Purpose:Many studies have investigated the association between serum IGF-1 and IGFBP levels with gastric cancer (GC), but the results remained inconclusive. In this work, we performed a systematic review and meta-analysis to examine the precise association of serum levels of IGF-1 and IGFBP with GC.Methods:A comprehensive systematic search was carried out in PubMed/MEDLINE, SCOPUS, Web of Science, and EMBASE databases for (nested) case-control studies that reported the levels of IGF-1 and IGFBP in GC cases and healthy controls, from inception until October 2020. Weighted mean difference (WMD) was calculated for estimating combined effect size. Subgroup analysis was performed to identify the source of heterogeneity among studies.
Results:We found eight and five eligible studies (with 1541 participants) which provided data for IGF-1 and IGFBP, respectively. All studies on IGFBP reported the IGFBP-3 isoform. The pooled results indicate that GC patients had significantly lower serum IGF-1 [WMD = −26.21 ng/mL (95% CI, −45.58 to −6.85; P = .008)] and IGFBP-3 [WMD = −0.41 ng/mL (95% CI, −0.80 to −0.01; P = .04; I 2 = 89.9%; P < .001)] levels than those in healthy subjects. Significant heterogeneity was observed in the association, which could be attributed to the sample size of the studies.
Conclusions:In conclusion, our study reveals a significantly lower level of IGF-1 and IGFBP-3 in GC patients compared with healthy control subjects.
We aimed to explore MRPL23-AS1’s role in the pre-metastatic microenvironment of malignancy during epithelial-mesenchymal transition (EMT). Identification and verification of lncRNA-interacting proteins in salivary adenoid cystic carcinoma (SACC) cells were conducted via RNA-pulldown,
silver staining, and Western blotting. RIP and RIP-seq were sequentially administered to verify the binding partners of lncRNA. CHIRP was performed to detect the promoter DNA in the downstream of lncRNA-protein complex. Ultimately CHIP-qPCR detected the effects of lncRNA on the binding degree
of its interacting protein to the promoter DNA in the downstream genes and the methyla-tion level of histones in the promoter region. The exosomes secreted by different SACC cells were extracted from culture supernatant to measure lncRNA expression via qPCR. MRPL23-AS1 interacted with EZH2
protein and promoted EZH2 binding to E-cadherin gene promoter region along with the H3K27 methylation. MRPL23-AS1 could promote EMT of SACC cells and increase pulmonary vascular endothelial cells permeability via exosomes secretion. MRPL23-AS1 up-regulated VEGFA, while down-regulated E-cadherin
and VE-cadherin in endothelial cells. Exosomes rich in MRPL23-AS1 could boost lung metastasis in vivo. MRPL23-AS1 inhibits E-cadherin level and promotes EMT of SACC cells, suggesting that it might be a biomarker and therapeutic target for lung cancer.
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