Identification of ryanodine receptor isoforms in prostate DU-145, LNCaP, and PWR-1E cells

Kobylewski, Sarah; Henderson, Kimberly A.; Eckhert, Curtis D.

doi:10.1016/j.bbrc.2012.07.119

Cited by 11 publications

(6 citation statements)

References 24 publications

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“…The ryanodine receptor (RyR, three isoforms) is a large, intracellular calcium channel and a recently published study demonstrated a mechanistic link between spinophilin and RyR2 activation in heart disease [ 31 ]. This calcium channel has also been connected to prostate [ 32 ] and breast cancer [ 33 ]. Abdul et al found a correlation between RyR expression and tumor grade in BC [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

Low spinophilin expression enhances aggressive biological behavior of breast cancer

et al. 2015

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Spinophilin, a putative tumor suppressor gene, has been shown to be involved in the pathogenesis of certain types of cancer, but its role has never been systematically explored in breast cancer. In this study, we determined for the first time the expression pattern of spinophilin in human breast cancer molecular subtypes (n = 489) and correlated it with survival (n = 921). We stably reduced spinophilin expression in breast cancer cells and measured effects on cellular growth, apoptosis, anchorage-independent growth, migration, invasion and self-renewal capacity in vitro and metastases formation in vivo. Microarray profiling was used to determine the most abundantly expressed genes in spinophilin-silenced breast cancer cells. Spinophilin expression was significantly lower in basal-like breast cancer (p<0.001) and an independent poor prognostic factor in breast cancer patients (hazard ratio = 1.93, 95% confidence interval: 1.24-3.03; p = 0.004) A reduction of spinophilin levels increased cellular growth in breast cancer cells (p<0.05), without influencing activation of apoptosis. Anchorage-independent growth, migration and self-renewal capacity in vitro and metastatic potential in vivo were also significantly increased in spinophilin-silenced cells (p<0.05). Finally, we identified several differentially expressed genes in spinophilin-silenced cells. According to our data, low levels of spinophilin are associated with aggressive behavior of breast cancer.

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Section: Discussionmentioning

confidence: 99%

Low spinophilin expression enhances aggressive biological behavior of breast cancer

et al. 2015

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“…So far, only a few studies addressed RYR2 regulation and function in epithelial tumor cells. RYR2 expression and Caffeine‐stimulated Ca 2+ release were reported for prostate and breast cancer cell lines . Mariot et al .…”

Section: Discussionmentioning

confidence: 93%

“…RYR2 expression and Caffeine-stimulated Ca 2+ release were reported for prostate and breast cancer cell lines. 57,58 Mariot et al 59 provided experimental data that a RYR-related Ca 2+ mobilization augments apoptosis of LNCaP cells, a RYR1-and RYR2-positive prostate cancer cell line. In contrast, a strong RYR2 up-regulation was found in a breast cancer cell line upon EGF-induced epithelial-to-mesenchymal transition, 58 a process which is related with a higher risk for tumor cell dissemination and treatment failure in many epithelial malignancies, including HNSCC.…”

Section: Discussionmentioning

confidence: 99%

Somatic mutations and promotor methylation of the ryanodine receptor 2 is a common event in the pathogenesis of head and neck cancer

Schmitt

Molfenter

Laureano

et al. 2019

Intl Journal of Cancer

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Genomic sequencing projects unraveled the mutational landscape of head and neck squamous cell carcinoma (HNSCC) and provided a comprehensive catalog of somatic mutations. However, the limited number of significant cancer‐related genes obtained so far only partially explains the biological complexity of HNSCC and hampers the development of novel diagnostic biomarkers and therapeutic targets. We pursued a multiscale omics approach based on whole‐exome sequencing, global DNA methylation and gene expression profiling data derived from tumor samples of the HIPO‐HNC cohort (n = 87), and confirmed new findings with datasets from The Cancer Genome Atlas (TCGA). Promoter methylation was confirmed by MassARRAY analysis and protein expression was assessed by immunohistochemistry and immunofluorescence staining. We discovered a set of cancer‐related genes with frequent somatic mutations and high frequency of promoter methylation. This included the ryanodine receptor 2 (RYR2), which showed variable promoter methylation and expression in both tumor samples and cell lines. Immunohistochemical staining of tissue sections unraveled a gradual loss of RYR2 expression from normal mucosa via dysplastic lesion to invasive cancer and indicated that reduced RYR2 expression in adjacent tissue and precancerous lesions might serve as risk factor for unfavorable prognosis and upcoming malignant conversion. In summary, our data indicate that impaired RYR2 function by either somatic mutation or epigenetic silencing is a common event in HNSCC pathogenesis. Detection of RYR2 expression and/or promoter methylation might enable risk assessment for malignant conversion of dysplastic lesions.

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“…Unlike that for InsP3Rs, much less is known about the role of RyRs in cancer, possibly because these channels are mainly studied in excitable cells, where the onset of cancer itself is rarer. RyRs are known to be expressed in breast cancer [128] and prostate cancer cells, where they may have a role in regulating apoptosis [129,130]. In a breast cancer cell line, for instance, EGF-induced EMT was associated with elevated mRNA levels of several ER Ca 2+ pumps and channels, of which RyR2 displayed the most prominent change in gene expression levels [89].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

ER Ca2+ release and store-operated Ca2+ entry – partners in crime or independent actors in oncogenic transformation?

et al. 2019

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The Graphical Abstract indicates the Hallmarks of Cancer and their relationship with a cell signalling module involving store operated Ca 2+ entry (SOCE) based on STIM/Orai and InsP3 dependent Ca 2+ release from the ER (via InsP3Rs; IICR). We propose that SOCE/IICR is dynamically modulated to meet the needs of the cell as it transitions through the various stages of oncogenic transformation. In turn, SOCE/IICR influences the physiology of the cell according to the transformation stage. Highlights: Ca 2+ signalling pathways control cellular life and death decisions  Ca 2+ signalling is remodelled during oncogenic transformation  Ca 2+ signalling contributes to oncogenic transformation  Ca 2+ release via ER InsP3R channels is remodelled in transformed cells  STIM/ORAI-associated store operated Ca 2+ entry is altered in cancer  ER Ca 2+ release and store operated Ca 2+ entry synergise to determine cell fate

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Identification of ryanodine receptor isoforms in prostate DU-145, LNCaP, and PWR-1E cells

Cited by 11 publications

References 24 publications

Low spinophilin expression enhances aggressive biological behavior of breast cancer

Low spinophilin expression enhances aggressive biological behavior of breast cancer

Somatic mutations and promotor methylation of the ryanodine receptor 2 is a common event in the pathogenesis of head and neck cancer

ER Ca2+ release and store-operated Ca2+ entry – partners in crime or independent actors in oncogenic transformation?

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