Silencing of cystatin M in metastatic oral cancer cell line MDA-686Ln by siRNA increases cysteine proteinases and legumain activities, cell proliferation and in vitro invasion

Life Sci. 2006 Jan 18;78(8):898-907. doi: 10.1016/j.lfs.2005.05.096. Epub 2005 Sep 8.

Abstract

Cystatins are inhibitors of lysosomal cysteine proteinases. Cystatin M demonstrates more diverse tissue distribution, target specificity and biological function than other cystatins from the same family. We utilized small interference RNAs (siRNA) to silence cystatin M gene expression in a metastatic oral cancer cell line (MDA-686Ln) that expresses a high level of cystatin M. We tested four different siRNAs targeted to different sites of the cystatin M mRNA, and found three out of the four siRNAs were effective in suppressing cystatin M expression by >50% at both mRNA and protein levels, as measured by quantitative real-time RT-PCR and Western blotting. We used siRNA-#1, which demonstrated highest efficiency of silencing cystatin M, to evaluate the phenotypic outcome of silencing cystatin M in MDA-686Ln cells. Cystatin M inhibition significantly increased the enzymatic activities of cathepsins B and L and legumain while reducing cysteine protease inhibitor activity both in the media and intracellularly. MDA-686Ln cells treated with siRNA#1 demonstrated markedly increased proliferation rate, in vitro motility and Matrigel invasiveness. Collectively, our data show that silencing of cystatin M in tumor cells not only increases their invasion and motility via cysteine-proteinase-dependent pathways, but also renders them hyperproliferative through a currently unknown mechanism.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Carcinoma, Squamous Cell / enzymology
  • Carcinoma, Squamous Cell / genetics*
  • Carcinoma, Squamous Cell / secondary
  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation
  • Cystatin M
  • Cystatins / genetics*
  • Cystatins / metabolism
  • Cysteine Endopeptidases / biosynthesis
  • Cysteine Endopeptidases / genetics*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Mouth Neoplasms / enzymology
  • Mouth Neoplasms / genetics*
  • Mouth Neoplasms / pathology
  • Neoplasm Invasiveness / genetics
  • RNA Interference*
  • RNA, Small Interfering / administration & dosage
  • RNA, Small Interfering / genetics*

Substances

  • CST6 protein, human
  • Cystatin M
  • Cystatins
  • RNA, Small Interfering
  • Cysteine Endopeptidases
  • asparaginylendopeptidase