Background: Activator of G-protein Signaling 3 (AGS3, also known as GPSM1), is related to cell cycle progression. We investigated the expression of AGS3 in human esophageal squamous cell carcinoma (ESCC) and the therapeutic effect of chemotherapy drugs.
Methods: Immunohistochemistry and Western blot analysis were performed for AGS3 in 85ESCC samples. The data were correlated with clinicopathological features. The univariate and multivariate survival analyses were also performed to determine its prognostic significance. The effect of overexpression of AGS3 on proliferation of esophageal carcinoma TE1 cells was analyzed by serum starvation.
Results: AGS3 was down regulated in ESCC as compared with the adjacent normal tissue. Low expression of AGS3 was associated with tumor grade (P=0.002), and AGS3 was negatively correlated with proliferation marker Ki-67 (P<0.01). Univariate analysis showed that AGS3 expression did have a remarkable prediction for poor prognosis (P=0.004), while in vitro, the expression of AGS3 was down regulated with release from serum starvation of TE1 cells.
Conclusions: This study shows that AGS3 is an important regulator of ESCC proliferation.
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http://dx.doi.org/10.1016/j.prp.2014.12.016 | DOI Listing |
Receptors for the vasoactive adipokine apelin, termed APJ receptors, are G-protein-coupled receptors and are widely expressed throughout the cardiovascular system. APJ receptors can also signal via G-protein-independent pathways, including G-protein-coupled-receptor kinase 2 (GRK2), which inhibits nitric oxide synthase (eNOS) activity and nitric oxide (NO) production in endothelial cells. Apelin causes endothelium-dependent, NO-mediated relaxation of coronary arteries from normotensive animals, but the effects of activating APJ receptor signaling pathways in hypertensive coronary arteries are largely unknown.
View Article and Find Full Text PDFFront Cell Dev Biol
January 2025
Department of Gastrointestinal Surgery, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
Background: The high morbidity and mortality rates of colorectal cancer (CRC) have been a public health concern globally, and the search for additional therapeutic options is imminent. Hyodeoxycholic acid (HDCA) has been receiving attention in recent years and has demonstrated potent efficacy in several diseases. Nonetheless, the antitumor effects and molecular pathways of HDCA in CRC remain largely unexplored.
View Article and Find Full Text PDFJ Cell Mol Med
January 2025
Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Recently, RIT1 has been implicated in a range of neurological disorders; however, its precise function in glioma pathogenesis is not yet well-defined. This study employed quantitative reverse transcription PCR (qRT-PCR), Western blotting (WB), immunohistochemistry (IHC) and additional methodologies to assess RIT1 expression levels in glioma tissues. Furthermore, the study investigated its influence on glioma progression through a series of functional experiments.
View Article and Find Full Text PDFBiochem Pharmacol
January 2025
School of Pharmacy, Xi'an Jiaotong University, Xi'an 710061, PR China; State Key Laboratory of Shaanxi for Natural Medicines Research and Engineering, Xi'an 710061, PR China. Electronic address:
Breast cancer is the most common malignant tumor endangering women's life and health. Tamoxifen citrate (TAM) is the first-line drug of adjuvant endocrine therapy for estrogen receptor-positive (ER) breast cancer patients. Some sporadic cases have described rare adverse reactions of TAM with potentially life-threatening dermatological manifestations, which were associated with skin allergy.
View Article and Find Full Text PDFThe GPCR-like protein Smoothened (Smo) plays a pivotal role in the Hedgehog (Hh) pathway. To initiate Hh signaling, active Smo binds to and inhibits the catalytic subunit of PKA in the primary cilium, a process facilitated by G protein-coupled receptor kinase 2 (Grk2). However, the precise regulatory mechanisms underlying this process, as well as the events preceding and following Smo activation, remain poorly understood.
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