Identification of novel splicing variants from RON proto-oncogene pre-mRNA

• Published in: Oncology reports Vol. 28; no. 6; pp. 2217 - 2220
• Main Authors: MOON, HEEGYUM, CHO, SUNGHEE, YANG, XIAOMING, ZHOU, JIANHUA, LOH, TIING JEN, ZHENG, XUEXIU, SHEN, HAIHONG
• Format: Journal Article
• Language: English
• Published: Athens D.A. Spandidos 01.12.2012; Spandidos; Spandidos Publications UK Ltd
• Subjects: Alternative Splicing; Base Sequence; Biological and medical sciences; Cell Line, Tumor; Colorectal cancer; exon; HeLa Cells; Humans; intron; Introns; Kinases; Medical sciences; Molecular Sequence Data; Protein Isoforms - genetics; Proteins; Receptor Protein-Tyrosine Kinases - genetics; RNA Precursors - genetics; RON; splicing; Studies; Tumors; variants; Alternative splicing; Genetic variability; Genotype; variants; Variant; RON; Cancerology; Exon; Messenger RNA; Intron; C-Onc gene; splicing; Protooncogene
• ISSN: 1021-335X; 1791-2431
• DOI: 10.3892/or.2012.2043

RON is a proto-oncogene that induces cell dissociation, migration and matrix invasion. RONΔ160, a splicing variant of RON, is a natural splicing product in colon cancers that is produced through skipping of exons 5 and 6 in alternative splicing process. RONΔ160 promotes cellular transformation in vitro and tumor formation in vivo. We present, here, two novel splicing variants of RON in the partial splicing events that involve exons 5 and 6. The common facts of these two novel splicing variants are that exons 4-7 are included. In addition, intron 4 is spliced whereas intron 5 is included in both variants. The difference of these two isoforms is the inclusion or skipping of intron 6. In one variant intron 6 is included, but intron 6 is skipped in another variant. These two variants should be truncated but these proteins have not yet been detected.