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Articles by J. S. Lee
Total Records ( 2 ) for J. S. Lee
  S. J You , S. H Lee and J. S. Lee
 

We kinetically analyzed RNA interference (RNAi) for lamin A/C in HeLa cells, assuming suppression and recovery phases of gene expression, and dilution of transfected small interfering RNA (siRNA) by cell divisions. We observed the inhibitory effect of RNAi over a period of 6 days using various siRNA concentrations, and the maximum gene silencing efficiency occurred at Day 2 or 3. The gene silencing efficiency as a function of time and siRNA concentration was further quantitatively evaluated using a kinetic analysis method, demonstrating that RNAi for lamin A/C can be understood as a conventional drug–response system. This work provides potentially important guidelines for future applications using nanomaterials as delivery vehicles of siRNA in RNAi for lamin A/C.

  H. O Byun , N. K Han , H. J Lee , K. B Kim , Y. G Ko , G Yoon , Y. S Lee , S. I Hong and J. S. Lee
 

Induction of premature senescence may be a promising strategy for cancer treatment. However, biomarkers for senescent cancer cells are lacking. To identify such biomarkers, we performed comparative proteomic analysis of MCF7 human breast cancer cells undergoing cellular senescence in response to ionizing radiation (IR). IR-induced senescence was associated with up-regulation of cathepsin D (CD) and down-regulation of eukaryotic translation elongation factor 1β2 (eEF1B2), as confirmed by Western blot. The other elongation factor, eukaryotic translation elongation factor 11 (eEF1A1), was also down-regulated. IR-induced senescence was associated with similar changes of CD and eEF1 (eEF1A1 and eEF1B2) levels in the HCT116 colon cancer cell line and the H460 lung cancer cell line. Up-regulation of CD and down-regulation of eEF1 seemed to be specific to senescence, as they were observed during cellular senescence induced by hydrogen peroxide or anticancer drugs (camptothecin, etoposide, or 50 ng doxorubicin) but not during apoptosis induced by Taxol or 10 µg doxorubicin or autophagy induced by tamoxifen. The same alterations in CD and eEF1A1 levels were observed during replicative senescence and Ras oncogene-induced senescence. Transient cell cycle arrest did not alter levels of eEF1 or CD. Chemical inhibition of CD (pepstatin A) and small interfering RNA–mediated knockdown of CD and eEF1 revealed that these factors participate in cell proliferation. Finally, the senescence-associated alteration in CD and eEF1 levels observed in cell lines was also observed in IR-exposed xenografted tumors. These findings show that CD and eEF1 are promising markers for the detection of cellular senescence induced by a variety of treatments. [Cancer Res 2009;69(11):4638–47]

 
 
 
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