Relationship between cellular morphology and abnormality of SWI/SNF complex subunits in pancreatic undifferentiated carcinoma
Purpose Pancreatic undifferentiated carcinoma (UDC) is a rare tumor with a worse prognosis than pancreatic ductal adenocarcinoma (PDAC). Recent study showed that UDC exhibits loss of SMARCB1, which is one of the subunits of the SWI/SNF complex. However, whether there are abnormalities of other SWI/S...
Gespeichert in:
| Veröffentlicht in: | Journal of cancer research and clinical oncology 2022-11, Vol.148 (11), p.2945-2957 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2957 |
|---|---|
| container_issue | 11 |
| container_start_page | 2945 |
| container_title | Journal of cancer research and clinical oncology |
| container_volume | 148 |
| creator | Yamamoto, Takeo Kohashi, Kenichi Yamada, Yutaka Kawata, Jun Sakihama, Kukiko Matsuda, Ryota Koga, Yutaka Aishima, Shinichi Nakamura, Masafumi Oda, Yoshinao |
| description | Purpose
Pancreatic undifferentiated carcinoma (UDC) is a rare tumor with a worse prognosis than pancreatic ductal adenocarcinoma (PDAC). Recent study showed that UDC exhibits loss of SMARCB1, which is one of the subunits of the SWI/SNF complex. However, whether there are abnormalities of other SWI/SNF complex subunits in UDC has remained unknown. In this study, we attempted to clarify whether the loss of SWI/SNF complex subunits is related to the pathogenesis of UDC by comparing undifferentiated component (UC) and ductal adenocarcinoma component (DAC).
Methods
Genetic analysis of the ten UCs and six DACs was performed. The expression of ARID1A, SMARCA2, SMARCA4, SMARCB1, SMARCC1, and SMARCC2 in formalin-fixed, paraffin-embedded tumor tissues collected by surgical resection from 18 UDC patients was evaluated immunohistochemically. Moreover, two pancreatic cell lines were evaluated for the effects of siARID1A on the mRNA and protein expression of E-cadherin, vimentin, and epithelial-mesenchymal transition (EMT)-related markers by qRT-PCR, western blotting, and immunofluorescence staining.
Results
UCs tended to have a higher frequency of mutation in ARID1A, SMARCA4, and SMARCC2 than DACs. Immunohistochemically, UCs revealed reduced/lost expression of ARID1A (72%), SMARCB1 (44%), SMARCC1 (31%), and SMARCC2 (67%). Reduced/lost expression of ARID1A, SMARCB1, and SMARCC2 was significantly more frequently observed in UCs than in DACs. In the pancreatic cell lines, western blotting and qRT-PCR showed that the downregulation of ARID1A increased the expression of vimentin and EMT-related markers.
Conclusion
Our results suggest that the abnormality of SWI/SNF complex subunits, especially ARID1A, is one of the factors behind the morphological change of UDC. |
| doi_str_mv | 10.1007/s00432-021-03860-8 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2601979368</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2717193376</sourcerecordid><originalsourceid>FETCH-LOGICAL-c503t-9be024e2e4de1d1193b046aa1a289945bb1259a8ea5101ca28bc1ed0734cdcc53</originalsourceid><addsrcrecordid>eNp9kU1rFTEUhoMo9lr9Ay4k4MbN2JxkPpdSWlsoFtqKy3CSOdOmzCRjMoPehf-9ud6q0IWrkHOevMnJw9hbEB9BiOYoCVEqWQgJhVBtLYr2GdvArgRKVc_ZRkADRSWhPmCvUroXeV818iU7UGULTV3Dhv26ohEXF3y6czM3tPwg8tzSOK4jRj6FON-FMdxuOfqeo_EhTji6ZcvDwK-_nR9dfznlNkzzSD95Ws3q3ZK483xGbyPlaMtX37thoEh-cbhQzy1G63yY8DV7MeCY6M3jesi-np7cHJ8VF5efz48_XRS2EmopOkNCliSp7Al6gE4ZUdaIgLLturIyBmTVYUtYgQCbq8YC9aJRpe2trdQh-7DPnWP4vlJa9OTSbkj0FNakZS2gazpVtxl9_wS9D2v0-XVaNvk_O6WaOlNyT9kYUoo06Dm6CeNWg9A7OXovR2c5-rccvYt-9xi9mon6v0f-2MiA2gMpt_wtxX93_yf2AQcOnAM</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2717193376</pqid></control><display><type>article</type><title>Relationship between cellular morphology and abnormality of SWI/SNF complex subunits in pancreatic undifferentiated carcinoma</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Yamamoto, Takeo ; Kohashi, Kenichi ; Yamada, Yutaka ; Kawata, Jun ; Sakihama, Kukiko ; Matsuda, Ryota ; Koga, Yutaka ; Aishima, Shinichi ; Nakamura, Masafumi ; Oda, Yoshinao</creator><creatorcontrib>Yamamoto, Takeo ; Kohashi, Kenichi ; Yamada, Yutaka ; Kawata, Jun ; Sakihama, Kukiko ; Matsuda, Ryota ; Koga, Yutaka ; Aishima, Shinichi ; Nakamura, Masafumi ; Oda, Yoshinao</creatorcontrib><description>Purpose
