Supplementary Tables S1-S6 from STAT1 Drives Tumor Progression in Serous Papillary Endometrial Cancer

Kharma, Budiman; Baba, Tsukasa; Matsumura, Noriomi; Kang, Hyun Sook; Hamanishi, Junzo; Murakami, Ryusuke; McConechy, Melissa M.; Leung, Samuel; Yamaguchi, Ken; Hosoe, Yuko; Yoshioka, Yumiko; Murphy, Susan K.; Mandai, Masaki; Hunstman, David G.; Konishi, Ikuo

doi:10.1158/0008-5472.22403913.v1

00085472can140847-sup-128828_1_supp_0_ncdgzc.docx (66.21 kB)

Supplementary Tables S1-S6 from STAT1 Drives Tumor Progression in Serous Papillary Endometrial Cancer

journal contribution

posted on 2023-03-30, 22:48 authored by Budiman Kharma, Tsukasa Baba, Noriomi Matsumura, Hyun Sook Kang, Junzo Hamanishi, Ryusuke Murakami, Melissa M. McConechy, Samuel Leung, Ken Yamaguchi, Yuko Hosoe, Yumiko Yoshioka, Susan K. Murphy, Masaki Mandai, David G. Hunstman, Ikuo Konishi

Supplementary Tables S1-S6. Primer sequences (S1); Correlation between histological subtypes of 294 endometrial cancers and FIGO stage (S2); Overlapping upregulated/downregulated genes between Kyoto University Microarray data and TCGA_UCEC-2013 (S3); Significantly differentially expressed genes in GSE56026 from comparison of serous-like versus endometrioid-like clusters by SAM analysis (S4); Multivariate analysis of tumor stage, histology subtype and STAT1 with regard to patients' survival (S5); Connectivity Map analysis for potential candidate drugs based on STAT1 pathway gene expression (S6).

History

ARTICLE ABSTRACT

Recent studies of the interferon-induced transcription factor STAT1 have associated its dysregulation with poor prognosis in some cancers, but its mechanistic contributions are not well defined. In this study, we report that the STAT1 pathway is constitutively upregulated in type II endometrial cancers. STAT1 pathway alteration was especially prominent in serous papillary endometrial cancers (SPEC) that are refractive to therapy. Our results defined a “SPEC signature” as a molecular definition of its malignant features and poor prognosis. Specifically, we found that STAT1 regulated MYC as well as ICAM1, PD-L1, and SMAD7, as well as the capacity for proliferation, adhesion, migration, invasion, and in vivo tumorigenecity in cells with a high SPEC signature. Together, our results define STAT1 as a driver oncogene in SPEC that modulates disease progression. We propose that STAT1 functions as a prosurvival gene in SPEC, in a manner important to tumor progression, and that STAT1 may be a novel target for molecular therapy in this disease. Cancer Res; 74(22); 6519–30. ©2014 AACR.