Stromal interaction molecule 1 plays an important role in gastric cancer progression

Xu, Jing; Zhou, Yan; Gao, Long; Zhou, Shuxian; Liu, Weihua; Li, Xiao-an

doi:10.3892/or.2016.4704

Cited by 14 publications

(14 citation statements)

References 27 publications

(30 reference statements)

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“…Although the presence of cancer associated fibroblasts and adipocytes are known to contribute to cancer progression via calcium signalling [77,78], the role of ORAI and STIM isoforms in these microenvironmental components has not yet been fully elucidated. Oesophageal cancer ↑ ↑ ↑ [24] Renal cancer ↑ [26] Stomach cancer ↑ [25] Lung cancer ↑ ↑ ↑ [80] ORAI3 Renal cancer ↔ [26] Breast cancer ↑ ↑ [22,66] Lung cancer ↑ ↑ ↑ [27,28] STIM1 Cervical cancer ↑ [40] Stomach cancer ↑ ↔ [81] Liver cancer ↑ ↑ [35,82] Colorectal cancer ↑ ↑ [83] STIM2 Colorectal cancer ↑ [84] A C C E P T E D M A N U S C R I P T…”

Section: Accepted Manuscriptmentioning

confidence: 99%

ORAI channels and cancer

Chalmers

Monteith

2018

Cell Calcium

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Cancer is a major cause of death. The diversity of cancer types and the propensity of cancers to acquire resistance to therapies, including new molecularly targeted and immune-based therapies, drives the search for new ways to understand cancer progression. The remodelling of calcium (Ca) signalling and the role of the Ca signal in controlling key events in cancer cells such as proliferation, invasion and the acquisition of resistance to cell death pathways is well established. Most of the work defining such changes has focused on Ca permeable Transient Receptor Potential (TRP) Channels and some voltage gated Ca channels. However, the identification of ORAI channels, a little more than a decade ago, has added a new dimension to how a Ca influx pathway can be remodelled in some cancers and also how calcium signalling could contribute to tumour progression. ORAI Ca channels are now an exemplar for how changes in the expression of specific isoforms of a Ca channel component can occur in cancer, and how such changes can vary between cancer types (e.g. breast cancer versus prostate cancer), and even subtypes (e.g. oestrogen receptor positive versus oestrogen receptor negative breast cancers). ORAI channels and store operated Ca entry are also highlighting the diverse roles of Ca influx pathways in events such as the growth and metastasis of cancers, the development of therapeutic resistance and the contribution of tumour microenvironmental factors in cancer progression. In this review we will highlight some of the studies that have provided evidence for the need to deepen our understanding of ORAI Ca channels in cancer. Many of these studies have also suggested new ways on how we can exploit the role of ORAI channels in cancer relevant processes to develop or inform new therapeutic strategies.

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Section: Accepted Manuscriptmentioning

confidence: 99%

ORAI channels and cancer

Chalmers

Monteith

2018

Cell Calcium

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“…In particular, STIM1 levels are upregulated in colorectal cancer and are positively correlated with tumor invasion and metastasis in this malignancy ( 45 ). STIM1 knockdown inhibited cell migration and invasion in both gastric cancer and glioblastoma ( 46 , 47 ). ORAI1 and STIM1 regulate focal adhesion kinase at the front or at the rear edge of migrating cells, respectively ( 48 ).…”

