Sialylation of FGFR1 by ST6Gal‑I overexpression contributes to ovarian cancer cell migration and chemoresistance
Fibroblast growth factor receptors (FGFRs) have been implicated in the malignant transformation and chemoresistance of epithelial ovarian cancer; however, the underlying molecular mechanisms are poorly understood. Increased sialyltransferase activity that enhances protein sialylation is an important...
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| Veröffentlicht in: | Molecular medicine reports 2020-03, Vol.21 (3), p.1449-1460 |
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| creator | Ou, Lingling He, Xiuzhen Liu, Naihua Song, Yuwei Li, Jinyuan Gao, Lvfen Huang, Xinke Deng, Zhendong Wang, Xiaoyu Lin, Shaoqiang |
| description | Fibroblast growth factor receptors (FGFRs) have been implicated in the malignant transformation and chemoresistance of epithelial ovarian cancer; however, the underlying molecular mechanisms are poorly understood. Increased sialyltransferase activity that enhances protein sialylation is an important post‑translational process promoting cancer progression and malignancy. In the present study, α2,6‑sialyltransferase (ST6Gal‑I) overexpression or knockdown cell lines were developed, and FGFR1 was examined to understand the effect of sialylation on migration and drug resistance, and the underlying mechanisms. It was identified that cells with ST6Gal‑I overexpression had increased cell viability and migratory ability upon serum deprivation. Moreover, ST6Gal‑I overexpression cells had strong resistance to paclitaxel, as demonstrated by low growth inhibition rate and cell apoptosis level. A mechanistic study showed that ST6Gal‑I overexpression induced high α2,6‑sialylation of FGFR1 and increased the expression of phospho‑ERK1/2 and phospho‑focal adhesion kinase. Further study demonstrated that the FGFR1 inhibitor PD173047 reduced cell viability and induced apoptosis; however, ST6Gal‑I overexpression decreased the anticancer effect of PD173047. In addition, ST6Gal‑I overexpression attenuated the effect of Adriamycin on cancer cells. Collectively, these results suggested that FGFR1 sialylation plays an important role in cell migration and drug chemoresistance in ovarian cancer cells. |
| doi_str_mv | 10.3892/mmr.2020.10951 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7003046</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A617388023</galeid><sourcerecordid>A617388023</sourcerecordid><originalsourceid>FETCH-LOGICAL-c485t-7074756e8cc77d17fb89de43fb6846d1316571268f212756053e7891cea7fec93</originalsourceid><addsrcrecordid>eNptkk1r3DAQhk1padK01x6LoZdcdjOSbH1cCiF0t4FAoEnPQpZHGwXb2kp26N7yF_oX-0sqN9v0gyCBxOiZdzTDWxRvCSyZVPSk7-OSAoUlAVWTZ8UhEYosGED1fH-nSomD4lVKtwC8prV6WRwwCoRXAg6LeOVNt-vM6MNQBleu1qvPpGx25dU1X5vux_338zLcYcRv24gpzZQNwxh9M42YyjHkVxO9yWEzWIylxa4re7-JD5JmaEt7g33I2T6NM_O6eOFMl_DN_jwqvqw-Xp99Wlxcrs_PTi8WtpL1uBAgKlFzlNYK0RLhGqlarJhruKx4SxjhtSCUS0cJzSDUDIVUxKIRDq1iR8WHB93t1PTYWszfNp3eRt-buNPBeP3vy-Bv9CbcaQHAoOJZ4HgvEMPXCdOoe5_m_syAYUqashoU5D3Xev8fehumOOT2ZooqqmQNf6iN6VD7wYVc186i-pQTwaQEyjK1fILKq8Xe5-Gj8zn-VIKNIaWI7rFHAnp2ic4u0bNL9C-X5IR3f0_mEf9tC_YTnRu4gA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2352929850</pqid></control><display><type>article</type><title>Sialylation of FGFR1 by ST6Gal‑I overexpression contributes to ovarian cancer cell migration and chemoresistance</title><source>Spandidos Publications Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Ou, Lingling ; He, Xiuzhen ; Liu, Naihua ; Song, Yuwei ; Li, Jinyuan ; Gao, Lvfen ; Huang, Xinke ; Deng, Zhendong ; Wang, Xiaoyu ; Lin, Shaoqiang</creator><creatorcontrib>Ou, Lingling ; He, Xiuzhen ; Liu, Naihua ; Song, Yuwei ; Li, Jinyuan ; Gao, Lvfen ; Huang, Xinke ; Deng, Zhendong ; Wang, Xiaoyu ; Lin, Shaoqiang</creatorcontrib><description>Fibroblast growth factor receptors (FGFRs) have been implicated in the malignant transformation and chemoresistance of epithelial ovarian cancer; however, the underlying molecular mechanisms are poorly understood. Increased sialyltransferase activity that enhances protein sialylation is an important post‑translational process promoting cancer progression and malignancy. In the present study, α2,6‑sialyltransferase (ST6Gal‑I) overexpression or knockdown cell lines were developed, and FGFR1 was examined to understand the effect of sialylation on migration and drug resistance, and the underlying mechanisms. It was identified that cells with