Wnt/β-Catenin Signaling Exacerbates Keloid Cell Proliferation by Regulating Telomerase
Abstract Objectives: Our goal was to investigate the relationship between keloid and telomerase as well as clarifying the influence of Wnt/β-catenin signaling on keloid cell proliferation. Methods: Tissues from 18 keloid patients were collected for further study. Keloid progenitor cells (KPC) and sk...
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| Veröffentlicht in: | Cellular physiology and biochemistry 2016-01, Vol.39 (5), p.2001-2013 |
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| creator | Yu, Dongmei Shang, Yong Yuan, Jian Ding, Shuang Luo, Sai Hao, Lijun |
| description | Abstract
Objectives: Our goal was to investigate the relationship between keloid and telomerase as well as clarifying the influence of Wnt/β-catenin signaling on keloid cell proliferation. Methods: Tissues from 18 keloid patients were collected for further study. Keloid progenitor cells (KPC) and skin progenitor cells (SKP) were both included in this study. Lenti-virus transfection was used to divide cells into different groups in which cells were treated with different substances: negative control (NC) group, wnt10a siRNA group, β-catenin siRNA group and TERT siRNA group. KPC cells were injected into 20 male BALB/c nude mice in order to build tumor models. Several experiments including immunohistochemistry, western blot and RT-PCR were conducted in order to detect the corresponding protein expressions and relative mRNA levels. MTT assay and flow cytometry were also conducted for assessing cell proliferation and apoptosis status. Results: β-catenin and telomerase expression levels in keloid tissues were elevated compared to normal tissues (all P < 0.05). KPC cells in keloid exhibited more dynamic telomerase activity than SKP cells (P < 0.05). Luciferase activity assay confirmed that β-catenin could directly interact with telomerase. After wnt10a/β-catenin signaling pathway was inhibited, the proliferation of KPC cells was significantly suppressed and the apoptosis rate was remarkably increased (all P < 0.05). Results from tumor models also validated that wnt10a/β-catenin signaling pathway influenced the activity and length of telomerase. Conclusions: Wnt/β-catenin signaling pathway is able to exacerbate keloid cell proliferation and inhibit the apoptosis of keloid cells through its interaction with telomerase. |
| doi_str_mv | 10.1159/000447896 |
| format | Article |
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Objectives: Our goal was to investigate the relationship between keloid and telomerase as well as clarifying the influence of Wnt/β-catenin signaling on keloid cell proliferation. Methods: Tissues from 18 keloid patients were collected for further study. Keloid progenitor cells (KPC) and skin progenitor cells (SKP) were both included in this study. Lenti-virus transfection was used to divide cells into different groups in which cells were treated with different substances: negative control (NC) group, wnt10a siRNA group, β-catenin siRNA group and TERT siRNA group. KPC cells were injected into 20 male BALB/c nude mice in order to build tumor models. Several experiments including immunohistochemistry, western blot and RT-PCR were conducted in order to detect the corresponding protein expressions and relative mRNA levels. MTT assay and flow cytometry were also conducted for assessing cell proliferation and apoptosis status. Results: β-catenin and telomerase expression levels in keloid tissues were elevated compared to normal tissues (all P < 0.05). KPC cells in keloid exhibited more dynamic telomerase activity than SKP cells (P < 0.05). Luciferase activity assay confirmed that β-catenin could directly interact with telomerase. After wnt10a/β-catenin signaling pathway was inhibited, the proliferation of KPC cells was significantly suppressed and the apoptosis rate was remarkably increased (all P < 0.05). Results from tumor models also validated that wnt10a/β-catenin signaling pathway influenced the activity and length of telomerase. Conclusions: Wnt/β-catenin signaling pathway is able to exacerbate keloid cell proliferation and inhibit the apoptosis of keloid cells through its interaction with telomerase.