Research Article The Role of PinX1 in Growth Control of Breast Cancer Cells and Its Potential Molecular Mechanism by mRNA and lncRNA Expression Profiles Screening Rong Shi, 1 Jue-Yu Zhou, 1 Hui Zhou, 1 Zhen Zhao, 2 Sang-Hua Liang, 1 Wen-Ling Zheng, 1 and Wen-Li Ma 1 1 Institute of Genetic Engineering, Southern Medical University, Guangzhou 510515, China 2 Nan Fang Hospital, Southern Medical University, Guangzhou 510515, China Correspondence should be addressed to Wen-Li Ma; igesmu@126.com Received 9 May 2013; Revised 12 November 2013; Accepted 3 December 2013; Published 3 February 2014 Academic Editor: Xin-yuan Guan Copyright © 2014 Rong Shi et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. As a major tumor suppressor gene, the role of PinX1 in breast cancer and its molecular mechanism remain unclear. In this study, overexpression of PinX1 was generated in 3 breast cancer cell lines, and knockdown of PinX1 was performed in a nontumorigenic breast cell line. Te regulation of PinX1 on cell proliferation and cell cycle was observed. A microarray-based lncRNA and mRNA expression profle screening was also performed. We found a lower growth rate, G0/G1 phase arrest, and S phase inhibition in the PinX1 overexpressed breast cancer cells, while a higher growth rate, decreased G0/G1 phase, and increased S phase rate in the PinX1 knocked-down nontumorigenic breast cell. A total of 977 mRNAs and 631 lncRNAs were identifed as diferentially expressed transcripts between PinX1 overexpressed and control MCF-7 cells. Further analysis identifed the involvement of these mRNAs in 52 cancer related pathways and various other biological processes. 11 enhancer-like lncRNAs and 25 lincRNAs with their adjacent mRNA pairs were identifed as coregulated transcripts. Our results confrmed the role of PinX1 as a major tumor suppressor gene in breast cancer cell lines and provided information for further research on the molecular mechanisms of PinX1 in tumorigenesis. 1. Introduction Te potent tumor suppressor PinX1 was originally isolated as one of the Pin2/TRF1 interaction proteins. Unlike other telomere-associated proteins, PinX1 is unique because it can directly interact with the telomerase catalytic component TERT and inhibit telomerase activity [1]. Previous stud- ies determined that PinX1, recruited to the telomeres by TRF1, provided a critical link between TRF1 and telom- erase inhibition to help maintain telomere homeostasis [2]. Te inhibition of endogenous PinX1 in human cancer cells increases the telomerase activity and elongates the telomeres, whereas overexpression of PinX1 inhibits telomerase activity and induces cell crisis [1]. PinX1 knockout in mice can result in embryonic lethality in the PinX1 null mice (PinX1−/−) and the spontaneous development of a variety of malignant tumors in the PinX1 knockout heterozygous mice (PinX1+/−) [3], indicating that PinX1 is a potent telomerase inhibitor and a putative tumor suppressor [1, 4]. Te functions of PinX1 are mainly attributable to the maintenance of telomerase activity and chromosomal stability [3, 4]. Although decreased expression of PinX1 was observed in breast cancer cell lines, and knockout of PinX1 in mice could cause breast cancer [3], the role of PinX1 in growth control of breast cancer cells and its molecular mechanism remains unclear. Terefore, in this study, we generated MCF-7, MDA-MB-231, and SK-BR- 3 breast cancer cells stably overexpressing PinX1 and MCF- 10A nontumorigenic breast cell knocking down PinX1 and assessed the role of PinX1 in growth control of the cells by MTT assay, focus formation, and fow cytometry. Te localization of PinX1 in diferent phases in the cell cycle was observed. In addition, we also performed a genome wide screen of the mRNA and lncRNA expression profle alterations. Hindawi Publishing Corporation BioMed Research International Volume 2014, Article ID 978984, 10 pages http://dx.doi.org/10.1155/2014/978984