World J Gastroenterol
Research Center of Reproductive Medicine, Shantou University Medical College (SUMC), shantou 515041, Guangdong Province, China.
Published: October 2004
Aim: To construct a pEgr-IFNgamma plasmid and to investigate its expression properties of interferon-gamma (INF-gamma) induced by irradiation and the effect of gene-radiotherapy on the growth of melanoma.
Methods: A recombined plasmid, pEgr-IFNgamma, was constructed and transfected into B16 cell line with lipofectamine. The expression properties of pEgr-IFNgamma were investigated by ELISA. Then, a B16 melanoma-bearing model was established in mice, and the plasmid was injected into the tumor tissue. The tumor received 20 Gy X-ray irradiation 36 h after injection, and IFN-gamma expression was detected from the tumor tissue. A tumor growth curve at different time points was determined.
Results: The eukaryotic expression vector, pEgr-IFNgamma, was successfully constructed and transfected into B16 cells. IFN-gamma expression was significantly increased in transfected cells after X-ray irradiation in comparison with 0 Gy group (77.73-94.60 pg/mL, P<0.05-0.001), and was significantly higher at 4 h and 6 h than that of control group after 2 Gy X-ray irradiation (78.90-90.00 pg/mL, P<0.01-0.001). When the transfected cells were given 2 Gy irradiation 5 times at an interval of 24 h, IFN-gamma expression decreased in a time-dependent manner. From d 3 to d 15 after IFNgamma gene-radiotherapy, the tumor growth was significantly slower than that after irradiation or gene therapy alone.
Conclusion: The anti-tumor effect of pEgr-IFNgamma gene-radiotherapy is better than that of genetherapy or radiotherapy alone for melanoma. These results may establish an important experimental basis for gene-radiotherapy of cancer.
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http://dx.doi.org/10.3748/wjg.v10.i20.3011 | DOI Listing |
ACS Nano
January 2025
Laboratory of Molecular Immunology, Institute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Kunming 650031, China.
Immunogenic cell death (ICD) of tumor cells, which is characterized by releasing immunostimulatory "find me" and "eat me" signals, expressing proinflammatory cytokines and providing personalized and broad-spectrum tumor antigens draws increasing attention in developing a tumor vaccine. In this study, we aimed to investigate whether the influenza virus (IAV) is efficient enough to induce ICD in tumor cells and an extra modification of IAV components such as hemeagglutinin (HA) will be helpful for the ICD-induced cells to elicit robust antitumor effects; in addition, to evaluate whether the membrane-engineering polylactic coglycolic acid nanoparticles (PLGA NPs) simulating ICD immune stimulation mechanisms hold the potential to be a promising vaccine candidate, a mouse melanoma cell line (B16-F10 cell) was infected with IAV rescued by the reverse genetic system, and the prepared cells and membrane-modified PLGA NPs were used separately to immunize the melanoma-bearing mice. IAV-infected tumor cells exhibit dying status, releasing high mobility group box-1 (HMGB1) and adenosine triphosphate (ATP), and exposing calreticulin (CRT), IAV hemeagglutinin (HA), and tumor antigens like tyrosinase-related protein 2 (TRP2).
View Article and Find Full Text PDFACS Appl Mater Interfaces
November 2024
Biomedical Polymers Laboratory, College of Chemistry, Chemical Engineering and Materials Science, and State Key Laboratory of Radiation Medicine and Protection, Soochow University, Suzhou 215123, P.R. China.
The clinical efficacy of cancer vaccines is closely related to immunoadjuvants that play a crucial role in magnifying and prolonging the immune response. Muramyl dipeptide (MDP), a minimal and conserved peptidoglycan found in almost all bacteria, can trigger robust immune activation by uniquely antagonizing the nucleotide-binding oligomerization domain 2 (NOD2) pathway. However, its effectiveness has been hindered by limited solubility, poor membrane penetration, and rapid clearance from the body.
View Article and Find Full Text PDFAdv Sci (Weinh)
November 2024
College of Biomedical Engineering, Sichuan University, Chengdu, 610064, China.
The effectiveness of Toll-like 9 agonists (CpG) as an adjuvant for tumor immunotherapy is restricted due to their insufficient ability to activate anti-tumor immunity. To address that, the common nutrient metal ions are explored (Mn, Cu, Ca, Mg, Zn, Fe, and Al), identifying Mn as a key enhancer of CpG to mediate immune activation by augmenting the STING-NF-κB pathway. Mn and CpG are then self-assembled with epigallocatechin gallate (EGCG) into a nanoadjuvant MPN/CpG.
View Article and Find Full Text PDFInt J Biol Sci
September 2024
C.A.I.R. Institute, The Safdiè AIDS and Immunology Research Center, The Mina & Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel.
Various cancer treatment approaches that inhibit the activity of the programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) axis, a key player in tumor immune evasion, have been developed. We show that the immunomodulatory small tellurium complexes AS101 (ammonium trichloro(dioxoethylene-o,o')tellurate) and SAS (octa-O-bis(R,R)-tartarate ditellurane) suppress PD-L1 expression in a variety of human and mouse malignant cells via the modulation of α4β1 very late antigen- (VLA-4) integrin activity. Consequently, the expression of pAkt and its downstream effector pNFκB are inhibited.
View Article and Find Full Text PDFMol Pharm
August 2024
Department of Radiology, University of Colorado Denver, Aurora, Colorado 80045, United States.
The purpose of this study was to examine how the introduction of ibuprofen (IBU) affected tumor-targeting and biodistribution properties of Lu-labeled IBU-conjugated alpha-melanocyte-stimulating hormone peptides. The IBU was used as an albumin binder and conjugated to the DOTA-Lys moiety without or with a linker to yield DOTA-Lys(IBU)-GG-Nle-CycMSH {1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid-Lys(IBU)-Gly-Gly-Nle-c[Asp-His-DPhe-Arg-Trp-Lys]-CONH}, DOTA-Lys(Asp-IBU)-GGNle-CycMSH, DOTA-Lys(Asn-IBU)-GGNle-CycMSH, and DOTA-Lys(Dab-IBU)-GGNle-CycMSH peptides. Their melanocortin-receptor 1 (MC1R) binding affinities were determined on B16/F10 melanoma cells first.
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