ST6Gal‑I overexpression had increased cell viability and migratory ability upon serum deprivation. Moreover, ST6Gal‑I overexpression cells had strong resistance to paclitaxel, as demonstrated by low growth inhibition rate and cell apoptosis level. A mechanistic study showed that ST6Gal‑I overexpression induced high α2,6‑sialylation of FGFR1 and increased the expression of phospho‑ERK1/2 and phospho‑focal adhesion kinase. Further study demonstrated that the FGFR1 inhibitor PD173047 reduced cell viability and induced apoptosis; however, ST6Gal‑I overexpression decreased the anticancer effect of PD173047. In addition, ST6Gal‑I overexpression attenuated the effect of Adriamycin on cancer cells. Collectively, these results suggested that FGFR1 sialylation plays an important role in cell migration and drug chemoresistance in ovarian cancer cells.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2020.10951</identifier><identifier>PMID: 32016470</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Anthracyclines ; Apoptosis ; Biotechnology ; Cancer cells ; Cancer metastasis ; Cancer therapies ; Cancer treatment ; Cell adhesion & migration ; Cell cycle ; Cell growth ; Cell migration ; Cell viability ; Chemoresistance ; Cloning ; Drug resistance ; Extracellular signal-regulated kinase ; Fibroblast growth factor receptor 1 ; Fibroblast growth factor receptors ; Fibroblast growth factors ; Fibroblasts ; Focal adhesion kinase ; Gene expression ; Growth factor receptors ; Kinases ; Laboratories ; Malignancy ; Medical prognosis ; Molecular modelling ; Mutation ; Ovarian cancer ; Paclitaxel ; Pharmaceutical industry ; Post-translation ; Prostate ; Scientific equipment industry ; Wound healing</subject><ispartof>Molecular medicine reports, 2020-03, Vol.21 (3), p.1449-1460</ispartof><rights>COPYRIGHT 2020 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2020</rights><rights>Copyright: © Ou et al. 2020</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c485t-7074756e8cc77d17fb89de43fb6846d1316571268f212756053e7891cea7fec93</citedby><cites>FETCH-LOGICAL-c485t-7074756e8cc77d17fb89de43fb6846d1316571268f212756053e7891cea7fec93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32016470$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ou, Lingling</creatorcontrib><creatorcontrib>He, Xiuzhen</creatorcontrib><creatorcontrib>Liu, Naihua</creatorcontrib><creatorcontrib>Song, Yuwei</creatorcontrib><creatorcontrib>Li, Jinyuan</creatorcontrib><creatorcontrib>Gao, Lvfen</creatorcontrib><creatorcontrib>Huang, Xinke</creatorcontrib><creatorcontrib>Deng, Zhendong</creatorcontrib><creatorcontrib>Wang, Xiaoyu</creatorcontrib><creatorcontrib>Lin, Shaoqiang</creatorcontrib><title>Sialylation of FGFR1 by ST6Gal‑I overexpression contributes to ovarian cancer cell migration and chemoresistance</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Fibroblast growth factor receptors (FGFRs) have been implicated in the malignant transformation and chemoresistance of epithelial ovarian cancer; however, the underlying molecular mechanisms are poorly understood. Increased sialyltransferase activity that enhances protein sialylation is an important post‑translational process promoting cancer progression and malignancy. In the present study, α2,6‑sialyltransferase (ST6Gal‑I) overexpression or knockdown cell lines were developed, and FGFR1 was examined to understand the effect of sialylation on migration and drug resistance, and the underlying mechanisms. It was identified that cells with ST6Gal‑I overexpression had increased cell viability and migratory ability upon serum deprivation. Moreover, ST6Gal‑I overexpression cells had strong resistance to paclitaxel, as demonstrated by low growth inhibition rate and cell apoptosis level. A mechanistic study showed that ST6Gal‑I overexpression induced high α2,6‑sialylation of FGFR1 and increased the expression of phospho‑ERK1/2 and phospho‑focal adhesion kinase. Further study demonstrated that the FGFR1 inhibitor PD173047 reduced cell viability and induced apoptosis; however, ST6Gal‑I overexpression decreased the anticancer effect of PD173047. In addition, ST6Gal‑I overexpression attenuated the effect of Adriamycin on cancer cells. Collectively, these results suggested that FGFR1 sialylation plays an important role in cell migration and drug chemoresistance in ovarian cancer cells.