In this study, to assess an involvement of LPA receptor genes in the development of human cancer cells, we looked for the presence of mutations in LPA receptor 1-6 (LPA1-6) genes in MG63 osteosarcoma, HT1080 fibrosarcoma, A549 lung adenocarcinoma, MCF-7 breast carcinoma, and G-361 melanoma cells.
The expression of ATX was highest in MC, while the LPA1 expression was higher in PDC and AC, and the expression of LPA2 and LPA3 was highest in PTC (p < 0.001).
Consistency of effects between rs7030789 and rs1409986 in LPAR1 and PTGER3 and apnea phenotypes were observed in independent clinic-based cohorts.Novel genetic loci for apnea phenotypes were identified through the use of customized gene chips and meta-analyses of cohort data with replication in clinic-based samples.
Using a panel of 46,449 polymorphisms from roughly 2,100 candidate genes on a customized Illumina iSelect chip, we tested for association with the apnea hypopnea index (AHI) as well as moderate to severe OSA (AHI≥15) in 3,551 participants of the Cleveland Family Study and two cohorts participating in the Sleep Heart Health Study.Among 647 African-Americans, rs11126184 in the pleckstrin (PLEK) gene was associated with OSA while rs7030789 in the lysophosphatidic acid receptor 1 (LPAR1) gene was associated with AHI using a chip-wide significance threshold of p-value<2×10(-6).
We suggest that the distribution of LpA-I is different in CAD and the Preβ1-HDL/LpA-I ratio may have additional value in assessing anti-atherogenic potential of HDL particles and it is likely to become a clinically valuable indicator of atherosclerosis development.
Recently, we reported that abrogation of LPA receptor 1 (LPA1) ameliorated murine collagen-induced arthritis, probably via inhibition of inflammatory cell migration, Th17 differentiation and osteoclastogenesis.
We suggest that the distribution of LpA-I is different in CAD and the Preβ1-HDL/LpA-I ratio may have additional value in assessing anti-atherogenic potential of HDL particles and it is likely to become a clinically valuable indicator of atherosclerosis development.
The expression level of LPA(1) mRNA was significantly higher in normal ovarian tissue compared with that in benign tumor and in ovarian cancer tissue (p<0.01).
Collectively, our results elucidate a new molecular pathway driving LPA-induced metastasis, thus underscoring the therapeutic potential of targeting LPA1 in patients with basal breast carcinomas.
Stromal LPA1 positivity (<i>p</i> = 0.017) and stromal LPA3 positivity (<i>p</i> = 0.004) were higher in breast cancer with adipose stroma containing CD68-positive crown-like structures (CLS).
We have recently reported that β-arrestin2 regulates LPA(1)-mediated breast cancer cell migration and invasion, although the underlying molecular mechanisms are not clearly understood.