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000447896</identifier><identifier>PMID: 27771714</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Animals ; Antibodies ; Apoptosis ; Apoptosis - genetics ; beta Catenin - antagonists & inhibitors ; beta Catenin - genetics ; beta Catenin - metabolism ; Cancer ; Cell growth ; Cell Proliferation ; Cloning ; Disease ; Epithelial-Mesenchymal Transition - genetics ; Gene Expression Regulation ; Genes ; Genes, Reporter ; Growth models ; Hospitals ; Humans ; Keloid ; Keloid - genetics ; Keloid - metabolism ; Keloid - pathology ; Kinases ; Laboratory animals ; Luciferases - genetics ; Luciferases - metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Original Paper ; Patients ; Plasmids ; Primary Cell Culture ; RNA, Small Interfering - genetics ; RNA, Small Interfering - metabolism ; Signal Transduction - genetics ; Skin ; Stem cells ; Stem Cells - metabolism ; Stem Cells - pathology ; Telomerase ; Telomerase - antagonists & inhibitors ; Telomerase - genetics ; Telomerase - metabolism ; Transfection ; Wnt ; Wnt Proteins - antagonists & inhibitors ; Wnt Proteins - genetics ; Wnt Proteins - metabolism ; β-catenin</subject><ispartof>Cellular physiology and biochemistry, 2016-01, Vol.39 (5), p.2001-2013</ispartof><rights>2016 The Author(s) Published by S. Karger AG, Basel</rights><rights>2016 The Author(s) Published by S. Karger AG, Basel.</rights><rights>2016 The Author(s) Published by S. Karger AG, Basel. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the associated terms available at: https://uk.sagepub.com/en-gb/eur/reusing-open-access-and-sage-choice-content</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-7b94620bbc9ab0aa06310fa3c280923c4c644c3d9fb4e367f9b4eb6e7f79ffb73</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,865,2103,27637,27926,27927</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27771714$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yu, Dongmei</creatorcontrib><creatorcontrib>Shang, Yong</creatorcontrib><creatorcontrib>Yuan, Jian</creatorcontrib><creatorcontrib>Ding, Shuang</creatorcontrib><creatorcontrib>Luo, Sai</creatorcontrib><creatorcontrib>Hao, Lijun</creatorcontrib><title>Wnt/β-Catenin Signaling Exacerbates Keloid Cell Proliferation by Regulating Telomerase</title><title>Cellular physiology and biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Abstract
Objectives: Our goal was to investigate the relationship between keloid and telomerase as well as clarifying the influence of Wnt/β-catenin signaling on keloid cell proliferation. Methods: Tissues from 18 keloid patients were collected for further study. Keloid progenitor cells (KPC) and skin progenitor cells (SKP) were both included in this study. Lenti-virus transfection was used to divide cells into different groups in which cells were treated with different substances: negative control (NC) group, wnt10a siRNA group, β-catenin siRNA group and TERT siRNA group. KPC cells were injected into 20 male BALB/c nude mice in order to build tumor models. Several experiments including immunohistochemistry, western blot and RT-PCR were conducted in order to detect the corresponding protein expressions and relative mRNA levels. MTT assay and flow cytometry were also conducted for assessing cell proliferation and apoptosis status. Results: β-catenin and telomerase expression levels in keloid tissues were elevated compared to normal tissues (all P < 0.05). KPC cells in keloid exhibited more dynamic telomerase activity than SKP cells (P < 0.05). Luciferase activity assay confirmed that β-catenin could directly interact with telomerase. After wnt10a/β-catenin signaling pathway was inhibited, the proliferation of KPC cells was significantly suppressed and the apoptosis rate was remarkably increased (all P < 0.05). Results from tumor models also validated that wnt10a/β-catenin signaling pathway influenced the activity and length of telomerase. Conclusions: Wnt/β-catenin signaling pathway is able to exacerbate keloid cell proliferation and inhibit the apoptosis of keloid cells through its interaction with telomerase.