</description><subject>Anthracyclines</subject><subject>Apoptosis</subject><subject>Biotechnology</subject><subject>Cancer cells</subject><subject>Cancer metastasis</subject><subject>Cancer therapies</subject><subject>Cancer treatment</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell migration</subject><subject>Cell viability</subject><subject>Chemoresistance</subject><subject>Cloning</subject><subject>Drug resistance</subject><subject>Extracellular signal-regulated kinase</subject><subject>Fibroblast growth factor receptor 1</subject><subject>Fibroblast growth factor receptors</subject><subject>Fibroblast growth factors</subject><subject>Fibroblasts</subject><subject>Focal adhesion kinase</subject><subject>Gene expression</subject><subject>Growth factor receptors</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Malignancy</subject><subject>Medical prognosis</subject><subject>Molecular modelling</subject><subject>Mutation</subject><subject>Ovarian cancer</subject><subject>Paclitaxel</subject><subject>Pharmaceutical industry</subject><subject>Post-translation</subject><subject>Prostate</subject><subject>Scientific equipment industry</subject><subject>Wound healing</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkk1r3DAQhk1padK01x6LoZdcdjOSbH1cCiF0t4FAoEnPQpZHGwXb2kp26N7yF_oX-0sqN9v0gyCBxOiZdzTDWxRvCSyZVPSk7-OSAoUlAVWTZ8UhEYosGED1fH-nSomD4lVKtwC8prV6WRwwCoRXAg6LeOVNt-vM6MNQBleu1qvPpGx25dU1X5vux_338zLcYcRv24gpzZQNwxh9M42YyjHkVxO9yWEzWIylxa4re7-JD5JmaEt7g33I2T6NM_O6eOFMl_DN_jwqvqw-Xp99Wlxcrs_PTi8WtpL1uBAgKlFzlNYK0RLhGqlarJhruKx4SxjhtSCUS0cJzSDUDIVUxKIRDq1iR8WHB93t1PTYWszfNp3eRt-buNPBeP3vy-Bv9CbcaQHAoOJZ4HgvEMPXCdOoe5_m_syAYUqashoU5D3Xev8fehumOOT2ZooqqmQNf6iN6VD7wYVc186i-pQTwaQEyjK1fILKq8Xe5-Gj8zn-VIKNIaWI7rFHAnp2ic4u0bNL9C-X5IR3f0_mEf9tC_YTnRu4gA</recordid><startdate>20200301</startdate><enddate>20200301</enddate><creator>Ou, Lingling</creator><creator>He, Xiuzhen</creator><creator>Liu, Naihua</creator><creator>Song, Yuwei</creator><creator>Li, Jinyuan</creator><creator>Gao, Lvfen</creator><creator>Huang, Xinke</creator><creator>Deng, Zhendong</creator><creator>Wang, Xiaoyu</creator><creator>Lin, Shaoqiang</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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however, the underlying molecular mechanisms are poorly understood. Increased sialyltransferase activity that enhances protein sialylation is an important post‑translational process promoting cancer progression and malignancy. In the present study, α2,6‑sialyltransferase (ST6Gal‑I) overexpression or knockdown cell lines were developed, and FGFR1 was examined to understand the effect of sialylation on migration and drug resistance, and the underlying mechanisms. It was identified that cells with ST6Gal‑I overexpression had increased cell viability and migratory ability upon serum deprivation. Moreover, ST6Gal‑I overexpression cells had strong resistance to paclitaxel, as demonstrated by low growth inhibition rate and cell apoptosis level. A mechanistic study showed that ST6Gal‑I overexpression induced high α2,6‑sialylation of FGFR1 and increased the expression of phospho‑ERK1/2 and phospho‑focal adhesion kinase. Further study demonstrated that the FGFR1 inhibitor PD173047 reduced cell viability and induced apoptosis; however, ST6Gal‑I overexpression decreased the anticancer effect of PD173047. In addition, ST6Gal‑I overexpression attenuated the effect of Adriamycin on cancer cells. Collectively, these results suggested that FGFR1 sialylation plays an important role in cell migration and drug chemoresistance in ovarian cancer cells.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>32016470</pmid><doi>10.3892/mmr.2020.10951</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Anthracyclines Apoptosis Biotechnology Cancer cells Cancer metastasis Cancer therapies Cancer treatment Cell adhesion & migration Cell cycle Cell growth Cell migration Cell viability Chemoresistance Cloning Drug resistance Extracellular signal-regulated kinase Fibroblast growth factor receptor 1 Fibroblast growth factor receptors Fibroblast growth factors Fibroblasts Focal adhesion kinase Gene expression Growth factor receptors Kinases Laboratories Malignancy Medical prognosis Molecular modelling Mutation Ovarian cancer Paclitaxel Pharmaceutical industry Post-translation Prostate Scientific equipment industry Wound healing |
| title | Sialylation of FGFR1 by ST6Gal‑I overexpression contributes to ovarian cancer cell migration and chemoresistance |
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