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Article: Contactin 1 modulates pegylated arginase resistance in small cell lung cancer through induction of epithelial-mesenchymal transition
Title | Contactin 1 modulates pegylated arginase resistance in small cell lung cancer through induction of epithelial-mesenchymal transition |
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Authors | |
Keywords | Neural Cell Adhesion Molecule L1 Neoplasms Contactins |
Issue Date | 2019 |
Publisher | Nature Research (part of Springer Nature): Fully open access journals. The Journal's web site is located at http://www.nature.com/srep/index.html |
Citation | Scientific Reports, 2019, v. 9, p. article no. 12030 How to Cite? |
Abstract | Drug resistance is a major hurdle in the treatment of small cell lung cancer (SCLC). Previously we demonstrated the potential anticancer effect of pegylated arginase BCT-100 in SCLC cell lines and xenograft models. To facilitate future clinical application of BCT-100 in SCLC treatment, we elucidated the potential mechanisms that underlie acquired drug resistance to BCT-100. H446 and H526 SCLC cells were serially cultured in stepwise increasing concentrations of BCT-100 until stable BCT-100-resistant cell lines emerged (H446-BR and H526-BR). Compared with parent cells, H446-BR and H526-BR displayed stronger migration ability, anoikis resistance and EMT progression. Gene chip assay was employed to select three potential targets (CDH17, CNTN-1 and IGF2BP1). Silencing CNTN-1 rather than CDH17 or IGF2BP1 in H446-BR and H526-BR cells re-sensitized resistant cells to BCT-100 treatment and attenuated the epithelial-mesenchymal transition (EMT) phenotype. The AKT signaling pathway was activated in H446-BR and H526-BR cells accompanied by EMT progression, and AKT inhibitor LY294002 reversed the EMT progression in resistant cells. |
Persistent Identifier | http://hdl.handle.net/10722/277359 |
ISSN | 2023 Impact Factor: 3.8 2023 SCImago Journal Rankings: 0.900 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | XU, S | - |
dc.contributor.author | Lam, SK | - |
dc.contributor.author | Cheng, PNM | - |
dc.contributor.author | Ho, JCM | - |
dc.date.accessioned | 2019-09-20T08:49:30Z | - |
dc.date.available | 2019-09-20T08:49:30Z | - |
dc.date.issued | 2019 | - |
dc.identifier.citation | Scientific Reports, 2019, v. 9, p. article no. 12030 | - |
dc.identifier.issn | 2045-2322 | - |
dc.identifier.uri | http://hdl.handle.net/10722/277359 | - |
dc.description.abstract | Drug resistance is a major hurdle in the treatment of small cell lung cancer (SCLC). Previously we demonstrated the potential anticancer effect of pegylated arginase BCT-100 in SCLC cell lines and xenograft models. To facilitate future clinical application of BCT-100 in SCLC treatment, we elucidated the potential mechanisms that underlie acquired drug resistance to BCT-100. H446 and H526 SCLC cells were serially cultured in stepwise increasing concentrations of BCT-100 until stable BCT-100-resistant cell lines emerged (H446-BR and H526-BR). Compared with parent cells, H446-BR and H526-BR displayed stronger migration ability, anoikis resistance and EMT progression. Gene chip assay was employed to select three potential targets (CDH17, CNTN-1 and IGF2BP1). Silencing CNTN-1 rather than CDH17 or IGF2BP1 in H446-BR and H526-BR cells re-sensitized resistant cells to BCT-100 treatment and attenuated the epithelial-mesenchymal transition (EMT) phenotype. The AKT signaling pathway was activated in H446-BR and H526-BR cells accompanied by EMT progression, and AKT inhibitor LY294002 reversed the EMT progression in resistant cells. | - |
dc.language | eng | - |
dc.publisher | Nature Research (part of Springer Nature): Fully open access journals. The Journal's web site is located at http://www.nature.com/srep/index.html | - |
dc.relation.ispartof | Scientific Reports | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject | Neural Cell Adhesion Molecule L1 | - |
dc.subject | Neoplasms | - |
dc.subject | Contactins | - |
dc.title | Contactin 1 modulates pegylated arginase resistance in small cell lung cancer through induction of epithelial-mesenchymal transition | - |
dc.type | Article | - |
dc.identifier.email | Lam, SK: sklam77@hku.hk | - |
dc.identifier.email | Ho, JCM: jhocm@hku.hk | - |
dc.identifier.authority | Ho, JCM=rp00258 | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1038/s41598-019-48476-8 | - |
dc.identifier.pmid | 31427725 | - |
dc.identifier.pmcid | PMC6700313 | - |
dc.identifier.scopus | eid_2-s2.0-85070802797 | - |
dc.identifier.hkuros | 305937 | - |
dc.identifier.volume | 9 | - |
dc.identifier.spage | article no. 12030 | - |
dc.identifier.epage | article no. 12030 | - |
dc.identifier.isi | WOS:000481590200071 | - |
dc.publisher.place | United Kingdom | - |
dc.identifier.issnl | 2045-2322 | - |