Sugase, M, T. (VLDL) treatment increases cell proliferation in LSR-expressing GC cell lines LSR on GC cell line proliferation, as well as the anti-tumor effect of the anti-hLSR mAb (#1C25) and = 6 [5%]; 2; = 24 [22%]; 3: = 45 [41%], 4: = 35 [32%]). There were no significant differences in LSR expression according to age, sex, differentiation, lymphatic invasion, vascular invasion, pT, pN, or metastasis. We considered GC patients with total preoperative cholesterol 220 mg/mL as having hypercholesterolaemia; such patients (or those being treated for it) had significantly stronger expression of LSR (= 33, 87%) than those without (= 47, 65%; = 0.037) (Table ?(Table11). Table 1 Comparison of LSR expression in patients with gastric cancer = 30= 80= 6= 24= 45= 35(%)0.775?male4 (67)15 (63)28 (62)25 (71)?female2 (33)9 (37)17 (38)10 (29)Differencition, (%)0.227?well differentiated3 (50)10 (42)23 (51)22 (63)?poorly differentiated3 (50)14 (58)22 (49)13 (37)Lymph invasion, (%)0.245?01 (17)9 (37)13 (29)5 (14)?1C25 (83)15 (63)32 (71)30 (86)Vascular invasion, (%)0.199?05 (83)19 (79)31 (69)23 (66)?1C21 (17)5 (21)14 (31)12 (34)pT, (%)0.052?12 (33)7 (29)11 (24)9 (26)?20 (0)1 (4)10 (22)11 (31)?32 (33)12 (50)15 (33)9 (26)?42 (33)4 (17)9 (21)6 (17)pN, (%)0.070?04 (67)18 (75)24 (53)13 (37)?11 (17)3 (13)8 (18)6 (17)?21 (17)1 (4)5 (11)8 (23)?30 (0)2 (8)8 (18)8 (23)pStage, (%)0.871?I2 (33)8 (33)15 (33)8 (23)?II2 (33)11 (46)16 (36)15 (43)?III2 (33)5 (21)14 (31)12 (34)Preoperative Hyperlipidemia or Drug history0.037?Yes1 (17)4 (17)12 (27)18 (51)?No5 (83)20 Fluocinonide(Vanos) (83)33 (73)17 (49) Open in a separate window Hyperlipidemia; Total Cholesterol 220 mg/dl. The total 5-year RFS Emcn and OS rates of GC patients who underwent curative resection were Fluocinonide(Vanos) 66.7% and 67.0%, respectively. GC patients with strong LSR expression tended to have poorer RFS rates than those with weak expression (5-year RFS rates: 63.0% vs. 76.2%, respectively, log-rank = 0.189). Moreover, patients with strong LSR expression had significantly poorer OS rates than those with weak expression (5-year OS rates: 59.7% vs. 85.8%, respectively, log-rank = 0.017) (Figure ?(Figure2A).2A). In GC patients with poorly differentiated or advanced tumors (pT3-4), those with strong LSR expression had significantly poorer OS, while those with weak LSR expression had relatively good OS (poorly differentiated tumors: 48.6% vs. 83.4%, respectively, log-rank = 0.022; pT3C4: 49.5.% versus 79.4%, respectively, log-rank = 0.022) (Figure 2B, 2C). Open in a separate window Figure 2 Survival curves based on lipolysis-stimulated lipoprotein receptor (LSR) expression levels in gastric cancer patients (= 110)(A) Recurrence-free survival and overall survival (OS) in patients with weak vs. strong expression of LSR. (B) Subgroup OS analysis of patients according Fluocinonide(Vanos) to tumor differentiation Fluocinonide(Vanos) (well- vs. poorly differentiated). (C) Subgroup OS analysis of patients according to T stage (pT1-2 vs. pT3-4). Survival rates were compared using the log-rank test. Univariate analysis revealed that pT3C4, pN1C3, and strong expression of LSR were significant predictors of OS (= 0.026, 0.048, and 0.010, respectively). Multivariate analysis revealed that pT3-4 and strong expression of LSR were independent and significant prognostic factors for GC patients in terms of OS (= 0.009 and 0.007, respectively) (Table ?(Table22). Table 2 Univariate and multivariate Cox model analysis for overall survival disulfide bridges [15]. Western blotting showed that MKN74 and NUGC-3 expressed slightly stronger LSR than MKN45 at these molecular weights (Figure ?(Figure3B3B). Open in a separate window Figure 3 (A, B) Lipolysis-stimulated lipoprotein receptor (LSR) expression in the gastric cancer (GC) cell lines MKN74, NUGC-3, and MKN45 as determined by fluorescence-activated cell sorting and western blotting. (C) Cell proliferation was determined by WST-8 assays at 48 h after very low density lipoprotein (VLDL) administration at 1, 5 and 10 g/mL. (D) Cell proliferation was determined by WST-8 assays at 2, 24, 48, and 72 h after replacing cell media (RPMI1640 + FBS, RPMI1640 + VLDL [5 g/mL], RPMI1640, RPMI1640 [non-Glu] + VLDL [5 g/mL], and RPMI1640 [non-Glu]). (E) Proliferation at 48 h after VLDL (MKN74 Fluocinonide(Vanos) 5 g/mL, NUGC-3 10 g/mL) or control IgG2a mAb or anti-hLSR mAb (#1C25) administration. (F) Evaluation of the anti-proliferative mechanisms 24 h after VLDL (MKN74 5 g/mL, NUGC-3 10 g/mL) or control IgG2a mAb or anti-hLSR mAb (#1-25) administration by western.