Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Thus, we recognize the importance of several kinase inhibitors to the current landscape of drug development for cancer therapy and the use of G-protein Coupled Receptor (GPCR) modulators.
|
31659944 |
2019 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The differentially expressed genes were functionally enriched in regulating the cell proliferation, cell death, and response to endogenous stimulus, and clustered in pathways such as cancer and signaling by the G protein-coupled receptor (GPCR).
|
31496800 |
2019 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Taken together with their GPCR properties, this makes them an attractive drug target for the development of highly specific and efficient targeted therapies against cancer.
|
30616827 |
2019 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Here, we overview the recent advances provided by the information theory, focusing on the nuclear factor (NF)-κB, extracellular signal-regulated kinase (ERK), and G-protein-coupled receptor (GPCR) pathways, which are frequently hijacked in cancer.
|
31630880 |
2019 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The growing impact of polypharmacology for complex diseases like schizophrenia, cancer etc. warrants the need for novel targets and considering the undiscriminating and selectivity of GPCRs, they can fulfill this purpose.
|
30394207 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Treatment with LINK-A locked nucleic acids or GPCR antagonists stabilized the PLC components, Rb and p53, and sensitized mammary gland tumors to immune checkpoint blockers.
|
31160797 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The oncoprotein Smoothened (SMO), a G-protein-coupled receptor (GPCR) of the Frizzled-class (class-F), transduces the Hedgehog signal from the tumour suppressor Patched-1 (PTCH1) to the glioma-associated-oncogene (GLI) transcription factors, which activates the Hedgehog signalling pathway<sup>1,2</sup>.
|
31168089 |
2019 |
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
Overall, we link a cancer cell-specific GPCR with the nuclear AR and show that targeting PSGR can provide us a new target to combat PCa better.
|
30928381 |
2019 |
Malignant neoplasm of prostate
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
G protein-coupled receptor family C group 6 member A (GPRC6A) is activated by testosterone and modulates prostate cancer progression.
|
30894404 |
2019 |
Prostate carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
G protein-coupled receptor family C group 6 member A (GPRC6A) is activated by testosterone and modulates prostate cancer progression.
|
30894404 |
2019 |
Prostate carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Overall, we link a cancer cell-specific GPCR with the nuclear AR and show that targeting PSGR can provide us a new target to combat PCa better.
|
30928381 |
2019 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
The differentially expressed genes were functionally enriched in regulating the cell proliferation, cell death, and response to endogenous stimulus, and clustered in pathways such as cancer and signaling by the G protein-coupled receptor (GPCR).
|
31496800 |
2019 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Taken together with their GPCR properties, this makes them an attractive drug target for the development of highly specific and efficient targeted therapies against cancer.
|
30616827 |
2019 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
The growing impact of polypharmacology for complex diseases like schizophrenia, cancer etc. warrants the need for novel targets and considering the undiscriminating and selectivity of GPCRs, they can fulfill this purpose.
|
30394207 |
2019 |
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Thus, we recognize the importance of several kinase inhibitors to the current landscape of drug development for cancer therapy and the use of G-protein Coupled Receptor (GPCR) modulators.
|
31659944 |
2019 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Here, we overview the recent advances provided by the information theory, focusing on the nuclear factor (NF)-κB, extracellular signal-regulated kinase (ERK), and G-protein-coupled receptor (GPCR) pathways, which are frequently hijacked in cancer.
|
31630880 |
2019 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
RHBDF1 is an indispensable component of the protein trafficking machinery involved in GPCR-mediated EGFR transactivation, and is an attractive therapeutic target for cancer.
|
30279141 |
2018 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In conclusion, P-REX2a enhanced cell motility via the GPCR downstream pathway independently of PTEN leading to progression of uterine endometrioid malignancies and poor prognosis of the patients.
|
29872505 |
2018 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Only a few GPCR members have been exploited as targets for developing drugs with therapeutic benefit in cancer.
|
29596308 |
2018 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
G protein‑coupled receptor 56 (GPR56), a member of the orphan GPCR family, has been reported to be an oncogene in various malignancies.
|
30066935 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The role of YAP (Yes-associated protein 1) and MRTF-A (myocardin-related transcription factor A), two transcriptional co-activators regulated downstream of GPCRs (G protein-coupled receptors) and RhoA, in the growth of glioblastoma cells and in vivo glioblastoma multiforme (GBM) tumor development was explored using human glioblastoma cell lines and tumor-initiating cells derived from patient-derived xenografts (PDX).
|
29887596 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These findings are the first to identify a critical link between the tumor suppressor ARRDC3 and regulation of GPCR trafficking and signaling in breast cancer.
|
29348172 |
2018 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
<i>Pten</i> knockout mice were used to examine the effect of <i>Runx2</i> heterozygous deletion or abiraterone acetate (ABA), a prodrug of the CYP17A1 inhibitor abiraterone on <i>Cyp11a1</i> and <i>Cyp17a1</i> expression, testosterone level and tumor microenvironment (TME) remodeling <i>in vivo</i><b>Results:</b> We uncovered that activation of the AKT-RUNX2-OCN-GPRC6A-CREB signaling axis induced expression of <i>CYP11A1</i> and <i>CYP17A1</i> and testosterone production in PTEN-null prostate cancer cell lines in culture.
|
29167276 |
2018 |
Malignant neoplasm of prostate
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
However, signaling pathways driving aberrant IAS remain poorly understood.<b>Experimental Design:</b> The effect of components of the AKT-RUNX2-osteocalcin (OCN)-GPRC6A-CREB signaling axis on expression of steroidogenesis genes <i>CYP11A1</i> and <i>CYP17A1</i> and testosterone level were examined in PTEN-null human prostate cancer cell lines.
|
29167276 |
2018 |
Prostate carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
However, signaling pathways driving aberrant IAS remain poorly understood.<b>Experimental Design:</b> The effect of components of the AKT-RUNX2-osteocalcin (OCN)-GPRC6A-CREB signaling axis on expression of steroidogenesis genes <i>CYP11A1</i> and <i>CYP17A1</i> and testosterone level were examined in PTEN-null human prostate cancer cell lines.
|
29167276 |
2018 |