Pancreatic undifferentiated carcinoma (UDC) is a rare tumor with a worse prognosis than pancreatic ductal adenocarcinoma (PDAC). Recent study showed that UDC exhibits loss of SMARCB1, which is one of the subunits of the SWI/SNF complex. However, whether there are abnormalities of other SWI/SNF complex subunits in UDC has remained unknown. In this study, we attempted to clarify whether the loss of SWI/SNF complex subunits is related to the pathogenesis of UDC by comparing undifferentiated component (UC) and ductal adenocarcinoma component (DAC).
Methods
Genetic analysis of the ten UCs and six DACs was performed. The expression of ARID1A, SMARCA2, SMARCA4, SMARCB1, SMARCC1, and SMARCC2 in formalin-fixed, paraffin-embedded tumor tissues collected by surgical resection from 18 UDC patients was evaluated immunohistochemically. Moreover, two pancreatic cell lines were evaluated for the effects of siARID1A on the mRNA and protein expression of E-cadherin, vimentin, and epithelial-mesenchymal transition (EMT)-related markers by qRT-PCR, western blotting, and immunofluorescence staining.
Results
UCs tended to have a higher frequency of mutation in ARID1A, SMARCA4, and SMARCC2 than DACs. Immunohistochemically, UCs revealed reduced/lost expression of ARID1A (72%), SMARCB1 (44%), SMARCC1 (31%), and SMARCC2 (67%). Reduced/lost expression of ARID1A, SMARCB1, and SMARCC2 was significantly more frequently observed in UCs than in DACs. In the pancreatic cell lines, western blotting and qRT-PCR showed that the downregulation of ARID1A increased the expression of vimentin and EMT-related markers.
Conclusion
Our results suggest that the abnormality of SWI/SNF complex subunits, especially ARID1A, is one of the factors behind the morphological change of UDC.</description><identifier>ISSN: 0171-5216</identifier><identifier>EISSN: 1432-1335</identifier><identifier>DOI: 10.1007/s00432-021-03860-8</identifier><identifier>PMID: 34817661</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Adenocarcinoma ; Adenocarcinoma - pathology ; Cadherins - genetics ; Cancer ; Cancer Research ; DNA Helicases - genetics ; DNA-Binding Proteins - genetics ; E-cadherin ; Formaldehyde ; Gene expression ; Genetic analysis ; Hematology ; Humans ; Immunofluorescence ; Immunohistochemistry ; Internal Medicine ; Medicine ; Medicine & Public Health ; Mesenchyme ; mRNA ; Nuclear Proteins - genetics ; Oncology ; Original Article – Clinical Oncology ; Pancreas ; Pancreatic carcinoma ; Pancreatic Neoplasms ; Paraffin ; RNA, Messenger ; SWI/SNF complex ; Transcription Factors - genetics ; Tumors ; Vimentin ; Western blotting</subject><ispartof>Journal of cancer research and clinical oncology, 2022-11, Vol.148 (11), p.2945-2957</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2021</rights><rights>2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-9be024e2e4de1d1193b046aa1a289945bb1259a8ea5101ca28bc1ed0734cdcc53</citedby><cites>FETCH-LOGICAL-c503t-9be024e2e4de1d1193b046aa1a289945bb1259a8ea5101ca28bc1ed0734cdcc53</cites><orcidid>0000-0001-9636-1182</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/s00432-021-03860-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00432-021-03860-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34817661$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yamamoto, Takeo</creatorcontrib><creatorcontrib>Kohashi, Kenichi</creatorcontrib><creatorcontrib>Yamada, Yutaka</creatorcontrib><creatorcontrib>Kawata, Jun</creatorcontrib><creatorcontrib>Sakihama, Kukiko</creatorcontrib><creatorcontrib>Matsuda, Ryota</creatorcontrib><creatorcontrib>Koga, Yutaka</creatorcontrib><creatorcontrib>Aishima, Shinichi</creatorcontrib><creatorcontrib>Nakamura, Masafumi</creatorcontrib><creatorcontrib>Oda, Yoshinao</creatorcontrib><title>Relationship between cellular morphology and abnormality of SWI/SNF complex subunits in pancreatic undifferentiated carcinoma</title><title>Journal of cancer research and clinical oncology</title><addtitle>J Cancer Res Clin Oncol</addtitle><addtitle>J Cancer Res Clin Oncol</addtitle><description>Purpose