Section: Oncogenes and Tumor Suppressorsmentioning

confidence: 99%

Regulation of Endoplasmic Reticulum–Mitochondria Ca2+ Transfer and Its Importance for Anti-Cancer Therapies

et al. 2017

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Inter-organelle membrane contact sites are emerging as major sites for the regulation of intracellular Ca2+ concentration and distribution. Here, extracellular stimuli operate on a wide array of channels, pumps, and ion exchangers to redistribute intracellular Ca2+ among several compartments. The resulting highly defined spatial and temporal patterns of Ca2+ movement can be used to elicit specific cellular responses, including cell proliferation, migration, or death. Plasma membrane (PM) also can directly contact mitochondria and endoplasmic reticulum (ER) through caveolae, small invaginations of the PM that ensure inter-organelle contacts, and can contribute to the regulation of numerous cellular functions through scaffolding proteins such as caveolins. PM and ER organize specialized junctions. Here, many components of the receptor-dependent Ca2+ signals are clustered, including the ORAI1-stromal interaction molecule 1 complex. This complex constitutes a primary mechanism for Ca2+ entry into non-excitable cells, modulated by intracellular Ca2+. Several contact sites between the ER and mitochondria, termed mitochondria-associated membranes, show a very complex and specialized structure and host a wide number of proteins that regulate Ca2+ transfer. In this review, we summarize current knowledge of the particular action of several oncogenes and tumor suppressors at these specialized check points and analyze anti-cancer therapies that specifically target Ca2+ flow at the inter-organelle contacts to alter the metabolism and fate of the cancer cell.

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“…Ca 2+ is a crucial second messenger modulating various cellular processes，thereby STIM1 is also involved in a variety of biological processes including immune activation [4], cardiovascular damage [5], pulmonary disease [6] and so on. Moreover, it is demonstrated that STIM1 is also associated with the development and metastasis of several cancers [7-10] and has emerged as a target for cancer therapeutics [11]. Yang and his colleagues [12] were the first to report that STIM1 mediated breast cancer cells migration and metastasis in 2009.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-223 Targeting STIM1 Inhibits the Biological Behavior of Breast Cancer

Yang¹,

Jiang

Ma³

et al. 2018

Cell Physiol Biochem

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Background/Aims: To investigate the cellular effects and clinical significance of microRNA-223 (miR-223) in breast cancer by targeting stromal interaction molecule1 (STIM1). Methods: Breast cancer cell lines (T47D, MCF-7, SKB-R3, MDA-MB-231 and MDA-MB-435) and a normal breast epithelial cell line (MCF-10A) were prepared for this study. MiR-223 mimics, anti-miR-223 and pcDNA 3.1-STIM1 were transiently transfected into cancer cells independently or together, and then RT-qPCR was performed to detect the expressions of miR-223 and STIM1 mRNA, dual-luciferase reporter assay was conducted to examine the effects of miR-223 on STIM1, Western blotting was used to measure the expressions of the STIM1 proteins, MTT and Trans-well assays were performed to detect cell proliferation and invasion. Finally, the correlation of miR-223 and STIM1 was investigated by detecting with ISH and IHC in breast cancer specimens or the corresponding adjacent normal tissues. Results: Compared with normal cells and tissues, breast cancer tissues and cells exhibited significantly lower expression of miR-223, but higher expression of STIM1. MiR-223 could inhibit the proliferation and invasiveness of breast cancer cells by negatively regulating the expressions of STIM1. Reimplantation with STIM1 partially rescued the miRNA-223-induced inhibition of breast cancer cells. Clinical data revealed that high expression of STIM1 and miR-223 was respectively detrimental and beneficial factor impacting patient’s disease-free survival (DFS) rather than overall survival (OS). Moreover, Pearson correlation analysis also confirmed that STIM1 was inversely correlated with miR-223. Conclusion: MiR-223 inhibits the proliferation and invasion of breast cancer by targeting STIM1. The miR-223/STIM1 axis could possibly be a potential therapeutic target for treating breast cancer patients.

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Stromal interaction molecule 1 plays an important role in gastric cancer progression

Cited by 14 publications

References 27 publications

ORAI channels and cancer

ORAI channels and cancer

Regulation of Endoplasmic Reticulum–Mitochondria Ca2+ Transfer and Its Importance for Anti-Cancer Therapies

MicroRNA-223 Targeting STIM1 Inhibits the Biological Behavior of Breast Cancer

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