GPR78 promotes lung cancer cell migration and metastasis by activation of Gαq-Rho GTPase pathway

Dong, Di; Zhou, Hui; Gao, Li

doi:10.5483/bmbrep.2016.49.11.133

Cited by 20 publications

(15 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The GPR78 protein, belongs to the family of G-protein-coupled receptors, whose main function is to mediate physiological responses to various extracellular signals, including hormones and neurotransmitters 36 . However, the specific function of GPR78 is still largely unknown, although it has been shown to play a role in lung cancer metastasis 37 .…”

Section: Discussionmentioning

confidence: 99%

A meta-analysis of genome-wide association studies identifies multiple longevity genes

et al. 2019

View full text Add to dashboard Cite

Human longevity is heritable, but genome-wide association (GWA) studies have had limited success. Here, we perform two meta-analyses of GWA studies of a rigorous longevity phenotype definition including 11,262/3484 cases surviving at or beyond the age corresponding to the 90th/99th survival percentile, respectively, and 25,483 controls whose age at death or at last contact was at or below the age corresponding to the 60th survival percentile. Consistent with previous reports, rs429358 (apolipoprotein E (ApoE) ε4) is associated with lower odds of surviving to the 90th and 99th percentile age, while rs7412 (ApoE ε2) shows the opposite. Moreover, rs7676745, located near GPR78 , associates with lower odds of surviving to the 90th percentile age. Gene-level association analysis reveals a role for tissue-specific expression of multiple genes in longevity. Finally, genetic correlation of the longevity GWA results with that of several disease-related phenotypes points to a shared genetic architecture between health and longevity.

show abstract

Section: Discussionmentioning

confidence: 99%

A meta-analysis of genome-wide association studies identifies multiple longevity genes

et al. 2019

View full text Add to dashboard Cite

show abstract

“…GRP (100 nM) or WP1066 (10 μM) in DMEM was added into the lower chamber. VSMCs migrating through the filter and appearing on the lower side were fixed by careful immersion of the filter into methanol for 1 minute, stained with H&E solution and cells counted in three random fields per well ( 30 ). Each experiment was performed in duplicate and three separate experiments were performed for each group.…”

Section: Methodsmentioning

confidence: 99%

Gastrin-releasing peptide promotes the migration of vascular smooth muscle cells through upregulation of matrix metalloproteinase-2 and -9

et al. 2017

View full text Add to dashboard Cite

Gastrin-releasing peptide (GRP) has been reported to be implicated in the pathogenesis of inflammatory disorders. The migration and proliferation of vascular smooth muscle cells (VSMCs) are key components of vascular inflammation that leads to the development of atherosclerosis. The present study aimed to investigate the molecular effect of GRP on VSMC proliferation and migration. We report that GRP significantly enhanced the proliferation and migration of rat VSMCs. GRP increased mRNA and protein expression of matrix metalloproteinase-2 and -9 (MMP-2/9) in VSMCs. The induction of MMP-2/9 by GRP was regulated by the activation of the signal transducer and activator of transcription-3 (STAT3). In addition, STAT3-knockdown of VSMCs by siRNA or blockade of the GRP receptor inhibited GRP-induced migration of VSMCs. Taken together, our findings indicate that GRP promotes the migration of VSMCs through upregulation of MMP-2/9 via STAT3 activation.

show abstract

“…Although it is not clear what causes unique DOR functions, alternative G protein coupling may be relevant. In contrast to MOR and KOR, DOR also activates G q/11 proteins (34) and these were found to regulate cancer cell metastasis (53).…”

Section: Discussionmentioning

confidence: 99%

Opioids trigger breast cancer metastasis through E-Cadherin downregulation and STAT3 activation promoting epithelial-mesenchymal transition

Tripolt

Knab

Neubauer

et al. 2018

Preprint

View full text Add to dashboard Cite

The opioid crisis of pain medication bears risks from addiction to cancer progression, but little experimental facts exist. Expression of δ-opioid receptors (DORs) correlates with poor prognosis for breast cancer (BCa) patients, but mechanism and genetic/pharmacologic proof of key changes in opioid-triggered cancer biology are lacking. We show that oncogenic STAT3 signaling and E-Cadherin downregulation are triggered by opioid-ligated DORs, promoting metastasis. Human and murine transplanted BCa cells (MDA-MB-231, 4T1) displayed enhanced metastasis upon opioid-induced DOR stimulation, and DOR-antagonist blocked metastasis. Opioid-exposed BCa cells showed enhanced migration, STAT3 activation, down-regulation of E-Cadherin and expression of epithelial-mesenchymal transition (EMT) markers. STAT3 knockdown or upstream inhibition through the JAK1/2 kinase inhibitor ruxolitinib prevented opioid-induced BCa cell metastasis and migration. We conclude that opioids trigger metastasis through oncogenic JAK1/2-STAT3 signaling.

show abstract

GPR78 promotes lung cancer cell migration and metastasis by activation of Gαq-Rho GTPase pathway

Cited by 20 publications

References 25 publications

A meta-analysis of genome-wide association studies identifies multiple longevity genes

A meta-analysis of genome-wide association studies identifies multiple longevity genes

Gastrin-releasing peptide promotes the migration of vascular smooth muscle cells through upregulation of matrix metalloproteinase-2 and -9

Opioids trigger breast cancer metastasis through E-Cadherin downregulation and STAT3 activation promoting epithelial-mesenchymal transition

Contact Info

Product

Resources

About