Pancreatic undifferentiated carcinoma (UDC) is a rare tumor with a worse prognosis than pancreatic ductal adenocarcinoma (PDAC). Recent study showed that UDC exhibits loss of SMARCB1, which is one of the subunits of the SWI/SNF complex. However, whether there are abnormalities of other SWI/SNF complex subunits in UDC has remained unknown. In this study, we attempted to clarify whether the loss of SWI/SNF complex subunits is related to the pathogenesis of UDC by comparing undifferentiated component (UC) and ductal adenocarcinoma component (DAC).
Methods
Genetic analysis of the ten UCs and six DACs was performed. The expression of ARID1A, SMARCA2, SMARCA4, SMARCB1, SMARCC1, and SMARCC2 in formalin-fixed, paraffin-embedded tumor tissues collected by surgical resection from 18 UDC patients was evaluated immunohistochemically. Moreover, two pancreatic cell lines were evaluated for the effects of siARID1A on the mRNA and protein expression of E-cadherin, vimentin, and epithelial-mesenchymal transition (EMT)-related markers by qRT-PCR, western blotting, and immunofluorescence staining.
Results
UCs tended to have a higher frequency of mutation in ARID1A, SMARCA4, and SMARCC2 than DACs. Immunohistochemically, UCs revealed reduced/lost expression of ARID1A (72%), SMARCB1 (44%), SMARCC1 (31%), and SMARCC2 (67%). Reduced/lost expression of ARID1A, SMARCB1, and SMARCC2 was significantly more frequently observed in UCs than in DACs. In the pancreatic cell lines, western blotting and qRT-PCR showed that the downregulation of ARID1A increased the expression of vimentin and EMT-related markers.
Conclusion
Our results suggest that the abnormality of SWI/SNF complex subunits, especially ARID1A, is one of the factors behind the morphological change of UDC.</description><subject>Adenocarcinoma</subject><subject>Adenocarcinoma - pathology</subject><subject>Cadherins - genetics</subject><subject>Cancer</subject><subject>Cancer Research</subject><subject>DNA Helicases - genetics</subject><subject>DNA-Binding Proteins - genetics</subject><subject>E-cadherin</subject><subject>Formaldehyde</subject><subject>Gene expression</subject><subject>Genetic analysis</subject><subject>Hematology</subject><subject>Humans</subject><subject>Immunofluorescence</subject><subject>Immunohistochemistry</subject><subject>Internal Medicine</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mesenchyme</subject><subject>mRNA</subject><subject>Nuclear Proteins - genetics</subject><subject>Oncology</subject><subject>Original Article – Clinical Oncology</subject><subject>Pancreas</subject><subject>Pancreatic carcinoma</subject><subject>Pancreatic Neoplasms</subject><subject>Paraffin</subject><subject>RNA, Messenger</subject><subject>SWI/SNF complex</subject><subject>Transcription Factors - genetics</subject><subject>Tumors</subject><subject>Vimentin</subject><subject>Western blotting</subject><issn>0171-5216</issn><issn>1432-1335</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kU1rFTEUhoMo9lr9Ay4k4MbN2JxkPpdSWlsoFtqKy3CSOdOmzCRjMoPehf-9ud6q0IWrkHOevMnJw9hbEB9BiOYoCVEqWQgJhVBtLYr2GdvArgRKVc_ZRkADRSWhPmCvUroXeV818iU7UGULTV3Dhv26ohEXF3y6czM3tPwg8tzSOK4jRj6FON-FMdxuOfqeo_EhTji6ZcvDwK-_nR9dfznlNkzzSD95Ws3q3ZK483xGbyPlaMtX37thoEh-cbhQzy1G63yY8DV7MeCY6M3jesi-np7cHJ8VF5efz48_XRS2EmopOkNCliSp7Al6gE4ZUdaIgLLturIyBmTVYUtYgQCbq8YC9aJRpe2trdQh-7DPnWP4vlJa9OTSbkj0FNakZS2gazpVtxl9_wS9D2v0-XVaNvk_O6WaOlNyT9kYUoo06Dm6CeNWg9A7OXovR2c5-rccvYt-9xi9mon6v0f-2MiA2gMpt_wtxX93_yf2AQcOnAM</recordid><startdate>20221101</startdate><enddate>20221101</enddate><creator>Yamamoto, Takeo</creator><creator>Kohashi, Kenichi</creator><creator>Yamada, Yutaka</creator><creator>Kawata, Jun</creator><creator>Sakihama, Kukiko</creator><creator>Matsuda, Ryota</creator><creator>Koga, Yutaka</creator><creator>Aishima, Shinichi</creator><creator>Nakamura, Masafumi</creator><creator>Oda, Yoshinao</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</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>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-9636-1182</orcidid></search><sort><creationdate>20221101</creationdate><title>Relationship