| Literature DB >> 28351319 |
Wentao Zhou1, Ning Ma2, Hao Jiang3, Yefei Rong1, Yuezhen Deng2, Yuanyuan Feng2, Hongxu Zhu1, Tiantao Kuang1, Wenhui Lou1, Dong Xie2,3, Dansong Wang1.
Abstract
Splicing factor 3b subunit 4, a critical component of pre-message RNA splicing complex, has been reported to play an important part in the tumorigenesis. However, the expression pattern and biological role of splicing factor 3b subunit 4 in pancreatic cancer have never been investigated. In this study, we found that both the messenger RNA ( p < 0.001) and protein level of splicing factor 3b subunit 4 were decreased significantly in pancreatic cancer specimens compared with their adjacent normal tissues. Overexpression of splicing factor 3b subunit 4 in pancreatic cancer cells inhibited cell growth and motility in vitro, while suppressing splicing factor 3b subunit 4 expression promoted the proliferation and migration of pancreatic cancer cells. In addition, splicing factor 3b subunit 4 was found to inhibit the activity of signal transducer and activator of transcription 3 signaling via downregulating the phosphorylation of signal transducer and activator of transcription 3 on a tyrosine residue at position 705. Taken together, these findings demonstrated that splicing factor 3b subunit 4 acted as a suppressive role in pancreatic cancer and indicated that restoring the function of splicing factor 3b subunit 4 might be a strategy for cancer therapy.Entities:
Keywords: Splicing factor 3b subunit 4; cell migration; cell proliferation; pancreatic cancer; signal transducer and activator of transcription 3 signaling
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Year: 2017 PMID: 28351319 DOI: 10.1177/1010428317695913
Source DB: PubMed Journal: Tumour Biol ISSN: 1010-4283