Upregulation of lncRNA snoRNA host gene 6 regulates NUAK family SnF1‐like kinase‐1 expression by competitively binding microRNA‐125b and interacting with Snail1/2 in bladder cancer

Backgrounds/aims Numerous studies have reported that long noncoding RNAs (lncRNAs) play critical roles in the development and progression of bladder cancer (BC). LncRNA snoRNA host gene 6 (SNHG6) is ectopically expressed in tumor tissues of patients with BC and BC cell lines. However, little is know...

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Veröffentlicht in:Journal of cellular biochemistry 2019-01, Vol.120 (1), p.357-367
Hauptverfasser: Wang, Chunyang, Tao, Weiyang, Ni, Shaobin, Chen, Qiyin
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Tao, Weiyang
Ni, Shaobin
Chen, Qiyin
description Backgrounds/aims Numerous studies have reported that long noncoding RNAs (lncRNAs) play critical roles in the development and progression of bladder cancer (BC). LncRNA snoRNA host gene 6 (SNHG6) is ectopically expressed in tumor tissues of patients with BC and BC cell lines. However, little is known about the molecular mechanism of SNHG6‐mediated bladder urothelial carcinoma cell migration and invasion. Methods We detected the SNHG6 levels in human BC specimens and cell lines by quantitative real‐time polymerase chain reaction and Western blot, and investigated its role in BC using in vitro assays. Results We showed that overexpression of SNHG6 induced epithelial‐mesenchymal transition (EMT) and promoted the migration and invasion capabilities of BC cells. Mechanistically, SNHG6 induced EMT of BC cells by upregulating the expression levels of Snail1/2 and regulated BC cell migration and invasion by tumor suppressive hsa‐miR‐125b and its target gene NUAK Family Kinase 1 (NUAK1). Furthermore, we found that SNHG6 was positively correlated with Snail1/2 expression, and negatively correlated with hsa‐miR‐125b expression in BC specimens. Further study showed that SNHG6 repressed hsa‐miR‐125b expression to upregulate Snail1/2. Conversely, hsa‐miR‐125b knockdown augmented SNHG6 expression in BC cells. Conclusion Overall, our study demonstrated that SNHG6 promotes BC cell migration and invasion partly via the hsa‐miR‐125b/Snail1/2/NUAK1 pathway. Therefore, SNHG6 may be a potential prognostic biomarker in BC, and targeting hsa‐miR‐125b/Snail1/2/NUAK1 axis may be a promising therapeutic approach for BC patients. In our study, we found that overexpression of snoRNA host gene 6 (SNHG6) can induce epithelial‐to‐mesenchymal transition (EMT), metastasis, and invasion. Furthermore, SNHG6 promoted invasion and metastasis of BC cells through the hsa‐miR‐125b ‐ Snail1/2‐ SNHG6 pathway. A reciprocal inhibition loop between SNHG6 and hsa‐miR‐125b was found in our research. This study attempted to elucidate the mechanism of SNHG6 to promote metastasis and invasion of BC cells and to provide new therapeutic targets for BC metastasis.
