SPRY2

Last update 23 Jan 2025

Basic Info

Synonyms

hSPRY2, Protein sprouty homolog 2, sprouty RTK signaling antagonist 2

+ [2]

Introduction

Antagonist of fibroblast growth factor (FGF) pathways via inhibition of FGF-mediated phosphorylation of ERK1/2 (By similarity). Thereby acts as an antagonist of FGF-induced retinal lens fiber differentiation, may inhibit limb bud outgrowth and may negatively modulate respiratory organogenesis (By similarity). Inhibits TGFB-induced epithelial-to-mesenchymal transition in retinal lens epithelial cells (By similarity). Inhibits CBL/C-CBL-mediated EGFR ubiquitination (PubMed:17974561).

100 Clinical Results associated with SPRY2

100 Translational Medicine associated with SPRY2

0 Patents (Medical) associated with SPRY2

407

Literatures (Medical) associated with SPRY2

01 Jan 2025·Cancer Medicine

Assessing the Causal Effect of Circulating Protein‐To‐Protein Ratio on the Risk of Morbidity of Hepatocellular Carcinoma

Article

Author: Zhang, Mingwei ; Wan, Xiaoye ; Yue, Qiuyuan ; Xu, Shaohua ; Lin, Xi ; Li, Xiaoxia ; Li, Yueming

ABSTRACTObjectiveSeveral observational studies have identified an association between plasma proteins and hepatocellular carcinoma (HCC). This study aimed to explore the potential causal relationship between the circulating protein‐to‐protein ratio and the morbidity risk of HCC.MethodsGenetic association data for circulating plasma proteins and 2821 protein‐to‐protein ratios were sourced from the UKB PPP and Suhre's study. Genetic association data for HCC were sourced from the FinnGen cohort (finngen‐R11‐HCC) and the IEU OpenGWAS project (ieu‐b‐4953). Subsequently, a two‐sample Mendelian randomization (MR) and drug‐targeted MR approach were used to evaluate causality associations. To bolster the robustness of our findings, we conducted a series of sensitivity analyses.ResultsEight protein–protein pairs were identified as causal factors for HCC in the two independent cohorts. For each standard deviation increase in protein–protein pair expression, susceptibility to HCC fluctuated from 0.4974 (95% confidence interval [CI]: 0.2506–0.9871) for the LAT2/SPRY2 protein pair to 1.9763 (95% CI: 1.3009–3.0026) for the ERBIN/LAT2 protein pair. However, among the significant protein pairs, only one circulating protein, TDRKH (odds ratio: 0.5964, 95% CI: 0.4196–0.8476), was causally associated with HCC.ConclusionUsing multiple datasets and methods, eight protein–protein pairs were identified as having causal associations with HCC. Protein–protein interactions can provide meaningful findings beyond simple pQTL analysis.

02 Dec 2024·Journal of Crohn's and Colitis

MSCs-exosomes Can Promote Macrophage M2 Polarisation via Exosomal miR-21-5p through Mesenteric Injection: A Promising Way to Attenuate Murine Colitis

Article

Author: Shen, Chen ; Li, Yi ; Zhou, Yudi ; Zhang, Yi ; Wang, Jin ; Qian, Wenwei ; Yao, Jun ; Wu, Enhao ; Wang, Sheng ; Bai, Yanjin ; Chen, Hong

AbstractBackground and AimsExosome-based therapies are gaining increasing attention, with growing evidence suggesting a link between alterations in mesentery adipose tissue [MAT] and intestinal disease in Crohn’s disease [CD]. However, the specific mechanism by which mesenchymal stem cells [MSCs]-Exos may alleviate colitis through targeting MAT remains not fully understood.MethodsHuman umbilical cord MSCs [HucMSCs] were cultured to isolate the corresponding exosomes [HucMSCs-Exos], which were confirmed by their morphology, size distribution, and expression of markers. In vivo, 2,4,6-trinitrobenzenesulphonic acid [TNBS]- and dextran sodium sulphate [DSS]-induced mouse colitis models were used to detect the therapeutic effects of HucMSCs-Exos. Enzyme-linked immunosorbent assay [ELISA], quantitative reverse transcription-polymerase chain reaction [qRT-PCR], western blotting, and immunofluorescence determined the expression of key molecules. Luciferase reporter assay was used to confirm the relationship between miR-21-5p and SPRY2.ResultsExosomes treatment through mesenteric injection demonstrated therapeutic effects on mesenteric inflammation and colitis. These therapeutic benefits were contingent on macrophages, significantly facilitating the M2 polarisation of mesenteric macrophages. The expression data from GSE159814 and GSE211008 revealed that exosomal miR-21-5p was enriched in HucMSCs-Exos and could be delivered to macrophages. Additionally, the results indicated that miR-21-5p could directly target the 3’UTR of SPRY2 and activate the phosphorylation of ERK to modify macrophage phenotypes. Mechanistically, exosomal miR-21-5p derived from HucMSCs could promote macrophage M2 polarisation via the SPRY2/ERK axis.ConclusionMesenteric injection of HucMSCs-Exos significantly alleviates mesenteric inflammation and colitis by promoting mesenteric macrophage M2 polarisation, making it a promising approach to treat colitis and suggesting therapeutic potential role of exosomal miR-21-5p in CD.

01 Sep 2024·Skin Research and Technology

LncRNA SLNCR1 facilitates angiogenesis and tumor growth in melanoma via DNMT1‐mediated epigenetically silencing SPRY2

Article

Author: Li, Ke ; Jiang, Jingting ; Wu, Lijun

AbstractBackgroundThe malignancy of melanoma is attributed to its pronounced invasiveness, extensive vascularization, and rapid tumor cell growth and metastasis. LncRNA SLNCR1 is closely associated with a variety of aggressive tumors. However, our understanding of SLNCR1 influences on malignant melanoma growth metastasis mechanism especially proangiogenic mechanism remains unclear.MethodsThe expression of SLNCR1 was evaluated in melanoma tissues, adjacent tissues, melanoma cell lines. The abilities of SLNCR1 on proliferation, migration, and angiogenesis of HUVECs were detected by CCK‐8, flow cytometry, and Western blot assays. The association between SLNCR1, DNMT1, and SPRY2 was assessed by ChIP, RIP, and Western blot assays. The effect of SLNCR1 on tumor growth was determined using a xenograft model in nude mice.ResultsSLNCR1 was confirmed to be highly expressed in melanoma tissues and cells. CM from melanoma cells transfected with sh‐SLNCR1 attenuated proliferation, migration, and angiogenesis of HUVECs. Moreover, loss of SLNCR1 hindered tumor growth and metastasis, as evidenced by reduced tumor size and weight, as well as angiogenesis. Mechanistic studies revealed that SLNCR1 silenced SPRY2 expression, likely through enhancing DNMT1‐mediated DNA methylation of SPRY2 promoter.ConclusionSLNCR1 is an oncogene that interacts with DNMT1 to mediate SPRY2 methylation, thereby suppressing SPRY2 expression and promoting the angiogenesis and tumor growth in melanoma. SLNCR1 may serve as a potential target for melanoma treatment.

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SPRY2

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