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>beta Catenin - antagonists & inhibitors</subject><subject>beta Catenin - genetics</subject><subject>beta Catenin - metabolism</subject><subject>Cancer</subject><subject>Cell growth</subject><subject>Cell Proliferation</subject><subject>Cloning</subject><subject>Disease</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Gene Expression Regulation</subject><subject>Genes</subject><subject>Genes, Reporter</subject><subject>Growth models</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Keloid</subject><subject>Keloid - genetics</subject><subject>Keloid - metabolism</subject><subject>Keloid - pathology</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Luciferases - genetics</subject><subject>Luciferases - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Original Paper</subject><subject>Patients</subject><subject>Plasmids</subject><subject>Primary Cell Culture</subject><subject>RNA, Small Interfering - genetics</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Signal Transduction - genetics</subject><subject>Skin</subject><subject>Stem cells</subject><subject>Stem Cells - metabolism</subject><subject>Stem Cells - pathology</subject><subject>Telomerase</subject><subject>Telomerase - antagonists & inhibitors</subject><subject>Telomerase - genetics</subject><subject>Telomerase - metabolism</subject><subject>Transfection</subject><subject>Wnt</subject><subject>Wnt Proteins - antagonists & inhibitors</subject><subject>Wnt Proteins - genetics</subject><subject>Wnt Proteins - metabolism</subject><subject>β-catenin</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DOA</sourceid><recordid>eNptkc9u1DAQxi0Eou3CgTtCkbiUQ6j_xY6PEBWoqEQFRT1aY8eOvGTjrZ1I9LV4EJ4Jl10WCXEaz_jnb77xIPSM4NeENOoMY8y5bJV4gI4Jp6RWUrYPyxmTpm5VK4_QSc5rXFKp6GN0RKWURBJ-jG5upvns54-6g9lNYaq-hGGCMUxDdf4drEum1HP10Y0x9FXnxrG6SnEM3iWYQ5wqc1d9dsMylqy8uS7cplxl9wQ98jBm93QfV-jru_Pr7kN9-en9RffmsrZcsLmWRnFBsTFWgcEAWDCCPTBLW6wos9wKzi3rlTfcMSG9KtEIJ71U3hvJVuhip9tHWOttChtIdzpC0L8LMQ0a0hzs6LQEbCh2jDe94b7nwDkzrbANVdRQS4vW6U5rm-Lt4vKsNyHbMjNMLi5Zk5Y1DRVNMblCL_9B13FJ5eeyZphjVqy294KvdpRNMefk_MEgwfp-c_qwucK-2CsuZuP6A_lnVX9bfoM0uHQAuqu3Owm97X2hnv-X2nf5BSYZp5c</recordid><startdate>20160101</startdate><enddate>20160101</enddate><creator>Yu, Dongmei</creator><creator>Shang, Yong</creator><creator>Yuan, Jian</creator><creator>Ding, Shuang</creator><creator>Luo, Sai</creator><creator>Hao, Lijun</creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20160101</creationdate><title>Wnt/β-Catenin Signaling Exacerbates Keloid Cell Proliferation by Regulating Telomerase</title><author>Yu, Dongmei ; Shang, Yong ; Yuan, Jian ; Ding, Shuang ; Luo, Sai ; Hao, Lijun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-7b94620bbc9ab0aa06310fa3c280923c4c644c3d9fb4e367f9b4eb6e7f79ffb73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>beta Catenin - antagonists & inhibitors</topic><topic>beta Catenin - genetics</topic><topic>beta Catenin - metabolism</topic><topic>Cancer</topic><topic>Cell growth</topic><topic>Cell Proliferation</topic><topic>Cloning</topic><topic>Disease</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Gene Expression Regulation</topic><topic>Genes</topic><topic>Genes, Reporter</topic><topic>Growth models</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Keloid</topic><topic>Keloid - genetics</topic><topic>Keloid - metabolism</topic><topic>Keloid - pathology</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Luciferases - genetics</topic><topic>Luciferases - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Original Paper</topic><topic>Patients</topic><topic>Plasmids</topic><topic>Primary Cell Culture</topic><topic>RNA, Small Interfering - genetics</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Signal Transduction - genetics</topic><topic>Skin</topic><topic>Stem cells</topic><topic>Stem Cells - metabolism</topic><topic>Stem Cells - pathology</topic><topic>Telomerase</topic><topic>Telomerase - antagonists & inhibitors</topic><topic>Telomerase - genetics</topic><topic>Telomerase - metabolism</topic><topic>Transfection</topic><topic>Wnt</topic><topic>Wnt Proteins - antagonists & inhibitors</topic><topic>Wnt Proteins - genetics</topic><topic>Wnt