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Article: Anoikis resistant mediated by FASN promoted growth and metastasis of osteosarcoma

TitleAnoikis resistant mediated by FASN promoted growth and metastasis of osteosarcoma
Authors
Keywordsanimal experiment
animal model
animal tissue
anoikis
apoptosis
Issue Date2019
PublisherNature Publishing Group: Open Access Journals - Option C. The Journal's web site is located at http://www.nature.com/cddis/index.html
Citation
Cell Death & Disease, 2019, v. 10, p. article no. 298 How to Cite?
AbstractThe pulmonary metastasis of osteosarcoma (OS) occurs commonly, which resulted from anoikis resistant (AR) of tumor cells as reported by previous studies, but the exact roles of AR in osteosarcoma were not fully studied. Our previous investigations showed fatty acid synthase (FASN) was relating to clinical features of patients with OS. In this study, we aim to explore the functions of FASN in the AR OS cells in vitro and in vivo and study the downstream effectors of FASN. In the present study, we used our established cell model to study the AR. We revealed that AR promoted cell proliferation and migration as determined by colony formation assay and transwell assay. In addition, AR assisted tumor growth in vivo. In the AR cells, the expression of FASN was higher. Thus, we constructed lentiviruses to silence or overexpress FASN in four cell lines to study functions of FASN. Silence of FASN reduced cell colonies and migration while overexpression of FASN increased colonies and migration in suspended cells. Loss of functions of FASN induced cell apoptosis in suspended OS cells while gain of function of FASN suppressed apoptosis as determined by flow cytometry. We found the levels of p-ERK1/2 and Bcl-xL declined when FASN was silenced while they increased when FASN was overexpressed. In addition, results showed that the levels of FASN and its potential related molecules (p-ERK1/2 and Bcl-xL) increased in 143B-AR and MG-63-AR cells. In vivo study showed that inhibition of FASN decreased pulmonary metastasis of OS. In conclusion, we showed that anoikis resistant and FASN as two interactional factors facilitated the progress of osteosarcoma.
Persistent Identifierhttp://hdl.handle.net/10722/276081
ISSN
2017 Impact Factor: 5.638
2015 SCImago Journal Rankings: 2.484
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorSUN, T-
dc.contributor.authorZhong, X-
dc.contributor.authorSong, H-
dc.contributor.authorLiu, J-
dc.contributor.authorLi, J-
dc.contributor.authorLeung, F-
dc.contributor.authorLu, WW-
dc.contributor.authorLiu, ZL-
dc.date.accessioned2019-09-10T02:55:34Z-
dc.date.available2019-09-10T02:55:34Z-
dc.date.issued2019-
dc.identifier.citationCell Death & Disease, 2019, v. 10, p. article no. 298-
dc.identifier.issn2041-4889-
dc.identifier.urihttp://hdl.handle.net/10722/276081-
dc.description.abstractThe pulmonary metastasis of osteosarcoma (OS) occurs commonly, which resulted from anoikis resistant (AR) of tumor cells as reported by previous studies, but the exact roles of AR in osteosarcoma were not fully studied. Our previous investigations showed fatty acid synthase (FASN) was relating to clinical features of patients with OS. In this study, we aim to explore the functions of FASN in the AR OS cells in vitro and in vivo and study the downstream effectors of FASN. In the present study, we used our established cell model to study the AR. We revealed that AR promoted cell proliferation and migration as determined by colony formation assay and transwell assay. In addition, AR assisted tumor growth in vivo. In the AR cells, the expression of FASN was higher. Thus, we constructed lentiviruses to silence or overexpress FASN in four cell lines to study functions of FASN. Silence of FASN reduced cell colonies and migration while overexpression of FASN increased colonies and migration in suspended cells. Loss of functions of FASN induced cell apoptosis in suspended OS cells while gain of function of FASN suppressed apoptosis as determined by flow cytometry. We found the levels of p-ERK1/2 and Bcl-xL declined when FASN was silenced while they increased when FASN was overexpressed. In addition, results showed that the levels of FASN and its potential related molecules (p-ERK1/2 and Bcl-xL) increased in 143B-AR and MG-63-AR cells. In vivo study showed that inhibition of FASN decreased pulmonary metastasis of OS. In conclusion, we showed that anoikis resistant and FASN as two interactional factors facilitated the progress of osteosarcoma.-
dc.languageeng-
dc.publisherNature Publishing Group: Open Access Journals - Option C. The Journal's web site is located at http://www.nature.com/cddis/index.html-
dc.relation.ispartofCell Death & Disease-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectanimal experiment-
dc.subjectanimal model-
dc.subjectanimal tissue-
dc.subjectanoikis-
dc.subjectapoptosis-
dc.titleAnoikis resistant mediated by FASN promoted growth and metastasis of osteosarcoma-
dc.typeArticle-
dc.identifier.emailLeung, F: klleunga@hkucc.hku.hk-
dc.identifier.emailLu, WW: wwlu@hku.hk-
dc.identifier.authorityLeung, F=rp00297-
dc.identifier.authorityLu, WW=rp00411-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/s41419-019-1532-2-
dc.identifier.pmid30931932-
dc.identifier.pmcidPMC6443797-
dc.identifier.scopuseid_2-s2.0-85063734204-
dc.identifier.hkuros305083-
dc.identifier.volume10-
dc.identifier.spagearticle no. 298-
dc.identifier.epagearticle no. 298-
dc.publisher.placeUnited Kingdom-

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