The long non-coding RNA NONHSAT062994 inhibits colorectal cancer by inactivating Akt signaling
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Xiao-Shun He1,*, Ling-Chuan Guo1,*, Ming-Zhan Du1,*, Shan Huang1, Ren-Peng Huang1, Sheng-Hua Zhan1, Dong-Mei Gu1, Wei-Shuo Liu1, Xi-Ming Wang3, Hua Wu2 and Wen-Juan Gan1
1Department of Pathology, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou 215006, China
2Pathology Center and Department of Pathology, Soochow University, Suzhou 215123, China
3Department of Radiology, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou 215006, China
*These authors have contributed equally to this work
Wen-Juan Gan, email: firstname.lastname@example.org
Hua Wu, email: email@example.com
Xi-Ming Wang, email: firstname.lastname@example.org
Keywords: LncRNA NONHSAT062994, colorectal cancer, growth, Akt signaling
Abbreviations: lncRNA, long noncoding RNAs (lncRNAs); qPCR, Quantitative PCR; CRC, Colorectal Cancer; ISH, In Situ Hybridization; FISH, fluorescent in situ hybridization
Received: May 05, 2017 Accepted: June 28, 2017 Published: August 02, 2017
The aberrant expression of long noncoding RNAs (lncRNAs) is implicated in cancer development and progression. However, the clinical significance and mechanism by which NONHSAT062994 regulates colorectal cancer (CRC) is unknown. We here reported that NONHSAT062994 was significantly downregulated in human CRC tissues and cell lines. Moreover, its expression was inversely correlated with tumor size and overall survival (OS) time in CRC patients. In CRC cells, the overexpression and knockdown of NONHSAT062994 inhibited and enhanced CRC cell growth, respectively, in vitro and in vivo. Mechanistically, NONHSAT062994 functioned as a tumor suppressor to inhibit CRC cell growth by inactivating Akt signaling. Notably, the NONHSAT062994 expression status was negatively correlated with the Akt downstream targets c-Myc and Cyclin D1 in clinical CRC samples. The current findings suggest that NONHSAT062994 plays a critical role in the development of CRC by regulating Akt signaling, and identified a candidate prognostic biomarker or potential therapeutic target for CRC patients.
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