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LncRNA snoRNA host gene 6 (SNHG6) is ectopically expressed in tumor tissues of patients with BC and BC cell lines. However, little is known about the molecular mechanism of SNHG6‐mediated bladder urothelial carcinoma cell migration and invasion. Methods We detected the SNHG6 levels in human BC specimens and cell lines by quantitative real‐time polymerase chain reaction and Western blot, and investigated its role in BC using in vitro assays. Results We showed that overexpression of SNHG6 induced epithelial‐mesenchymal transition (EMT) and promoted the migration and invasion capabilities of BC cells. Mechanistically, SNHG6 induced EMT of BC cells by upregulating the expression levels of Snail1/2 and regulated BC cell migration and invasion by tumor suppressive hsa‐miR‐125b and its target gene NUAK Family Kinase 1 (NUAK1). Furthermore, we found that SNHG6 was positively correlated with Snail1/2 expression, and negatively correlated with hsa‐miR‐125b expression in BC specimens. Further study showed that SNHG6 repressed hsa‐miR‐125b expression to upregulate Snail1/2. Conversely, hsa‐miR‐125b knockdown augmented SNHG6 expression in BC cells. Conclusion Overall, our study demonstrated that SNHG6 promotes BC cell migration and invasion partly via the hsa‐miR‐125b/Snail1/2/NUAK1 pathway. Therefore, SNHG6 may be a potential prognostic biomarker in BC, and targeting hsa‐miR‐125b/Snail1/2/NUAK1 axis may be a promising therapeutic approach for BC patients. In our study, we found that overexpression of snoRNA host gene 6 (SNHG6) can induce epithelial‐to‐mesenchymal transition (EMT), metastasis, and invasion. Furthermore, SNHG6 promoted invasion and metastasis of BC cells through the hsa‐miR‐125b ‐ Snail1/2‐ SNHG6 pathway. A reciprocal inhibition loop between SNHG6 and hsa‐miR‐125b was found in our research. This study attempted to elucidate the mechanism of SNHG6 to promote metastasis and invasion of BC cells and to provide new therapeutic targets for BC metastasis.</description><identifier>ISSN: 0730-2312</identifier><identifier>ISSN: 1097-4644</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.27387</identifier><identifier>PMID: 30168179</identifier><language>eng</language><publisher>United States</publisher><subject>Aged ; Binding Sites ; biomarker ; bladder cancer (BC) ; Cell Line, Tumor ; Cell Movement ; Epithelial-Mesenchymal Transition ; Female ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Humans ; invasion ; long noncoding RNAs (lncRNA) ; Male ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Middle Aged ; migration ; Neoplasm Invasiveness ; Protein Kinases - genetics ; Protein Kinases - metabolism ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Snail Family Transcription Factors - genetics ; Snail Family Transcription Factors - metabolism ; snoRNA host gene 6 (SNHG6) ; Transfection ; Up-Regulation ; Urinary Bladder Neoplasms - metabolism ; Urinary Bladder Neoplasms - pathology</subject><ispartof>Journal of cellular biochemistry, 2019-01, Vol.120 (1), p.357-367</ispartof><rights>2018 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3267-e99ddff2e155bd51e4a725c2264ad11e33484a9f2738160b13237b355355b21f3</citedby><orcidid>0000-0003-2302-9933</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcb.27387$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.27387$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30168179$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Chunyang</creatorcontrib><creatorcontrib>Tao, Weiyang</creatorcontrib><creatorcontrib>Ni, Shaobin</creatorcontrib><creatorcontrib>Chen, Qiyin</creatorcontrib><title>Upregulation of lncRNA snoRNA host gene 6 regulates NUAK family SnF1‐like kinase‐1 expression by competitively binding microRNA‐125b and interacting with Snail1/2 in bladder cancer</title><title>Journal of cellular biochemistry</title><addtitle>J Cell Biochem</addtitle><description>Backgrounds/aims Numerous studies have reported that long noncoding RNAs (lncRNAs) play critical roles in the development and progression of bladder cancer (BC). LncRNA snoRNA host gene 6 (SNHG6) is ectopically expressed in tumor tissues of patients with BC and BC cell lines. However, little is known about the molecular mechanism of SNHG6‐mediated bladder urothelial carcinoma cell migration and invasion. Methods We detected the SNHG6 levels in human BC specimens and cell lines by quantitative real‐time polymerase chain reaction and Western