Research Papers:

Pseudogene PHBP1 promotes esophageal squamous cell carcinoma proliferation by increasing its cognate gene PHB expression

Feiyue Feng _, Bin Qiu, Ruochuan Zang, Peng Song and Shugeng Gao

PDF  |  HTML  |  How to cite  |  Order a Reprint

Oncotarget. 2017; 8:29091-29100. https://doi.org/10.18632/oncotarget.16196

Metrics: PDF 1406 views  |   HTML 1751 views  |   ?  


Feiyue Feng1, Bin Qiu1, Ruochuan Zang1, Peng Song1, Shugeng Gao1

1Department of Thoracic Surgery, National Cancer Center, Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China

Correspondence to:

Feiyue Feng, email: feiyuefeng_cn@aliyun.com

Shugeng Gao, email: gaoshugeng@vip.sina.com

Keywords: natural antisense transcript (NAT), long noncoding RNA (lncRNA), esophageal squamous cell carcinoma (ESCC), quantitative real-time PCR (qRT-PCR), SDS-polyacrylamide gel electrophoresis (SDS-PAGE)

Received: January 02, 2017     Accepted: January 25, 2017     Published: March 16, 2017


Natural antisense transcripts (NATs) as one of the most diverse classes of long noncoding RNAs (lncRNAs), have been demonstrated involved in fundamental biological processes in human. Here, we reported that human prohibitin gene pseudogene 1 (PHBP1) was upregulated in ESCC, and increased PHBP1 expression in ESCC was associated with clinical advanced stage. Functional experiments showed that PHBP1 knockdown inhibited ESCC cells proliferation, colony formation and xenograft tumor growth in vitro and in vivo by causing cell-cycle arrest at the G1-G0 phase. Mechanisms analysis revealed that PHBP1 transcript as an antisense transcript of PHB is partially complementary to PHB mRNA and formed an RNA-RNA hybrid with PHB, consequently inducing an increase of PHB expression at both the mRNA and protein levels. Furthermore, PHBP1 expression is strongly correlated with PHB expression in ESCC tissues. Collectively, this study elucidates an important role of PHBP1 in promoting ESCC partly via increasing PHB expression.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 16196