Upregulation of long non-coding RNA HOXA-AS2 promotes proliferation and induces epithelial-mesenchymal transition in gallbladder carcinoma
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Peng Zhang1,*, Peihua Cao1,*, Xiaofeng Zhu2, Mingxin Pan1, Kebo Zhong1, Rui He2, Yang Li1,3, Xingyuan Jiao2, Yi Gao1,3,4
1Department of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, Guangdong, P. R. China
2Organ Transplant Center, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, Guangdong, P. R. China
3Guangdong Provincial Research Center of Artificial Organ and Tissue Engineering, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, Guangdong, P. R. China
4State Key Laboratory of Organ Failure Research, Southern Medical University, Guangzhou 510515, Guangdong, P. R. China
*These authors contributed equally to this work
Yi Gao, email: email@example.com
Xingyuan Jiao, email: firstname.lastname@example.org
Keywords: HOXA-AS2, LncRNA, GBC, metastasis, EMT
Received: January 19, 2017 Accepted: March 09, 2017 Published: March 25, 2017
Gallbladder carcinoma (GBC) is the most common malignancy of the bile duct and patients with GBC have extremely poor prognoses. Increasing evidence indicates that long non-coding RNAs (lncRNAs) regulate diverse cellular processes, including cell growth, differentiation, apoptosis, and cancer progression. However, the function of lncRNAs in the progression of GBC remains largely unknown. Here, we reported that HOXA cluster antisense RNA2 (HOXA-AS2) was upregulated in GBC. In vitro experiments revealed that HOXA-AS2 knockdown significantly inhibited GBC cells proliferation by causing G1 arrest and promoting apoptosis, whereas HOXA-AS2 overexpression promoted cell growth. Further functional assays indicated that HOXA-AS2 overexpression significantly promoted GBC cell migration and invasion by promoting EMT. Taken together, our study demonstrates that HOXA-AS2 could act as a functional oncogene in GBC, as well as a potential therapeutic target to inhibit GBC metastasis.
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