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Review
. 2021 Sep 28:516:64-72.
doi: 10.1016/j.canlet.2021.05.036. Epub 2021 Jun 2.

Store-operated Ca2+ entry as a key oncogenic Ca2+ signaling driving tumor invasion-metastasis cascade and its translational potential

Jiazhang Wei  1 , Yayan Deng  2 , Jiaxiang Ye  2 , Yue Luo  2 , Jingjin Weng  1 , Qian He  3 , Fei Liu  4 , Min Li  1 , Rong Liang  2 , Yan Lin  2 , Yongqiang Li  2 , Jinyan Zhang  5 , Jianrong Yang  6 , Shenhong Qu  7
Affiliations
Review

Store-operated Ca2+ entry as a key oncogenic Ca2+ signaling driving tumor invasion-metastasis cascade and its translational potential

Jiazhang Wei et al. Cancer Lett. .

Abstract

Tumor metastasis is the primary cause of treatment failure and cancer-related deaths. Store-operated Ca2+ entry (SOCE), which is mediated by stromal interaction molecules (STIM) and ORAI proteins, has been implicated in the tumor invasion-metastasis cascade. Epithelial-mesenchymal transition (EMT) is a cellular program that enables tumor cells to acquire the capacities needed for migration and invasion and the formation of distal metastases. Tumor-associated angiogenesis contributes to metastasis because aberrantly developed vessels offer a path for tumor cell dissemination as well as supply sufficient nutrients for the metastatic colony to develop into metastasis. Recently, increasing evidence has indicated that SOCE alterations actively participate in the multi-step process of tumor metastasis. In addition, the dysregulated expression of STIM/ORAI has been reported to be a predictor of poor prognosis. Herein, we review the latest advances about the critical role of SOCE in the tumor metastasis cascade and the underlying regulatory mechanisms. We emphasize the contributions of SOCE to the EMT program, tumor cell migration and invasion, and angiogenesis. We further discuss the possibility of modulating SOCE or intervening in the downstream signaling pathways as a feasible targeting therapy for cancer treatment.

Keywords: Angiogenesis; Epithelial-mesenchymal transition; Migration; ORAI; STIM.

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