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Volume 69, Issue 2, Pages 232-238 (August 2010)


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Expression of Mina53, a novel c-Myc target gene, is a favorable prognostic marker in early stage lung cancer

Kazutoshi Komiyaa, Naoko Sueoka-AraganeaCorresponding Author Informationemail address, Akemi Satoa, Takashi Hisatomia, Toru Sakuragib, Masahiro Mitsuokab, Toshimi Satoc, Shinichiro Hayashia, Hiroto Izumid, Makoto Tsuneokae, Eisaburo Sueokaa

Received 5 August 2009; received in revised form 29 September 2009; accepted 19 October 2009. published online 16 November 2009.

Abstract 

Mina53, a novel target gene product of c-Myc, is overexpressed in various malignancies. We previously demonstrated that Mina53 is overexpressed in lung cancer patients from the early clinical stages. In this paper, the association between disease prognosis and Mina53 expression in lung cancer patients is analyzed; we found that overexpression of Mina53 in lung cancer patients is associated with favorable prognosis. Statistical analysis using the Kaplan–Meier method showed that patients with negative staining for Mina53 had significantly shorter survival than patients with positive staining for Mina53, especially in stage I or with squamous cell carcinoma. Because the major cause of death in lung cancer patients after surgery is distant metastasis, the effect on cancer cell invasiveness was analyzed for the mechanisms involved in the association with favorable outcome. Overexpression of Mina53 in H226B, a lung squamous cell carcinoma cell line, inhibited cancer cell invasion. Transfection with mina53 shRNA increased the number of invading cells. These results suggest that Mina53 immunostaining is a useful prognostic marker – especially in the early stage of lung cancer – and that Mina53 negative patients should be managed particularly carefully after surgery.

a Department of Internal Medicine, Faculty of Medicine, Saga University, 5-1-1 Nabeshima, Saga 849-8501, Japan

b Department of Thoracic Surgery, Faculty of Medicine, Saga University, 5-1-1 Nabeshima, Saga 849-8501, Japan

c Department of Pathology, Faculty of Medicine, Saga University, 5-1-1 Nabeshima, Saga 849-8501, Japan

d Department of Molecular Biology, University of Occupational and Environmental Health, Kitakyushu, Fukuoka 807-8555, Japan

e Department of Pharmacology, Takasaki University of Health and Welfare, Takasaki 370-0033, Japan

Corresponding Author InformationCorresponding author. Tel.: +81 952 34 3531; fax: +81 952 34 2017.

PII: S0169-5002(09)00541-8

doi:10.1016/j.lungcan.2009.10.010


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