The impact of the RBM4-initiated splicing cascade on modulating the carcinogenic signature of colorectal cancer cells

Jung Chun Lin, Yuan Chii Lee, Yu Chih Liang, Yang C. Fann, Kory R. Johnson, Ying Ju Lin

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

A growing body of studies has demonstrated that dysregulated splicing profiles constitute pivotal mechanisms for carcinogenesis. In this study, we identified discriminative splicing profiles of colorectal cancer (CRC) cells compared to adjacent normal tissues using deep RNA-sequencing (RNA-seq). The RNA-seq results and cohort studies indicated a relatively high ratio of exon 4-excluded neuro-oncological ventral antigen 1 (Nova1 -4) and intron 2-retained SRSF6 (SRSF6 +intron 2) transcripts in CRC tissues and cell lines. Nova1 variants exhibited differential effects on eliminating SRSF6 expression in CRC cells by inducing SRSF6 +intron 2 transcripts which were considered to be the putative target of alternative splicing-coupled nonsense-mediated decay mechanism. Moreover, the splicing profile of vascular endothelial growth factor (VEGF)165/VEGF165b transcripts was relevant to SRSF6 expression, which manipulates the progression of CRC calls. These results highlight the novel and hierarchical role of an alternative splicing cascade that is involved in the development of CRC.

Original languageEnglish
Article number44204
JournalScientific Reports
Volume7
DOIs
Publication statusPublished - Mar 9 2017

Fingerprint

Colorectal Neoplasms
Introns
Alternative Splicing
RNA
RNA Sequence Analysis
High-Throughput Nucleotide Sequencing
Exons
Carcinogenesis
Cohort Studies
Antigens
Cell Line

ASJC Scopus subject areas

  • General

Cite this

The impact of the RBM4-initiated splicing cascade on modulating the carcinogenic signature of colorectal cancer cells. / Lin, Jung Chun; Lee, Yuan Chii; Liang, Yu Chih; Fann, Yang C.; Johnson, Kory R.; Lin, Ying Ju.

In: Scientific Reports, Vol. 7, 44204, 09.03.2017.

Research output: Contribution to journalArticle

@article{6df493cef01045f28b39dd00af1587b5,
title = "The impact of the RBM4-initiated splicing cascade on modulating the carcinogenic signature of colorectal cancer cells",
abstract = "A growing body of studies has demonstrated that dysregulated splicing profiles constitute pivotal mechanisms for carcinogenesis. In this study, we identified discriminative splicing profiles of colorectal cancer (CRC) cells compared to adjacent normal tissues using deep RNA-sequencing (RNA-seq). The RNA-seq results and cohort studies indicated a relatively high ratio of exon 4-excluded neuro-oncological ventral antigen 1 (Nova1 -4) and intron 2-retained SRSF6 (SRSF6 +intron 2) transcripts in CRC tissues and cell lines. Nova1 variants exhibited differential effects on eliminating SRSF6 expression in CRC cells by inducing SRSF6 +intron 2 transcripts which were considered to be the putative target of alternative splicing-coupled nonsense-mediated decay mechanism. Moreover, the splicing profile of vascular endothelial growth factor (VEGF)165/VEGF165b transcripts was relevant to SRSF6 expression, which manipulates the progression of CRC calls. These results highlight the novel and hierarchical role of an alternative splicing cascade that is involved in the development of CRC.",
author = "Lin, {Jung Chun} and Lee, {Yuan Chii} and Liang, {Yu Chih} and Fann, {Yang C.} and Johnson, {Kory R.} and Lin, {Ying Ju}",
year = "2017",
month = "3",
day = "9",
doi = "10.1038/srep44204",
language = "English",
volume = "7",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "Nature Publishing Group",

}

TY - JOUR

T1 - The impact of the RBM4-initiated splicing cascade on modulating the carcinogenic signature of colorectal cancer cells

AU - Lin, Jung Chun

AU - Lee, Yuan Chii

AU - Liang, Yu Chih

AU - Fann, Yang C.

AU - Johnson, Kory R.

AU - Lin, Ying Ju

PY - 2017/3/9

Y1 - 2017/3/9

N2 - A growing body of studies has demonstrated that dysregulated splicing profiles constitute pivotal mechanisms for carcinogenesis. In this study, we identified discriminative splicing profiles of colorectal cancer (CRC) cells compared to adjacent normal tissues using deep RNA-sequencing (RNA-seq). The RNA-seq results and cohort studies indicated a relatively high ratio of exon 4-excluded neuro-oncological ventral antigen 1 (Nova1 -4) and intron 2-retained SRSF6 (SRSF6 +intron 2) transcripts in CRC tissues and cell lines. Nova1 variants exhibited differential effects on eliminating SRSF6 expression in CRC cells by inducing SRSF6 +intron 2 transcripts which were considered to be the putative target of alternative splicing-coupled nonsense-mediated decay mechanism. Moreover, the splicing profile of vascular endothelial growth factor (VEGF)165/VEGF165b transcripts was relevant to SRSF6 expression, which manipulates the progression of CRC calls. These results highlight the novel and hierarchical role of an alternative splicing cascade that is involved in the development of CRC.

AB - A growing body of studies has demonstrated that dysregulated splicing profiles constitute pivotal mechanisms for carcinogenesis. In this study, we identified discriminative splicing profiles of colorectal cancer (CRC) cells compared to adjacent normal tissues using deep RNA-sequencing (RNA-seq). The RNA-seq results and cohort studies indicated a relatively high ratio of exon 4-excluded neuro-oncological ventral antigen 1 (Nova1 -4) and intron 2-retained SRSF6 (SRSF6 +intron 2) transcripts in CRC tissues and cell lines. Nova1 variants exhibited differential effects on eliminating SRSF6 expression in CRC cells by inducing SRSF6 +intron 2 transcripts which were considered to be the putative target of alternative splicing-coupled nonsense-mediated decay mechanism. Moreover, the splicing profile of vascular endothelial growth factor (VEGF)165/VEGF165b transcripts was relevant to SRSF6 expression, which manipulates the progression of CRC calls. These results highlight the novel and hierarchical role of an alternative splicing cascade that is involved in the development of CRC.

UR - http://www.scopus.com/inward/record.url?scp=85014939040&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85014939040&partnerID=8YFLogxK

U2 - 10.1038/srep44204

DO - 10.1038/srep44204

M3 - Article

AN - SCOPUS:85014939040

VL - 7

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

M1 - 44204

ER -