Background: Gastric cancer is the second most common causes of cancer related death in the world and is responsible for two third of cancer related death in the developing countries. survival rate surgery is low and radiation therapy and chemotherapy as alternatives ways for treatment of gastric cancer are not very promising. Thus there is an urgent need for introducing novel treatment procedures and promising new anti-canceric drugs.
Aim: In this study we used pre-prepared liposomes and after necessary manipulations ,these modified liposomes were used for delivery of apoptosis activator 2 to gastric adenocarcinoma cell line (AGS).
Materials And Methods: we used pre-prepared liposomes and after necessary manipulations, these modified liposomes were used for delivery of apoptosis activator 2 to AGS cells and induced apoptosis was evaluated by related apoptotic DNA ladder, TUNNEL and Cell Death experiments.
Results: Evaluation of apoptosis by Apoptotic DNA Ladder in liposome treated and untreated AGS cells by DNA laddering and fragmentation, TUNEL and Cell Death Detection confirmed that treatment of AGS cell lines with apoptosis activator 2 loaded liposomes which targeted cell surface TROP2 antigen in cancer cells significantly increased apoptosis in these cells.
Conclusion: Nano drug delivery of apoptosis activator 2 to human gastric adenocarcinoma cell line with liposomes targeted TROP2 antigen is a possible way for smart killing of human gastric adenocarcinoma cells.
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http://dx.doi.org/10.4103/1947-2714.103319 | DOI Listing |
Curr Cancer Drug Targets
January 2025
Department of Pharmaceutical Chemistry, JSS College of Pharmacy, JSS Academy of Higher Education & Research, Ooty, Nilgiris, Tamil Nadu, India.
Cancer manifests as uncontrolled cell proliferation. Tankyrase, a poly(ADP-ribose) polymerase member, is vital in Wnt signal transmission, making it a promising cancer therapy target. The Wnt/β-catenin pathway regulates critical biological processes like genomic stability, gene expression, energy utilization, and apoptosis.
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January 2025
Department of Endocrinology, Tianjin 4th Center Hospital, Tianjin, 300140, China.
To investigate the role of silent information regulator 6 (SIRT6) in regulating podocyte injury in diabetic nephropathy (DN) through autophagy mediated by Notch signaling pathway. A blank control group (group A), a diabetic nephropathy group (group B), and a Sirt6 intervention group (group C) were established. The group A cells were human normal glomerular podocyte cell lines (HGPCs) without any treatment.
View Article and Find Full Text PDFACS Nano
January 2025
Zhejiang Key Laboratory of Intelligent Cancer Biomarker Discovery and Translation, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325035, Zhejiang, P. R. China.
The concept of immunogenic cell death (ICD) induced by chemotherapy as a potential synergistic modality for cancer immunotherapy has been widely discussed. Unfortunately, most chemotherapeutic agents failed to dictate effective ICD responses due to their defects in inducing potent ICD signaling. Here, we report a dual-enzyme-instructed peptide self-assembly platform of (CPT-GFFpY-PLGVRK-Caps) that cooperatively utilizes camptothecin (CPT) and capsaicin (Caps) to promote ICD and engage systemic adaptive immunity for tumor rejection.
View Article and Find Full Text PDFResveratrol (RES), a natural polyphenolic compound, has garnered significant attention for its therapeutic potential in various pathological conditions. This review explores how RES modulates mitophagy-the selective autophagic degradation of mitochondria essential for maintaining cellular homeostasis. RES promotes the initiation and execution of mitophagy by enhancing PINK1/Parkin-mediated mitochondrial clearance, reducing reactive oxygen species production, and mitigating apoptosis, thereby preserving mitochondrial integrity.
View Article and Find Full Text PDFImmunol Rev
January 2025
Department of Internal Medicine and Paediatrics, Ghent University, Ghent, Belgium.
Inflammasomes are crucial mediators of both antimicrobial host defense and inflammatory pathology, requiring stringent regulation at multiple levels. This review explores the pivotal role of mitogen-activated protein kinase (MAPK) signaling in modulating inflammasome activation through various regulatory mechanisms. We detail recent advances in understanding MAPK-mediated regulation of NLRP3 inflammasome priming, licensing and activation, with emphasis on MAPK-induced activator protein-1 (AP-1) signaling in NLRP3 priming, ERK1 and JNK in NLRP3 licensing, and TAK1 in connecting death receptor signaling to NLRP3 inflammasome activation.
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