Presenilins are the enzymatic components of γ-secretase complex that cleaves amyloid precursor protein, Notch and β-catenin, which has critical roles in the development of Alzheimer's disease and cancer cell growth. Therefore, in the present study, we studied the effects and mechanisms of PS2 knockout on lung cancer development and possible mechanisms as a key regulator of lung tumor development. We compared carcinogen-induced tumor growth between PS2 knockout mice and wild-type mice. PS2 knockout mice showed increased urethane (1 mg/g)-induced lung tumor incidence when compared with that of wild-type mice with decreased activity of γ-secretase in the lung tumor tissues. Consequently, iPLA2 activities in lung tumor tissues of PS2 knockout mice were much higher than in tumor tissues of wild-type mice. Furthermore, knockdown of PS2 using PS2 siRNA decreased γ-secretase activity with increased iPLA2 activity in the lung cancer cells (A549 and NCI-H460), leading to increased lung cancer cell growth. PS2 knockout mice and PS2 knockdown lung cancer cells showed increased DNA-binding activities of nuclear factor kappa-beta, signal transducer and activator of transcription 3 (STAT3) and AP-1 which are critical transcriptional factors of iPLA2 than those of PS2 wild-type mice and control lung cancer cells. Taken together, these results suggest that the loss of PS2 could have a critical role in lung tumor development through the upregulation of iPLA2 activity by reducing γ-secretase.

Background In this study, we describe our clinical experience with the fifth-generation of a breast implant with a smooth, fine surface from a Korean manufacturer (BellaGelÒ SmoothFine; HansBiomed Co. Ltd., Seoul, Korea) in Asian women. Methods We analyzed 223 women (mean age=35.28±9.45 years and mean follow-up period=12.03±2.48 months), comprising 118 bilateral cases and 109 unilateral ones, who received breast augmentation using the BellaGelÒ SmoothFine at our hospital between June 4, 2018 and February 28, 2019. For safety assessment, we analyzed frequencies of postoperative complications and overall survival of the BellaGelÒ SmoothFine. Results Postoperatively, complications (12 cases, 5.38%) include asymmetry (3 cases, 1.35%), hematoma (2 cases, 0.90%), hypertrophic scars (2 cases, 0.90%), wound disruption (2 cases, 0.90%), rippling (1 case, 0.45%), capsular contracture (1 case, 0.45%), stretch deformities with skin excess (1 case, 0.45%). In addition, time-to-events were calculated as 10.94±0.64 months (95% CI 9.69-12.19). Conclusions Here, we describe our clinical experience with the BellaGelÒ SmoothFine. Our results are of significance in that this is the first report about the fifth-generation of a breast implant with a smooth, fine surface from a Korean manufacturer in Asian women.

The current study measured alterations in the inducible nitric oxide synthase (iNOS)‑mediated cyclooxygenase‑2 (COX‑2) induction pathway, inflammasome pathway, NF-kB activation, and inflammatory cytokine expressions in the transverse colon of C3 knockout (KO) mice, to determine whether complement component 3 (C3) deficiency affects its receptor downstream-mediated inflammatory response. Compared to wild type (WT) mice, the expression level of C3 protein was successfully suppressed in the transverse colon of C3 KO mice. Significant enhancement was observed in expression levels of important members of the iNOS‑mediated COX‑2 induction pathway, and in the phosphorylation of mitogen‑activated protein (MAP) kinase members. Also, a similar pattern of increase was observed in the expression levels of inflammasome proteins in C3 KO mice. Moreover, compared to WT mice, C3 KO mice showed remarkably enhanced phosphorylation of NF-kB and IkB-a, which was reflected in entirety as increased expressions of TNF-a, IL-6 and IL-1a. Taken together, results of the current study indicate that C3 deficiency induces activation of the iNOS‑mediated COX‑2 induction pathway, ASC-inflammasome pathway, and NF-kB signaling pathway, resulting in the enhancement of inflammatory cytokine expressions in the transverse colon of C3 KO mice.