between cellular morphology and abnormality of SWI/SNF complex subunits in pancreatic undifferentiated carcinoma</title><author>Yamamoto, Takeo ; Kohashi, Kenichi ; Yamada, Yutaka ; Kawata, Jun ; Sakihama, Kukiko ; Matsuda, Ryota ; Koga, Yutaka ; Aishima, Shinichi ; Nakamura, Masafumi ; Oda, Yoshinao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-9be024e2e4de1d1193b046aa1a289945bb1259a8ea5101ca28bc1ed0734cdcc53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adenocarcinoma</topic><topic>Adenocarcinoma - pathology</topic><topic>Cadherins - genetics</topic><topic>Cancer</topic><topic>Cancer Research</topic><topic>DNA Helicases - genetics</topic><topic>DNA-Binding Proteins - genetics</topic><topic>E-cadherin</topic><topic>Formaldehyde</topic><topic>Gene expression</topic><topic>Genetic analysis</topic><topic>Hematology</topic><topic>Humans</topic><topic>Immunofluorescence</topic><topic>Immunohistochemistry</topic><topic>Internal Medicine</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mesenchyme</topic><topic>mRNA</topic><topic>Nuclear Proteins - genetics</topic><topic>Oncology</topic><topic>Original Article – Clinical Oncology</topic><topic>Pancreas</topic><topic>Pancreatic carcinoma</topic><topic>Pancreatic Neoplasms</topic><topic>Paraffin</topic><topic>RNA, Messenger</topic><topic>SWI/SNF complex</topic><topic>Transcription Factors - genetics</topic><topic>Tumors</topic><topic>Vimentin</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yamamoto, Takeo</creatorcontrib><creatorcontrib>Kohashi, Kenichi</creatorcontrib><creatorcontrib>Yamada, Yutaka</creatorcontrib><creatorcontrib>Kawata, Jun</creatorcontrib><creatorcontrib>Sakihama, Kukiko</creatorcontrib><creatorcontrib>Matsuda, Ryota</creatorcontrib><creatorcontrib>Koga, Yutaka</creatorcontrib><creatorcontrib>Aishima, Shinichi</creatorcontrib><creatorcontrib>Nakamura, Masafumi</creatorcontrib><creatorcontrib>Oda, Yoshinao</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>Oncogenes and Growth Factors Abstracts</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>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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>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>AIDS and Cancer Research Abstracts</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>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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cancer research and clinical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yamamoto, Takeo</au><au>Kohashi, Kenichi</au><au>Yamada, Yutaka</au><au>Kawata, Jun</au><au>Sakihama, Kukiko</au><au>Matsuda, Ryota</au><au>Koga, Yutaka</au><au>Aishima, Shinichi</au><au>Nakamura, Masafumi</au><au>Oda, Yoshinao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Relationship between cellular morphology and abnormality of SWI/SNF complex subunits in pancreatic undifferentiated carcinoma</atitle><jtitle>Journal of cancer research and clinical oncology</jtitle><stitle>J Cancer Res Clin Oncol</stitle><addtitle>J Cancer Res Clin Oncol</addtitle><date>2022-11-01</date><risdate>2022</risdate><volume>148</volume><issue>11</issue><spage>2945</spage><epage>2957</epage><pages>2945-2957</pages><issn>0171-5216</issn><eissn>1432-1335</eissn><abstract>Purpose
Pancreatic undifferentiated carcinoma (UDC) is a rare tumor with a worse prognosis than pancreatic ductal adenocarcinoma (PDAC). Recent study showed that UDC exhibits loss of SMARCB1, which is one of the subunits of the SWI/SNF complex. However, whether there are abnormalities of other SWI/SNF complex subunits in UDC has remained unknown. In this study, we attempted to clarify whether the loss of SWI/SNF complex subunits is related to the pathogenesis of UDC by comparing undifferentiated component (UC) and ductal adenocarcinoma component (DAC).
