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Specific-detection of clinical samples, systematic functional investigations, and transcriptome analysis reveals that splice variant MUC4/Y contributes to the malignant progression of pancreatic…

Overview of attention for article published in Journal of Translational Medicine, November 2014
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Title
Specific-detection of clinical samples, systematic functional investigations, and transcriptome analysis reveals that splice variant MUC4/Y contributes to the malignant progression of pancreatic cancer by triggering malignancy-related positive feedback loops signaling
Published in
Journal of Translational Medicine, November 2014
DOI 10.1186/s12967-014-0309-8
Pubmed ID
Authors

Yi Zhu, Jing-Jing Zhang, Kun-Ling Xie, Jie Tang, Wen-Biao Liang, Rong Zhu, Yan Zhu, Bin Wang, Jin-Qiu Tao, Xiao-Fei Zhi, Zheng Li, Wen-Tao Gao, Kui-Rong Jiang, Yi Miao, Ze-Kuan Xu

Abstract

BackgroundMUC4 plays important roles in the malignant progression of human pancreatic cancer. But the huge length of MUC4 gene fragment restricts its functional and mechanism research. As one of its splice variants, MUC4/Y with coding sequence is most similar to that of the full-length MUC4 (FL-MUC4), together with alternative splicing of the MUC4 transcript has been observed in pancreatic carcinomas but not in normal pancreas. So we speculated that MUC4/Y might be involved in malignant progression similarly to FL-MUC4, and as a research model of MUC4 in pancreatic cancer. The conjecture was confirmed in the present study.MethodsMUC4/Y expression was detected by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) using gene-specific probe in the clinic samples. The effects of MUC4/Y were observed by serial in vitro and in vivo experiments based on stable over-expressed cell model. The underlying mechanisms were investigated by sequence-based transcriptome analysis and verified by qRT-PCR, Western blot and enzyme-linked immunosorbent assays.ResultsThe detection of clinical samples indicates that MUC4/Y is significantly positive-correlated with tumor invasion and distant metastases. Based on stable forced-expressed pancreatic cancer PANC-1 cell model, functional studies show that MUC4/Y enhances malignant activity in vitro and in vivo, including proliferation under low-nutritional-pressure, resistance to apoptosis, motility, invasiveness, angiogenesis, and distant metastasis. Mechanism studies indicate the novel finding that MUC4/Y triggers malignancy-related positive feedback loops for concomitantly up-regulating the expression of survival factors to resist adverse microenvironment and increasing the expression of an array of cytokines and adhesion molecules to affect the tumor milieu.ConclusionsIn light of the enormity of the potential regulatory circuitry in cancer afforded by MUC4 and/or MUC4/Y, repressing MUC4 transcription, inhibiting post-transcriptional regulation, including alternative splicing, or blocking various pathways simultaneously may be helpful for controlling malignant progression. MUC4/Y- expression model is proven to a valuable tool for the further dissection of MUC4-mediated functions and mechanisms.

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Mendeley readers

The data shown below were compiled from readership statistics for 20 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
France 1 5%
Unknown 19 95%

Demographic breakdown

Readers by professional status Count As %
Researcher 6 30%
Student > Ph. D. Student 6 30%
Student > Master 3 15%
Student > Bachelor 1 5%
Unspecified 1 5%
Other 0 0%
Unknown 3 15%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 6 30%
Medicine and Dentistry 4 20%
Agricultural and Biological Sciences 2 10%
Environmental Science 1 5%
Nursing and Health Professions 1 5%
Other 3 15%
Unknown 3 15%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 27 February 2016.
All research outputs
#18,968,277
of 21,321,610 outputs
Outputs from Journal of Translational Medicine
#3,063
of 3,686 outputs
Outputs of similar age
#212,620
of 253,680 outputs
Outputs of similar age from Journal of Translational Medicine
#201
of 285 outputs
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