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Conference Paper: NFATc2 in non-small cell lung cancer mediates inhibition of peripheral blood mononuclear cell proliferation

TitleNFATc2 in non-small cell lung cancer mediates inhibition of peripheral blood mononuclear cell proliferation
Authors
Issue Date2017
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Proceedings of 108th Annual Meeting of the American Association for Cancer Research (AACR), Washington, DC, USA, 1-5 April 2017. In Cancer Research, 2017, v. 77 n. 13, Suppl.1, abstract 2699 How to Cite?
AbstractLung cancer is the leading cause of cancer death worldwide. While genetic mutations that provide growth advantages to cancer cells are fundamental to malignant transformation, ability to evade the immune system is also crucial in tumorigenesis. We have previously shown that human lung cancers with high expression of nuclear factor of activated T cells, cytoplasmic 2, (NFATc2) are associated with reduced recurrence-free and overall survival. NFATc2 is expressed in most immune cells and has been extensively studied in immune cells. However, its function in cancer development is not completely understood. In this study, the role of NFATc2 in lung cancer on immune escape is explored. Lung cancer cell lines with high NFATc2 expression were co-cultured with peripheral blood mononuclear cells (PBMC) and a significant inhibition of PBMC proliferation was observed compared to PBMC only control. However, the inhibitory effect of PBMC proliferation was reversed in co-culture with NFATc2 knockdown cancer cells. When cancer cells and PBMC were separated by a membrane using Transwell inserts, the anti-proliferative effect on PBMC was not observed suggesting that cell-cell contact was required for the NFATc2-mediated inhibition. Moreover, interleukin-2 (IL-2) was produced by PBMC irrespective of the presence or absence of lung cancer cells. These results showed that the inhibition of proliferation was independent of the activation of PBMC. Taken together, we have shown NFATc2 in lung cancer plays a role in immune modulation by inhibiting PBMC proliferation and this could be a novel mechanism of immune evasion in lung cancer.
Persistent Identifierhttp://hdl.handle.net/10722/259743
ISSN
2017 Impact Factor: 9.13
2015 SCImago Journal Rankings: 5.372
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLam, KYI-
dc.contributor.authorXiao, Z-
dc.contributor.authorTin, VPC-
dc.contributor.authorHuang, F-
dc.contributor.authorWong, MP-
dc.date.accessioned2018-09-03T04:13:11Z-
dc.date.available2018-09-03T04:13:11Z-
dc.date.issued2017-
dc.identifier.citationProceedings of 108th Annual Meeting of the American Association for Cancer Research (AACR), Washington, DC, USA, 1-5 April 2017. In Cancer Research, 2017, v. 77 n. 13, Suppl.1, abstract 2699-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/259743-
dc.description.abstractLung cancer is the leading cause of cancer death worldwide. While genetic mutations that provide growth advantages to cancer cells are fundamental to malignant transformation, ability to evade the immune system is also crucial in tumorigenesis. We have previously shown that human lung cancers with high expression of nuclear factor of activated T cells, cytoplasmic 2, (NFATc2) are associated with reduced recurrence-free and overall survival. NFATc2 is expressed in most immune cells and has been extensively studied in immune cells. However, its function in cancer development is not completely understood. In this study, the role of NFATc2 in lung cancer on immune escape is explored. Lung cancer cell lines with high NFATc2 expression were co-cultured with peripheral blood mononuclear cells (PBMC) and a significant inhibition of PBMC proliferation was observed compared to PBMC only control. However, the inhibitory effect of PBMC proliferation was reversed in co-culture with NFATc2 knockdown cancer cells. When cancer cells and PBMC were separated by a membrane using Transwell inserts, the anti-proliferative effect on PBMC was not observed suggesting that cell-cell contact was required for the NFATc2-mediated inhibition. Moreover, interleukin-2 (IL-2) was produced by PBMC irrespective of the presence or absence of lung cancer cells. These results showed that the inhibition of proliferation was independent of the activation of PBMC. Taken together, we have shown NFATc2 in lung cancer plays a role in immune modulation by inhibiting PBMC proliferation and this could be a novel mechanism of immune evasion in lung cancer.-
dc.languageeng-
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/-
dc.relation.ispartofCancer Research-
dc.relation.ispartof108th Annual Meeting of the American Association for Cancer Research (AACR), 2017-
dc.titleNFATc2 in non-small cell lung cancer mediates inhibition of peripheral blood mononuclear cell proliferation-
dc.typeConference_Paper-
dc.identifier.emailLam, KYI: lamkyian@hku.hk-
dc.identifier.emailXiao, Z: xiaozj@hku.hk-
dc.identifier.emailTin, VPC: pctin@hku.hk-
dc.identifier.emailHuang, F: fphuang@hku.hk-
dc.identifier.emailWong, MP: mwpik@hku.hk-
dc.identifier.authorityHuang, F=rp01922-
dc.identifier.authorityWong, MP=rp00348-
dc.identifier.doi10.1158/1538-7445.AM2017-2699-
dc.identifier.hkuros288317-
dc.identifier.volume77-
dc.identifier.issue13, Suppl.1-
dc.identifier.isiWOS:000442496706013-
dc.publisher.placeUnited States-

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