SOX7: From a developmental regulator to an emerging tumor suppressor

Daniel B. Stovall, Paul Cao* and Guangchao Sui

Department of Cancer Biology and Comprehensive Cancer Center, and Center for Cancer Genomics, Wake Forest University School of Medicine, Winston-Salem, NC, USA
*Current address: Department of Pathology, Yale University, School of Medicine, New Haven CT, USA

Offprint requests to: Guangchao Sui, Hanes Building, Room 5055, Medical Center Boulevard, Winston Salem, NC 27157, USA, e-mail: gsui@wakehealth.edu


Summary. SOX7 belongs to the SOX (SRY-related HMG-box) family of transcription factors that have been shown to regulate multiple biological processes, such as hematopoiesis, vasculogenesis and cardiogenesis during embryonic development. Recent studies indicate that several SOX family members play important roles in tumorigenesis. In this review, we introduce SOX7 gene and protein structures, and discuss its expression and functional role in cancer development and progression. SOX7 is frequently downregulated in many human cancers and its reduced expression correlates with poor prognoses of several cancers. Functional studies reveal many tumor suppressive properties of SOX7 in prostate, colon, lung, and breast cancers. To date, although a few target genes of SOX7 have been identified, SOX7-mediated gene expression has not been investigated in a cancer-relevant context. Our recent studies not only for the first time demonstrate a tumor suppressive role of SOX7 in a xenograft mouse model, but also unravel that many genes regulating cell death, growth and apoptosis are affected by SOX7, strongly supporting a pivotal role of SOX7 in tumorigenesis. Thus, currently available data clearly indicate a tumor suppressive role of SOX7, but the mechanisms underlying its gene expression and tumor suppressive activity remain undetermined. The research of SOX7 in cancers remains a fertile area to be explored. Histol Histopathol 29, 439-445 (2014)

Key words: SOX7, Tumor suppressor, Gene expression, Transcription factor, Cancer

DOI: 10.14670/HH-29.10.439