Calcium entry via ORAI1 regulates glioblastoma cell proliferation and apoptosis

Liu, Huiling; Hughes, Joshua D.; Rollins, Shadon; Chen, Betty; Perkins, Eddie

doi:10.1016/j.yexmp.2011.09.005

Cited by 102 publications

(84 citation statements)

References 28 publications

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“…We also observed a small but significant decrease in GBMs proliferation upon Orai1 knockdown (69). On the other hand, Liu et al (61) reported that in established human (U251) and rat (C6) glioblastoma cell lines, both STIM1 and Orai1 are essential for cell proliferation and cell survival. In a recent study, STIM1 knockdown significantly decreased U251 human glioblastoma proliferation by causing cell cycle arrest in G 0 /G 1 phase (55).…”

Section: Brain Tumors: Glioblastomas and Neuroblastomassupporting

confidence: 56%

STIM and Orai proteins as novel targets for cancer therapy. A Review in the Theme: Cell and Molecular Processes in Cancer Metastasis

Vashisht

Trebak

Motiani

2015

American Journal of Physiology-Cell Physiology

109

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Section: Brain Tumors: Glioblastomas and Neuroblastomassupporting

confidence: 56%

STIM and Orai proteins as novel targets for cancer therapy. A Review in the Theme: Cell and Molecular Processes in Cancer Metastasis

Vashisht

Trebak

Motiani

2015

American Journal of Physiology-Cell Physiology

109

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“…The involvement of the Orai1-driven Ca 2+ entry in apoptosis has been demonstrated in various cell types (23)(24)(25). However, its proor antiapoptotic role seems highly dependent on the stimulus and cell type studied.…”

Section: Role Of Calcium Influx In Rtx-induced Apoptosismentioning

confidence: 99%

Localized Store-Operated Calcium Influx Represses CD95-Dependent Apoptotic Effects of Rituximab in Non-Hodgkin B Lymphomas

Vacher

Pineau

et al. 2015

The Journal of Immunology

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International audienceThe anti-CD20 mAb, rituximab, is routinely used to treat B cell malignancies. However, a majority of patients relapse. An improvement in the complete response was obtained by combining rituximab with chemotherapy, at the cost of increased toxicity. We reported that rituximab induced the colocalization of both the Orai1 Ca(2+) release-activated Ca(2+) channel (CRAC) and the endoplasmic reticulum Ca(2+) sensor stromal interaction molecule 1 with CD20 and CD95 into a cluster, eliciting a polarized store-operated Ca(2+) entry (SOCE). We observed that blocking this Ca(2+) entry with downregulation of Orai1, pharmacological inhibitors, or reducing calcemia with hypocalcemic drugs sensitized human B lymphoma cell lines and primary human lymphoma cells to rituximab-induced apoptosis in vitro, and improved the antitumoral effect of rituximab in xenografted mice. This revealed that Ca(2+) entry exerted a negative feedback loop on rituximab-induced apoptosis, suggesting that associating CRAC channel inhibitors or hypocalcemic agents with rituximab may improve the treatment of patients with B cell malignancies. The calcium-dependent proteins involved in this process appear to vary according to the B lymphoma cell type, suggesting that CRAC-channel targeting is likely to be more efficient than calcium-dependent protein targetin

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“…STIM1 and ORAI1 underlie I CRAC and regulate glioblastoma cell proliferation, apoptosis, and invasion (15,16) and are involved in neuroblastoma proliferation as well (17). ORAI3 may form Ca 2ϩ -permeable channels with roles in breast cancer (18) and in non-small cell lung adenocarcinoma (19).…”

mentioning

confidence: 99%

A Reciprocal Shift in Transient Receptor Potential Channel 1 (TRPC1) and Stromal Interaction Molecule 2 (STIM2) Contributes to Ca2+ Remodeling and Cancer Hallmarks in Colorectal Carcinoma Cells

Sobradillo

Hernández-Morales

Ubierna

et al. 2014

Journal of Biological Chemistry

122

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Calcium entry via ORAI1 regulates glioblastoma cell proliferation and apoptosis

Cited by 102 publications

References 28 publications

STIM and Orai proteins as novel targets for cancer therapy. A Review in the Theme: Cell and Molecular Processes in Cancer Metastasis

STIM and Orai proteins as novel targets for cancer therapy. A Review in the Theme: Cell and Molecular Processes in Cancer Metastasis

Localized Store-Operated Calcium Influx Represses CD95-Dependent Apoptotic Effects of Rituximab in Non-Hodgkin B Lymphomas

A Reciprocal Shift in Transient Receptor Potential Channel 1 (TRPC1) and Stromal Interaction Molecule 2 (STIM2) Contributes to Ca2+ Remodeling and Cancer Hallmarks in Colorectal Carcinoma Cells

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