NDLI: Enhanced Stim1 expression is associated with acquired chemo-resistance of cisplatin in osteosarcoma cells

Content Provider	Springer Nature Link
Author	Sun, Xilong Wei, Qiang Cheng, Jie Bian, Yanzhu Tian, Congna Hu, Yujing Li, Huijie
Copyright Year	2017
Abstract	Osteosarcoma is the most common primary malignant bone tumor. Although cisplatin is the primary chemotherapy used in osteosarcoma treatment, the cisplatin resistance remains a big challenge for improving overall survival. The store-operated calcium (Ca$^{2+}$) entry (SOCE) and its major mediator Stim1 have been shown to be implicated in a number of pathological processes typical for cancer. In this study, we showed that Stim1 expression was significantly increased in chemo-resistant osteosarcoma tissues compared with chemo-sensitivity tissues. Patients with Sitm1 expression exhibited poorer overall survival than Stim1-negative patients. Moreover, un-regulation of Stim1 expression and SOCE were also observed in cisplatin-resistant MG63/CDDP cells compared with their parental cells. Cisplatin treatment obviously reduced Stim1 expression and SOCE in cisplatin-sensitivity MG63 cells, but had no effects on MG63/CDDP cells. In addition, cisplatin resulted in a more pronounced increase of endoplasmic reticulum (ER) stress in MG63 cells than in their resistant variants, which was evidenced by the activation of molecular markers of ER stress, GRP78, CHOP and ATF4. Knockdown of Stim1 using siRNA remarkably enhanced cisplatin-induced apoptosis and ER stress in MG63/CDDP cells, thereby sensitizing cancer cells to cisplatin. On the other hand, overexpression of Stim1 markedly reversed apoptosis and ER stress following cisplatin treatment. Taken together, these results demonstrate that Stim1 as well as Ca$^{2+}$ entry contributes cisplatin resistance via inhibition of ER stress-mediated apoptosis, and provide important clues to the mechanisms involved in cisplatin resistance for osteosarcoma treatment. Stim1 represents as a target of cisplatin and blockade of Stim1-mediated Ca$^{2+}$ entry may be a useful strategy to improve the efficacy of cisplatin to treat osteosarcoma.
Starting Page	216
Ending Page	225
Page Count	10
File Format	PDF
ISSN	09147470
Journal	Human Cell
Volume Number	30
Issue Number	3
e-ISSN	17490774
Language	English
Publisher	Springer Japan
Publisher Date	2017-03-22
Publisher Place	Tokyo
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Cisplatin resistance Osteosarcoma Endoplasmic reticulum Apoptosis Stim1 Cell Biology Embryology Oncology Stem Cells Reproductive Medicine Cell Culture
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Cancer Research

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