Abstract

Commentary: HNRNPLL, a newly identified colorectal cancer metastasis suppressor, modulates alternative splicing of CD44 during epithelial-mesenchymal transition.

Highlights

  • Heterogeneous nuclear ribonucleoprotein L-like (HNRNPLL), located on the chromosome 2p22.1, is a RNA-binding protein that functions as a regulator of alternative splicing for multiple mRNAs target

  • ShRNA mediated silencing of HNRNPLL inhibits in-vitro cell proliferation and enhances matrigel invasion to promote metastasis in colon cancer cells

  • Knocking down HNRNPLL inhibits in-vivo primary tumor growth, and lung metastasis of colon cancer which is reverted by shRNA resistant HNRNPLL plasmid

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Summary

Introduction

A commentary on HNRNPLL, a newly identified colorectal cancer metastasis suppressor, modulates alternative splicing of CD44 during epithelial-mesenchymal transition by Sakuma, K., Sasaki, E., Kimura, K., Komori, K., Shimizu, Y., Yatabe, Y., et al (2017). MS gene inhibits metastasis without affecting in-vitro cell proliferation and in-vivo primary tumor growth (Smith and Theodorescu, 2009). Genome-wide screening using shRNA library in the orthotropic and lung metastasis mouse model has identified several MS genes in breast and colon cancer (Gumireddy et al, 2009; Duquet et al, 2014).Using a genome-wide silencing approach in non-metastatic CMT93 mouse cell line expressing Venus fluorescent protein in a syngeneic mouse model, Sakuma and colleagues have delineated the inverse relationship between HNRNPLL and CD44v6 expression in the metastasis of colon cancer (Sakuma et al, 2017).

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