PinX1: structure, regulation and its functions in cancer
Metrics: PDF 637 views | HTML 883 views | ?
Hai-Long Li1,2,*, Jun Song3,4,*, Hong-Mei Yong5,*, Ping-Fu Hou1,3, Yan-Su Chen1,3, Wen-Bo Song1, Jin Bai1 and Jun-Nian Zheng1,3
1 Jiangsu Key Laboratory of Biological Cancer Therapy, Xuzhou Medical College, Xuzhou, Jiangsu, China
2 Department of Urology, The Affiliated Hospital of Xuzhou Medical College, Xuzhou, Jiangsu, China
3 Jiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Cancer Institute, Xuzhou Medical College, Xuzhou, Jiangsu, China
4 Department of General Surgery, The Affiliated Hospital of Xuzhou Medical College, Xuzhou, Jiangsu, China
5 Department of Medical Oncology, Huai’an Hospital to Xuzhou Medical College, Huai’an, Jiangsu, China
* These authors have contributed equally to this study
Jun-Nian Zheng, email:
Jin Bai, email:
Keywords: PinX1; cancer; structure; regulation; function
Received: March 14, 2016 Accepted: August 09, 2016 Published: August 19, 2016
PIN2/TRF1-interacting telomerase inhibitor 1 (PinX1) is a novel cloned gene located at human chromosome 8p23, playing a vital role in maintaining telomeres length and chromosome stability. It has been demonstrated to be involved in tumor genesis and progression in most malignancies. However, some researches showed opposing molecular status of PinX1 gene and its expression patterns in several other types of tumors. The pathogenic mechanism of PinX1 expression in human malignancy is not yet clear. Moreover, emerging evidence suggest that PinX1 (especially its TID domain) might be a potential new target cancer treatment. Therefore, PinX1 may be a new potential diagnostic biomarker and therapeutic target for human cancers, and may play different roles in different human cancers. The functions and the mechanisms of PinX1 in various human cancers remain unclear, suggesting the necessity of further extensive works of its role in tumor genesis and progression.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.