topic>Laboratory Medicine</topic><topic>Lung cancer</topic><topic>Lung carcinoma</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>Male</topic><topic>Metastases</topic><topic>Middle Aged</topic><topic>Molecular Medicine</topic><topic>Neoplasm Grading</topic><topic>Neoplasm Staging</topic><topic>Non-small cell lung carcinoma</topic><topic>Original</topic><topic>Original Research Article</topic><topic>Patients</topic><topic>Pharmacotherapy</topic><topic>Prostate cancer</topic><topic>Proteins</topic><topic>Regulators</topic><topic>Reverse transcription</topic><topic>Samples</topic><topic>Signal Transduction</topic><topic>Signaling</topic><topic>Small cell lung carcinoma</topic><topic>Smoking</topic><topic>Squamous cell carcinoma</topic><topic>Stat6 protein</topic><topic>STAT6 Transcription Factor - metabolism</topic><topic>Statistical analysis</topic><topic>Statistical methods</topic><topic>Statistical significance</topic><topic>Studies</topic><topic>Suppressor of Cytokine Signaling 3 Protein - genetics</topic><topic>Thoracic surgery</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><toplevel>online_resources</toplevel><creatorcontrib>Pastuszak-Lewandoska, Dorota</creatorcontrib><creatorcontrib>Domańska-Senderowska, Daria</creatorcontrib><creatorcontrib>Antczak, Adam</creatorcontrib><creatorcontrib>Kordiak, Jacek</creatorcontrib><creatorcontrib>Górski, Paweł</creatorcontrib><creatorcontrib>Czarnecka, Karolina H.</creatorcontrib><creatorcontrib>Migdalska-Sęk, Monika</creatorcontrib><creatorcontrib>Nawrot, Ewa</creatorcontrib><creatorcontrib>Kiszałkiewicz, Justyna M.</creatorcontrib><creatorcontrib>Brzeziańska-Lasota, Ewa</creatorcontrib><collection>SpringerOpen</collection><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>Docstoc</collection><collection>Biotechnology Research Abstracts</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Biotechnology and BioEngineering Abstracts</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>Molecular diagnosis & therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pastuszak-Lewandoska, Dorota</au><au>Domańska-Senderowska, Daria</au><au>Antczak, Adam</au><au>Kordiak, Jacek</au><au>Górski, Paweł</au><au>Czarnecka, Karolina H.</au><au>Migdalska-Sęk, Monika</au><au>Nawrot, Ewa</au><au>Kiszałkiewicz, Justyna M.</au><au>Brzeziańska-Lasota, Ewa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Expression Levels of IL-4/IL-13/STAT6 Signaling Pathway Genes and SOCS3 Could Help to Differentiate the Histopathological Subtypes of Non-Small Cell Lung Carcinoma</atitle><jtitle>Molecular diagnosis & therapy</jtitle><stitle>Mol Diagn Ther</stitle><addtitle>Mol Diagn Ther</addtitle><date>2018-10-01</date><risdate>2018</risdate><volume>22</volume><issue>5</issue><spage>621</spage><epage>629</epage><pages>621-629</pages><issn>1177-1062</issn><eissn>1179-2000</eissn><abstract>Background
The interleukin (IL)-4/IL-13/signal transducer and activator of transcription (STAT) 6 signaling pathway and the
SOCS3
gene, one of its main regulators, constitute an important link between the inflammation process in the epithelial cells and inflammatory-related tumorigenesis. The present study is the first to evaluate
IL-4, IL-13, STAT6
, and
SOCS3
mRNA expression in non-small cell lung carcinoma (NSCLC) histopathological subtypes.
Methods
Gene expression levels were assessed using TaqMan
®
probes by quantitative reverse transcription PCR (qRT-PCR) in lung tumor samples and unchanged lung tissue samples.
Results
Increased expression of
IL-4
,
IL-13
, and
STAT6
was observed in all histopathological NSCLC subtypes (squamous cell carcinoma [SCC], adenocarcinoma [AC], and large cell carcinoma [LCC]). Significantly higher expression of
IL-13
and
STAT6
(
p
= 0.019 and
p
= 0.008, respectively) was found in SCC than in LCC. No statistically significant differences were found for
IL-4
. Significantly higher
SOCS3
expression was found in LCC than in AC (
p
= 0.027). A negative correlation (rho = –0.519) was observed for the
STAT6
and
SOCS3
genes in SCC (
p
= 0.005). No associations were found between gene expression and tumor staging (post-operative Tumor Node Metastasis [pTNM], American Joint Committee on Cancer [AJCC]), patients’ age, sex, or history of smoking.
Conclusions
As the number of LCC cases in our study was quite low, the statistically significant results obtained should be confirmed in a larger group of patients, particularly as the relationships identified between increased
IL-4, IL-13,
and
STAT6 mRNA
expression and decreased
SOCS3
expression suggest that these genes may serve as potential diagnostic markers for differentiating between NSCLC histopathological subtypes.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>30105735</pmid><doi>10.1007/s40291-018-0355-7</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0001-7602-9203</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1177-1062 |
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issn | 1177-1062 1179-2000 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6132440 |
source | MEDLINE; Springer Online Journals |
subjects | Adenocarcinoma Aged Apoptosis Biomedical and Life Sciences Biomedicine Breast cancer Cancer Research Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - metabolism Carcinoma, Non-Small-Cell Lung - pathology Cell Line, Tumor Cytokines Diagnostic systems Epithelial cells Female Gene expression Gene Expression Regulation, Neoplastic Genes Growth factors Human Genetics Humans Inflammation Inflammatory diseases Interleukin 13 Interleukin 4 Interleukin-13 - genetics Interleukin-4 - genetics Kinases Laboratory Medicine Lung cancer Lung carcinoma Lung Neoplasms - genetics Lung Neoplasms - metabolism Lung Neoplasms - pathology Male Metastases Middle Aged Molecular Medicine Neoplasm Grading Neoplasm Staging Non-small cell lung carcinoma Original Original Research Article Patients Pharmacotherapy Prostate cancer Proteins Regulators Reverse transcription Samples Signal Transduction Signaling Small cell lung carcinoma Smoking Squamous cell carcinoma Stat6 protein STAT6 Transcription Factor - metabolism Statistical analysis Statistical methods Statistical significance Studies Suppressor of Cytokine Signaling 3 Protein - genetics Thoracic surgery Tumorigenesis Tumors |
title | The Expression Levels of IL-4/IL-13/STAT6 Signaling Pathway Genes and SOCS3 Could Help to Differentiate the Histopathological Subtypes of Non-Small Cell Lung Carcinoma |
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