siRNA-mediated silencing of the 37/67-kDa high affinity laminin receptor in Hep3B cells induces apoptosis.

Cellular & Molecular Biology Letters
Tharinee Susantad, Duncan R Smith

Abstract

The laminin-binding protein, variously called the 37/67-kDa high affinity laminin receptor or p40, mediates the attachment of normal cells to the laminin network, and also has a role as a ribosomal protein. Over-expression of this protein has been strongly correlated with the metastatic phenotype. However, few studies have investigated the cellular consequence of the ablation of this gene's expression. To address this issue, the expression of the 37/67-kDa high affinity laminin receptor was knocked out with several siRNA constructs via RNA interference in transformed liver (Hep3B) cells. In each case where the message was specifically ablated, apoptosis was induced, as determined by annexin V/propidium iodide staining, and by double staining with annexin V and an antibody directed against the 37/67-kDa high affinity laminin receptor. These results suggest that this protein plays a critical role in maintaining cell viability.

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Citations

Aug 23, 2012·Journal of Proteome Research·Lisa Venticinque, Daniel Meruelo
Sep 3, 2009·Molecular Therapy : the Journal of the American Society of Gene Therapy·Jonathan ScheimanDaniel Meruelo
Nov 26, 2015·Free Radical Biology & Medicine·Filipe Vilas-BoasCarla Real
Sep 8, 2011·Journal of Cellular and Molecular Medicine·Pietro FormisanoNunzia Montuori
Jan 30, 2015·Biological Reviews of the Cambridge Philosophical Society·Vincent DiGiacomo, Daniel Meruelo
Mar 10, 2015·Expert Opinion on Therapeutic Patents·Katarina JovanovicStefan F T Weiss
Oct 2, 2015·PloS One·Thandokuhle KhumaloStefan F T Weiss
Nov 21, 2008·The Journal of Gene Medicine·Sonsoles DíezConchita Tros de ILarduya
Aug 25, 2011·Prion·Bianca Da Costa DiasStefan F T Weiss
Nov 30, 2010·Expert Opinion on Therapeutic Patents·Aadilah OmarStefan F T Weiss

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis