Further, ROC curve analysis revealed that PLG, FGG, and their combination could distinguish NSCLC and its subtypes from healthy controls with an AUC ranging from 0.827 to 0.947.
By comparing urine samples with matching plasma CEA from NSCLC stage I-IV patients (n=81) and healthy controls (n=31), the combination of CEA with PLG or FGG showed that the AUC was 0.889 and 0.806, respectively, which is superior to a single biomarker alone.
Direct sequencing analyses were performed on FGA, FGB, and FGG genes to confirm hypodysfibrinogenemia and on the protein C gene to confirm protein C deficiency.
Seven candidate proteins, Contactin-1 (CNTN1), fibrinogen gamma chain (FGG), hemopexin (HPX), cell adhesion molecule-3 (CADM3), alpha-1B-glycoprotein (A1BG), complement factor B (CFB), and beta-2-microglobulin (B2M), were selected for further studies based on identification by both univariate and multivariate analyses and reported detection in human CSF and known associations to arthritis.
FGG played important roles in enhancing cancer cell motility and invasiveness through EMT signaling, and might serve as a potential prognostic biomarker for HCC patients.
Decreased levels of FGG and CFB in CSF after treatment showed strong correlations with both erythrocyte sedimentation rate and disability scores, while CNTN1 and CADM3 were associated with pain.
Direct sequencing analyses were performed on FGA, FGB, and FGG genes to confirm hypodysfibrinogenemia and on the protein C gene to confirm protein C deficiency.
In vitro phenotype studies showed that overexpression of FGG could promote the migration and invasion in SK-HEP-1 cells; conversely, these phenotypes could be significantly inhibited by knocking down the expression of FGG.
In addition, the protein-protein interaction network indicated that the core proteins associated with ADRB3-KO-induced LVDD were FGG, ALDH1A1, FGA, APOC3, SLC4A1, SERPINF2, HP, CTNNB1, and TKT.
FGG played important roles in enhancing cancer cell motility and invasiveness through EMT signaling, and might serve as a potential prognostic biomarker for HCC patients.
Clinical pathological analysis demonstrated that upregulation of intracellular FGG was significantly associated with increased vascular invasion, more satellite nodules, and more advanced TNM stage, and HCC patients with stronger expression of FGG had a higher recurrence rate and correspondingly a shorter overall survival time.
A novel fibrinogen gamma-chain mutation, p.Cys165Arg, causes disruption of the γ165Cys-Bβ227Cys disulfide bond and ultimately leads to hypofibrinogenemia.
Loss of function mutations in FGG have been associated with fibrinogen deficiency, while the c.1423G > A mutation in TBCD causes a novel syndrome of neurodegeneration and early onset encephalopathy.
Certain core genes, including collagen type 12 α1 chain (COL12A1), glutathione S‑transferase α3 (GSTA3), fibrinogen α chain (FGA) and fibrinogen γ chain (FGG), were the first reported to be associated with GC.
A novel fibrinogen gamma-chain mutation, p.Cys165Arg, causes disruption of the γ165Cys-Bβ227Cys disulfide bond and ultimately leads to hypofibrinogenemia.