blot, and investigated its role in BC using in vitro assays. Results We showed that overexpression of SNHG6 induced epithelial‐mesenchymal transition (EMT) and promoted the migration and invasion capabilities of BC cells. Mechanistically, SNHG6 induced EMT of BC cells by upregulating the expression levels of Snail1/2 and regulated BC cell migration and invasion by tumor suppressive hsa‐miR‐125b and its target gene NUAK Family Kinase 1 (NUAK1). Furthermore, we found that SNHG6 was positively correlated with Snail1/2 expression, and negatively correlated with hsa‐miR‐125b expression in BC specimens. Further study showed that SNHG6 repressed hsa‐miR‐125b expression to upregulate Snail1/2. Conversely, hsa‐miR‐125b knockdown augmented SNHG6 expression in BC cells. Conclusion Overall, our study demonstrated that SNHG6 promotes BC cell migration and invasion partly via the hsa‐miR‐125b/Snail1/2/NUAK1 pathway. Therefore, SNHG6 may be a potential prognostic biomarker in BC, and targeting hsa‐miR‐125b/Snail1/2/NUAK1 axis may be a promising therapeutic approach for BC patients. In our study, we found that overexpression of snoRNA host gene 6 (SNHG6) can induce epithelial‐to‐mesenchymal transition (EMT), metastasis, and invasion. Furthermore, SNHG6 promoted invasion and metastasis of BC cells through the hsa‐miR‐125b ‐ Snail1/2‐ SNHG6 pathway. A reciprocal inhibition loop between SNHG6 and hsa‐miR‐125b was found in our research. This study attempted to elucidate the mechanism of SNHG6 to promote metastasis and invasion of BC cells and to provide new therapeutic targets for BC metastasis.</description><subject>Aged</subject><subject>Binding Sites</subject><subject>biomarker</subject><subject>bladder cancer (BC)</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Knockdown Techniques</subject><subject>Humans</subject><subject>invasion</subject><subject>long noncoding RNAs (lncRNA)</subject><subject>Male</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Middle Aged</subject><subject>migration</subject><subject>Neoplasm Invasiveness</subject><subject>Protein Kinases - genetics</subject><subject>Protein Kinases - metabolism</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Snail Family Transcription Factors - genetics</subject><subject>Snail Family Transcription Factors - metabolism</subject><subject>snoRNA host gene 6 (SNHG6)</subject><subject>Transfection</subject><subject>Up-Regulation</subject><subject>Urinary Bladder Neoplasms - metabolism</subject><subject>Urinary Bladder Neoplasms - pathology</subject><issn>0730-2312</issn><issn>1097-4644</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kc1u1DAUha0K1E5LF30BdJds0vFPEifLYdRSoCoSMOvIPzdTt44zxBna2fUReB4ehyfBaQckS9fW-e6xdA4hZ4yeM0r5_M7ocy5FJQ_IjNFaZnmZ56_IjEpBMy4YPyLHMd5RSuta8ENyJCgrKybrGfm92gy43no1uj5A34IP5uvNAmLop3HbxxHWGBBK2HMY4Wa1-Ayt6pzfwbdwyf48_fLuHuHeBRUxvRjgY_KNcTLVOzB9t8HRje4nphXtgnVhDZ0zw_TLtMALDSpYcGHEQZlx0h_ceJv8lfNszpMC2itrcQCjgsHhDXndKh_xdD9PyOry4vvyKrv-8uHjcnGdGcFLmWFdW9u2HFlRaFswzJXkheG8zJVlDIXIq1zV7RQgK6lmggupRVGkozlrxQl59-K7GfofW4xj07lo0HsVsN_GhtO6kilwWSX07R7d6g5tsxlcp4Zd8y_vBMxfgAfncfdfZ7SZimxSkc1zkc2n5fvni_gLagOS4w</recordid><startdate>201901</startdate><enddate>201901</enddate><creator>Wang, Chunyang</creator><creator>Tao, Weiyang</creator><creator>Ni, Shaobin</creator><creator>Chen, Qiyin</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-2302-9933</orcidid></search><sort><creationdate>201901</creationdate><title>Upregulation of lncRNA snoRNA host gene 6 regulates NUAK family SnF1‐like kinase‐1 expression by competitively binding microRNA‐125b and interacting with Snail1/2 in bladder cancer</title><author>Wang, Chunyang ; Tao, Weiyang ; Ni, Shaobin ; Chen, Qiyin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3267-e99ddff2e155bd51e4a725c2264ad11e33484a9f2738160b13237b355355b21f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Aged</topic><topic>Binding Sites</topic><topic>biomarker</topic><topic>bladder cancer (BC)</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Knockdown Techniques</topic><topic>Humans</topic><topic>invasion</topic><topic>long noncoding RNAs (lncRNA)</topic><topic>Male</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Middle Aged</topic><topic>migration</topic><topic>Neoplasm Invasiveness</topic><topic>Protein Kinases - genetics</topic><topic>Protein Kinases - metabolism</topic><topic>Repressor Proteins - genetics</topic><topic>Repressor Proteins - metabolism</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Snail