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Poster display session

3402 - Cathepsin S Regulates Cell Migration and Invasion through Mediating Store-Operated Calcium Entry and the Focal Adhesion Proteins


11 Sep 2017


Poster display session


Cancer Biology


Hsiao-Han Lin


Annals of Oncology (2017) 28 (suppl_5): v595-v604. 10.1093/annonc/mdx391


H. Lin1, M. Shen2, J. Chang3

Author affiliations

  • 1 Basic Medical Sciences, National Cheng Kung University, 701 - Tainan/TW
  • 2 Obstetrics And Gynecology, National Cheng Kung University Hospital, 704 - Tainan/TW
  • 3 Internal Medicine, National Cheng Kung University Hospital, 701 - Tainan/TW


Abstract 3402


Cathepsin S (CTSS), a lysosomal cysteine protease, plays an important role in inflammation, and it has been reported that it is also associated with angiogenesis and extracellular matrix (ECM) degradation promoting cell migration and invasion. Since CTSS is stably overexpressed in the different types of cancer cells, we explored a novel intracellular mechanism other than ECM degradation that regulates cell migration and metastasis.


Human oral cancer cells, OEC-M1, and breast cancer cells, MDA-MB-231, were used for this study. The expressions of CTSS were knockdown by siRNA transfection and the enzymatic activities were inhibited by highly-selective CTSS inhibitor, 58. The migratory and invasive abilities were determined by wound healing assay and transwell invasion assay, respectively. Microarray data and promoter prediction analysis were used to determine the intra-cellular targets of CTSS. Immunofluorescence assay was executed to evaluate STIM1 puncta formation and calcium influxes from store-operated calcium entry (SOCE) were measured by fura-2 calcium imaging. Western blot analysis was performed to detect the alteration of focal adhesion proteins.


Our data showed that either CTSS knockdown with siRNA or activity inhibition could significantly decrease cell spreading area, and suppress cell migratory and invasive activities in both OEC-M1 and MDA-MB-231 cells. Moreover, inhibition of CTSS enzymatic activity resulted in the suppression of STIM1 aggregation and decreasing calcium influx from SOCE. Furthermore, downregulation of CTSS expression with siRNA could reduce the protein expression of three focal adhesion proteins, including CD29, CD104 and vinculin, which could be restored by CTSS transfection.


These results exhibit a novel intracellular molecular mechanism of CTSS mediating STIM1 aggregation and the calcium influx from SOCE to regulate the focal adhesion proteins, which are crucial for ECM interactions, cell migration and invasion.

Clinical trial identification

Legal entity responsible for the study

Ministry of Science and Technology of Taiwan




All authors have declared no conflicts of interest.

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