Gregory R. Monteith
University of Queensland
CancerInternal medicineEndocrinologyChemistryVoltage-dependent calcium channelCalcium signalingBreast cancer cellsProgrammed cell deathCancer researchPlasma membrane Ca2+ ATPaseCalciumBreast cancerMedicineEpithelial–mesenchymal transitionIntracellularBiologyCalcium pumpCell biologyCancer cellPharmacology
372Publications
45H-index
5,125Citations
Publications 367
Newest
#6Patsy S. Soon (UNSW: University of New South Wales)
Cancer-associated fibroblasts (CAFs) represent an important component of the tumour microenvironment and are implicated in disease progression. Two outstanding questions in cancer biology are how CAFs arise and how they might be targeted therapeutically. The calcium signal also has an important role in tumorigenesis. To date, the role of calcium signalling pathways in the induction of the CAF phenotype remains unexplored. A CAF model was generated through exogenous transforming growth factor bet...
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Epithelial to mesenchymal transition (EMT) in cancer is important in therapeutic resistance and invasiveness. Calcium signaling is key to the induction of EMT in breast cancer cells. Although inhibition of specific calcium-permeable ion channels regulates the induction of a sub-set of EMT markers in breast cancer cells, it is still unclear if activation of a specific calcium channel can be a driver for the induction of EMT events. In this study, we exploited the availability of a selective pharm...
4 CitationsSource
#1Xuexin Zhang (PSU: Pennsylvania State University)H-Index: 24
#2Ping Xin (PSU: Pennsylvania State University)H-Index: 9
Last. Mohamed Trebak (PSU: Pennsylvania State University)H-Index: 55
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The ubiquitous Ca2+ release-activated Ca2+ (CRAC) channel is crucial to many physiological functions. Both gain and loss of CRAC function is linked to disease. While ORAI1 is a crucial subunit of CRAC channels, recent evidence suggests that ORAI2 and ORAI3 heteromerize with ORAI1 to form native CRAC channels. Furthermore, ORAI2 and ORAI3 can form CRAC channels independently of ORAI1, suggesting diverse native CRAC stoichiometries. Yet, most available CRAC modifiers are presumed to target ORAI1 w...
17 CitationsSource
#1Jack Taylor (UTS: University of Technology, Sydney)H-Index: 4
#2Iman Azimi (UTAS: University of Tasmania)H-Index: 15
Last. Mary Bebawy (UTS: University of Technology, Sydney)H-Index: 33
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ABSTRACTExtracellular vesicles (EVs) are small extracellular membrane vesicles that serve as important intercellular signalling intermediaries in both malignant and non-malignant cells. For EVs for...
15 CitationsSource
#1Francisco Sadras (UQ: University of Queensland)
#2Teneale A. Stewart (UQ: University of Queensland)H-Index: 9
Last. Gregory R. Monteith (UQ: University of Queensland)H-Index: 45
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Disruption of Ca2+ signaling during breast cancer tumorigenesis is now well-established. Despite the increasing recognition of the role of the tumour microenvironment, and cancer associated fibroblasts (CAFs), in tumorigenesis, very few studies have assessed alterations in Ca2+ influx pathways in this context. The aims of this study were to identify changes in the nature of Ca2+ influx in breast CAFs and to define the role of Ca2+ signaling in the induction of CAFs. We first developed a model fo...
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#1Alice H.L. Bong (UQ: University of Queensland)H-Index: 4
#2John J. Bassett (UQ: University of Queensland)H-Index: 3
Last. Gregory R. Monteith (UQ: University of Queensland)H-Index: 45
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Abstract Triple-negative breast cancers (TNBC) are often associated with high relapse rates, despite treatment with chemotherapy agents such as doxorubicin. A better understanding of the signaling and molecular changes associated with doxorubicin may provide novel insights into strategies to enhance treatment efficacy. Calcium signaling is involved in many pathways influencing the efficacy of chemotherapy agents such as proliferation and cell death. However, there are a limited number of studies...
3 CitationsSource
#1Teneale A. Stewart (UQ: University of Queensland)H-Index: 9
#2Iman AzimiH-Index: 15
Last. Gregory R. Monteith (UQ: University of Queensland)H-Index: 45
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The Ca2+ signal is essential in both hypoxia- and epidermal growth factor (EGF)-mediated epithelial to mesenchymal transition (EMT) in MDA-MB-468 breast cancer cells. This finding suggests that Ca2+-permeable ion channels participate in the induction of expression of some mesenchymal markers such as vimentin. However, the ion channels involved in vimentin expression induction have not been fully characterized. This work sought to define how differential modulation of the calcium signal effects t...
2 CitationsSource
#1Choon Leng So (UQ: University of Queensland)H-Index: 2
#2Michael J. G. Milevskiy (WEHI: Walter and Eliza Hall Institute of Medical Research)H-Index: 10
Last. Gregory R. Monteith (UQ: University of Queensland)H-Index: 45
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Transient receptor potential cation channel subfamily V (TRPV) channels play important roles in a variety of cellular processes. One example includes the sensory role of TRPV1 that is sensitive to elevated temperatures and acidic environments and is activated by the hot pepper component capsaicin. Another example is the importance of the highly Ca2+ selective channels TRPV5 and TRPV6 in Ca2+ absorption/reabsorption in the intestine and kidney. However, in some cases such as TRPV4 and TRPV6, brea...
8 CitationsSource
#1Iman Azimi (UTAS: University of Tasmania)H-Index: 15
#2Ralph J. Stevenson (University of Auckland)H-Index: 16
Last. Gregory R. MonteithH-Index: 45
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Store-operated calcium (Ca2+) entry is an important homeostatic mechanism in cells, whereby the release of Ca2+ from intracellular endoplasmic reticulum stores triggers the activation of a Ca2+ influx pathway. Mediated by Orai1, this Ca2+ influx has specific and essential roles in biological processes as diverse as lactation to immunity. Although pharmacological inhibitors of this Ca2+ influx mechanism have helped to define the role of store-operated Ca2+ entry in many cellular events, the lack ...
10 CitationsSource
#1Silke B. ChalmersH-Index: 5
Last. Gregory R. MonteithH-Index: 45
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