Cell division cycle-associated protein 1 as a new melanoma-associated antigen

Immune checkpoint inhibitors have increased the median survival of melanoma patients. To improve their effects, antigen‐specific therapies utilizing melanoma‐associated antigens should be developed. Cell division cycle‐associated protein 1 (CDCA1), which has a specific function at the kinetochores f...

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Published inJournal of dermatology Vol. 43; no. 12; pp. 1399 - 1405
Main Authors Tokuzumi, Aki, Fukushima, Satoshi, Miyashita, Azusa, Nakahara, Satoshi, Kubo, Yosuke, Yamashita, Junji, Harada, Miho, Nakamura, Kayo, Kajihara, Ikko, Jinnin, Masatoshi, Ihn, Hironobu
Format Journal Article
LanguageEnglish
Published England Blackwell Publishing Ltd 01.12.2016
Wiley Subscription Services, Inc
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Summary:Immune checkpoint inhibitors have increased the median survival of melanoma patients. To improve their effects, antigen‐specific therapies utilizing melanoma‐associated antigens should be developed. Cell division cycle‐associated protein 1 (CDCA1), which has a specific function at the kinetochores for stabilizing microtubule attachment, is overexpressed in various cancers. CDCA1, which is a member of cancer–testis antigens, does not show detectable expression levels in normal tissues. Quantitative reverse transcription polymerase chain reaction and immunoblotting analyses revealed that CDCA1 was expressed in all of the tested melanoma cell lines, 74% of primary melanomas, 64% of metastatic melanomas and 25% of nevi. An immunohistochemical analysis and a Cox proportional hazards model showed that CDCA1 could be a prognostic marker in malignant melanoma (MM) patients. CDCA1‐specific siRNA inhibited the cell proliferation of SKMEL2 and WM115 cells, but did not reduce the migration or invasion activity. These results suggest that CDCA1 may be a new therapeutic target of melanoma.
Bibliography:ark:/67375/WNG-2CGN2V57-5
ArticleID:JDE13436
istex:C27379244D254B5FF661281BDC9C13C58197C7E2
JSPS KAKENHI - No. 25870545; No. 15K09772
National Cancer Center Research and Development Fund - No. 26-A-4
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0385-2407
1346-8138
DOI:10.1111/1346-8138.13436