Family Transcription Factors - genetics</topic><topic>Snail Family Transcription Factors - metabolism</topic><topic>snoRNA host gene 6 (SNHG6)</topic><topic>Transfection</topic><topic>Up-Regulation</topic><topic>Urinary Bladder Neoplasms - metabolism</topic><topic>Urinary Bladder Neoplasms - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Chunyang</creatorcontrib><creatorcontrib>Tao, Weiyang</creatorcontrib><creatorcontrib>Ni, Shaobin</creatorcontrib><creatorcontrib>Chen, Qiyin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Chunyang</au><au>Tao, Weiyang</au><au>Ni, Shaobin</au><au>Chen, Qiyin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Upregulation of lncRNA snoRNA host gene 6 regulates NUAK family SnF1‐like kinase‐1 expression by competitively binding microRNA‐125b and interacting with Snail1/2 in bladder cancer</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J Cell Biochem</addtitle><date>2019-01</date><risdate>2019</risdate><volume>120</volume><issue>1</issue><spage>357</spage><epage>367</epage><pages>357-367</pages><issn>0730-2312</issn><issn>1097-4644</issn><eissn>1097-4644</eissn><abstract>Backgrounds/aims Numerous studies have reported that long noncoding RNAs (lncRNAs) play critical roles in the development and progression of bladder cancer (BC). LncRNA snoRNA host gene 6 (SNHG6) is ectopically expressed in tumor tissues of patients with BC and BC cell lines. However, little is known about the molecular mechanism of SNHG6‐mediated bladder urothelial carcinoma cell migration and invasion. Methods We detected the SNHG6 levels in human BC specimens and cell lines by quantitative real‐time polymerase chain reaction and Western blot, and investigated its role in BC using in vitro assays. Results We showed that overexpression of SNHG6 induced epithelial‐mesenchymal transition (EMT) and promoted the migration and invasion capabilities of BC cells. Mechanistically, SNHG6 induced EMT of BC cells by upregulating the expression levels of Snail1/2 and regulated BC cell migration and invasion by tumor suppressive hsa‐miR‐125b and its target gene NUAK Family Kinase 1 (NUAK1). Furthermore, we found that SNHG6 was positively correlated with Snail1/2 expression, and negatively correlated with hsa‐miR‐125b expression in BC specimens. Further study showed that SNHG6 repressed hsa‐miR‐125b expression to upregulate Snail1/2. Conversely, hsa‐miR‐125b knockdown augmented SNHG6 expression in BC cells. Conclusion Overall, our study demonstrated that SNHG6 promotes BC cell migration and invasion partly via the hsa‐miR‐125b/Snail1/2/NUAK1 pathway. Therefore, SNHG6 may be a potential prognostic biomarker in BC, and targeting hsa‐miR‐125b/Snail1/2/NUAK1 axis may be a promising therapeutic approach for BC patients. In our study, we found that overexpression of snoRNA host gene 6 (SNHG6) can induce epithelial‐to‐mesenchymal transition (EMT), metastasis, and invasion. Furthermore, SNHG6 promoted invasion and metastasis of BC cells through the hsa‐miR‐125b ‐ Snail1/2‐ SNHG6 pathway. A reciprocal inhibition loop between SNHG6 and hsa‐miR‐125b was found in our research. This study attempted to elucidate the mechanism of SNHG6 to promote metastasis and invasion of BC cells and to provide new therapeutic targets for BC metastasis.</abstract><cop>United States</cop><pmid>30168179</pmid><doi>10.1002/jcb.27387</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-2302-9933</orcidid><oa>free_for_read</oa></addata></record>
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subjects Aged
Binding Sites
biomarker
bladder cancer (BC)
Cell Line, Tumor
Cell Movement
Epithelial-Mesenchymal Transition
Female
Gene Expression Regulation, Neoplastic
Gene Knockdown Techniques
Humans
invasion
long noncoding RNAs (lncRNA)
Male
MicroRNAs - genetics
MicroRNAs - metabolism
Middle Aged
migration
Neoplasm Invasiveness
Protein Kinases - genetics
Protein Kinases - metabolism
Repressor Proteins - genetics
Repressor Proteins - metabolism
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
Snail Family Transcription Factors - genetics
Snail Family Transcription Factors - metabolism
snoRNA host gene 6 (SNHG6)
Transfection
Up-Regulation
Urinary Bladder Neoplasms - metabolism
Urinary Bladder Neoplasms - pathology
title Upregulation of lncRNA snoRNA host gene 6 regulates NUAK family SnF1‐like kinase‐1 expression by competitively binding microRNA‐125b and interacting with Snail1/2 in bladder cancer
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