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Updated: Oct 7, 2025

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma
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Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma

Published on: April 12, 2019

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STIM1 Controls the Focal Adhesion Dynamics and Cell Migration by Regulating SOCE in Osteosarcoma

Yu-Shan Lin1, Yi-Hsin Lin2, MyHang Nguyen Thi2

  • 1Institute of Basic Medical Sciences, National Cheng Kung University, Tainan 701, Taiwan.

International Journal of Molecular Sciences
|January 11, 2022
PubMed

Insights

Stromal interaction molecule 1 (STIM1) regulates calcium entry and focal adhesion turnover, impacting cancer cell migration. Appropriate calcium levels are crucial for metastasis, while excessive calcium hinders it.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Biochemistry

Background:

  • Store-operated calcium entry (SOCE) dysregulation is linked to cancer progression.
  • Stromal interaction molecule 1 (STIM1), a key SOCE component, is upregulated in cancers and drives metastasis.
  • STIM1's role in focal adhesion dynamics and cancer cell migration requires further investigation.

Purpose of the Study:

  • To investigate the impact of STIM1-mediated SOCE on focal adhesion turnover and cell migration in osteosarcoma.
  • To elucidate the relationship between STIM1 variants, calcium influx, and cancer cell motility.

Main Methods:

  • Overexpression of wild-type, constitutively active, and dominant-negative STIM1 variants in an osteosarcoma cell line.
  • Assessment of calcium influx, calpain activity, and focal adhesion protein turnover (FAK, paxillin, vinculin).
  • Evaluation of cancer cell migration capabilities.

Main Results:

  • Constitutively active STIM1 elevated calcium influx and calpain activity, increasing focal adhesion protein turnover and impeding migration.
  • Dominant-negative STIM1 decreased focal adhesion turnover, promoting cell migration compared to wild-type and control cells.
  • STIM1-mediated calcium influx influences focal adhesion dynamics and cancer cell metastasis.

Conclusions:

  • Cancer cells require optimal calcium levels for focal adhesion regulation and migration via calpain activity.
  • Excessive calcium influx due to STIM1 dysregulation impairs, rather than enhances, cancer cell metastasis.
  • STIM1-mediated SOCE presents a potential therapeutic target for controlling cancer progression.
Keywords:
SOCESTIM1cell migrationfocal adhesion

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