Mportant molecular markers of breast cancer, RNPC1 could develop to a novel molecular maker as a downstream factor of p53.Conclusions In summary, RNPC1 was frequently loss or low-expressed in breast cancer. RNPC1 inhibits breast cancer cells proliferation and further suppressed tumor-cell migration and invasion. RNPC1 significantly negative correlated between RNPC1 protein and mutp53, lymphonode metastasis, clinic stage. It suggested RNPC1 acting as a functional tumor suppressor in breast tumorigenesis and metastasis. RNPC1 may become a potential marker in the therapeutic or prognostic practice of breast cancer.Xue et al. BMC Cancer 2014, 14:322 12 ofAdditional filesAdditional file 1: Table S1. RNPC1a shRNA sequences. Figure S1. Identification of stably transfected MCF-7 and MB-231 cells. (A, C) Western blot was used to verify the efficiency of knockdown. The cells transduced with the three shRNAs and one control shRNA are designated as `sh1′, `sh2′, `sh3′ and `SCR’. RNPC1a-knockdown MCF-7 and MB-231 cells had 85 lower expression when compared with SCR cells. The fold change of RNPC1a is shown below each lane. Arbitrarily set at 1.0 in control cells. The intensity of the bands was determined using densitometric analysis. (B, D) qRT-PCR was used to detect RNPC1a expression. The results are similar to those seen in the Western blot analyses. Data were means of two separate experiments mean ?SEM, * p < 0.05. Additional file 2: Figure S2. Cell cycle was progress in RNPC1a knockdown MCF-7 cells. (A) The progression of MCF-7-SCR cells was more arrested in the G1 phase compared to MCF-7-shRNPC1a cells. (B) Histogram of cell cycle analyses. Data were means of three separate experiments mean ?SEM, *p < 0.05. Additional file 3: Figure S3. RNPC1a decreased migration and invasion in MCF-7 cells. (A) The number of migrating and invading cells was higher in MCF-7-NC than the MCF-7-RNPC1a cells. (B) The number of migrating and invading cells was lower in MCF-7-SCR than the MCF-7shRNPC1a cells. Data presented average number of cells/field for three fields. (C, D) Columns: average data of three independent experiments, mean ?SEM, *p < 0.05, ***p < 17.18.Competing interests The authors declare that have no competing interests. Authors' contributions QD and J-QX PubMed ID: have contributed to the conception and design of the study, T-SX performed the analysis and interpretation of data, as well as final approval of the version to be submitted. X-QL and WZ participated in the design of the study, performed the statistical analysis, drafted and revised the article. LC, LS, YW performed the experimental study. All authors read and approved the final version of manuscript. Acknowledgements This work was financially supported by the Natural Science Foundation of China (81272916 and 81202077), the Natural Science Foundation of Jiangsu Province (BK2011855), the key projects of Jiangsu Provincial Health Office (to Qiang Ding), the Project of Jiangsu Province Traditional Chinese medicine bureau (LZ11084), the Six Talents Peak projects of Jiangsu province (IB09), and a project Funded by the P144 Peptide site Priority Academic Program Development of Jiangsu higher Education Institutions (PAPD). Received: 5 November 2013 Accepted: 29 April 2014 Published: 7 May 2014 References 1. Smith RA, Cokkinides V, Brooks D, Saslow D, Brawley OW: Cancer screening in the United States, 2010 A Review of Current American Cancer Soci.