SF3B4 is decreased in pancreatic cancer and inhibits the growth and migration of cancer cells

• Published in: Tumor biology 2017-03, Vol.39 (3), p.1010428317695913-1010428317695913
• Main Authors: Zhou, Wentao, Ma, Ning, Jiang, Hao, Rong, Yefei, Deng, Yuezhen, Feng, Yuanyuan, Zhu, Hongxu, Kuang, Tiantao, Lou, Wenhui, Xie, Dong, Wang, Dansong
• Format: Article
• Language: English
• Subjects: Adult; Aged; Angiogenesis; Apoptosis; Cancer therapies; Cell cycle; Cell Line, Tumor; Cell migration; Cell Movement - genetics; Cell proliferation; Cell Proliferation - genetics; Female; Gene Expression Regulation, Neoplastic; Humans; Kinases; Liver cancer; Male; Medical prognosis; Metastasis; Middle Aged; mRNA; Pancreatic cancer; Pancreatic Neoplasms - genetics; Pancreatic Neoplasms - pathology; Phosphorylation; Polymerase chain reaction; Proteins; RNA Splicing - genetics; RNA Splicing Factors - genetics; Signal Transduction - genetics; Splicing factors; STAT3 Transcription Factor - biosynthesis; STAT3 Transcription Factor - genetics; Transcription; Tumorigenesis; Tyrosine
• ISSN: 1010-4283; 1423-0380
• DOI: 10.1177/1010428317695913

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.