Proteins - metabolism</topic><topic>β-catenin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yu, Dongmei</creatorcontrib><creatorcontrib>Shang, Yong</creatorcontrib><creatorcontrib>Yuan, Jian</creatorcontrib><creatorcontrib>Ding, Shuang</creatorcontrib><creatorcontrib>Luo, Sai</creatorcontrib><creatorcontrib>Hao, Lijun</creatorcontrib><collection>Karger Open Access Journals</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>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</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>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>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular physiology and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yu, Dongmei</au><au>Shang, Yong</au><au>Yuan, Jian</au><au>Ding, Shuang</au><au>Luo, Sai</au><au>Hao, Lijun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Wnt/β-Catenin Signaling Exacerbates Keloid Cell Proliferation by Regulating Telomerase</atitle><jtitle>Cellular physiology and biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2016-01-01</date><risdate>2016</risdate><volume>39</volume><issue>5</issue><spage>2001</spage><epage>2013</epage><pages>2001-2013</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Abstract
Objectives: Our goal was to investigate the relationship between keloid and telomerase as well as clarifying the influence of Wnt/β-catenin signaling on keloid cell proliferation. Methods: Tissues from 18 keloid patients were collected for further study. Keloid progenitor cells (KPC) and skin progenitor cells (SKP) were both included in this study. Lenti-virus transfection was used to divide cells into different groups in which cells were treated with different substances: negative control (NC) group, wnt10a siRNA group, β-catenin siRNA group and TERT siRNA group. KPC cells were injected into 20 male BALB/c nude mice in order to build tumor models. Several experiments including immunohistochemistry, western blot and RT-PCR were conducted in order to detect the corresponding protein expressions and relative mRNA levels. MTT assay and flow cytometry were also conducted for assessing cell proliferation and apoptosis status. Results: β-catenin and telomerase expression levels in keloid tissues were elevated compared to normal tissues (all P < 0.05). KPC cells in keloid exhibited more dynamic telomerase activity than SKP cells (P < 0.05). Luciferase activity assay confirmed that β-catenin could directly interact with telomerase. After wnt10a/β-catenin signaling pathway was inhibited, the proliferation of KPC cells was significantly suppressed and the apoptosis rate was remarkably increased (all P < 0.05). Results from tumor models also validated that wnt10a/β-catenin signaling pathway influenced the activity and length of telomerase. Conclusions: Wnt/β-catenin signaling pathway is able to exacerbate keloid cell proliferation and inhibit the apoptosis of keloid cells through its interaction with telomerase.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>27771714</pmid><doi>10.1159/000447896</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antibodies Apoptosis Apoptosis - genetics beta Catenin - antagonists & inhibitors beta Catenin - genetics beta Catenin - metabolism Cancer Cell growth Cell Proliferation Cloning Disease Epithelial-Mesenchymal Transition - genetics Gene Expression Regulation Genes Genes, Reporter Growth models Hospitals Humans Keloid Keloid - genetics Keloid - metabolism Keloid - pathology Kinases Laboratory animals Luciferases - genetics Luciferases - metabolism Male Mice Mice, Inbred BALB C Mice, Nude Original Paper Patients Plasmids Primary Cell Culture RNA, Small Interfering - genetics RNA, Small Interfering - metabolism Signal Transduction - genetics Skin Stem cells Stem Cells - metabolism Stem Cells - pathology Telomerase Telomerase - antagonists & inhibitors Telomerase - genetics Telomerase - metabolism Transfection Wnt Wnt Proteins - antagonists & inhibitors Wnt Proteins - genetics Wnt Proteins - metabolism β-catenin |
| title | Wnt/β-Catenin Signaling Exacerbates Keloid Cell Proliferation by Regulating Telomerase |
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