Methods
Genetic analysis of the ten UCs and six DACs was performed. The expression of ARID1A, SMARCA2, SMARCA4, SMARCB1, SMARCC1, and SMARCC2 in formalin-fixed, paraffin-embedded tumor tissues collected by surgical resection from 18 UDC patients was evaluated immunohistochemically. Moreover, two pancreatic cell lines were evaluated for the effects of siARID1A on the mRNA and protein expression of E-cadherin, vimentin, and epithelial-mesenchymal transition (EMT)-related markers by qRT-PCR, western blotting, and immunofluorescence staining.
Results
UCs tended to have a higher frequency of mutation in ARID1A, SMARCA4, and SMARCC2 than DACs. Immunohistochemically, UCs revealed reduced/lost expression of ARID1A (72%), SMARCB1 (44%), SMARCC1 (31%), and SMARCC2 (67%). Reduced/lost expression of ARID1A, SMARCB1, and SMARCC2 was significantly more frequently observed in UCs than in DACs. In the pancreatic cell lines, western blotting and qRT-PCR showed that the downregulation of ARID1A increased the expression of vimentin and EMT-related markers.
Conclusion
Our results suggest that the abnormality of SWI/SNF complex subunits, especially ARID1A, is one of the factors behind the morphological change of UDC.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>34817661</pmid><doi>10.1007/s00432-021-03860-8</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-9636-1182</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0171-5216 |
| ispartof | Journal of cancer research and clinical oncology, 2022-11, Vol.148 (11), p.2945-2957 |
| issn | 0171-5216 1432-1335 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2601979368 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Adenocarcinoma Adenocarcinoma - pathology Cadherins - genetics Cancer Cancer Research DNA Helicases - genetics DNA-Binding Proteins - genetics E-cadherin Formaldehyde Gene expression Genetic analysis Hematology Humans Immunofluorescence Immunohistochemistry Internal Medicine Medicine Medicine & Public Health Mesenchyme mRNA Nuclear Proteins - genetics Oncology Original Article – Clinical Oncology Pancreas Pancreatic carcinoma Pancreatic Neoplasms Paraffin RNA, Messenger SWI/SNF complex Transcription Factors - genetics Tumors Vimentin Western blotting |
| title | Relationship between cellular morphology and abnormality of SWI/SNF complex subunits in pancreatic undifferentiated carcinoma |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-19T03%3A25%3A21IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Relationship%20between%20cellular%20morphology%20and%20abnormality%20of%20SWI/SNF%20complex%20subunits%20in%20pancreatic%20undifferentiated%20carcinoma&rft.jtitle=Journal%20of%20cancer%20research%20and%20clinical%20oncology&rft.au=Yamamoto,%20Takeo&rft.date=2022-11-01&rft.volume=148&rft.issue=11&rft.spage=2945&rft.epage=2957&rft.pages=2945-2957&rft.issn=0171-5216&rft.eissn=1432-1335&rft_id=info:doi/10.1007/s00432-021-03860-8&rft_dat=%3Cproquest_cross%3E2717193376%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2717193376&rft_id=info:pmid/34817661&rfr_iscdi=true |