Since cancer cells inhibit T-cell activity, the authors investigated a method to reverse T-cell disfunction with gene therapy, so that the T-cells would become effective once again in fighting cancer cells. They used the inhibition of proprotein convertases (PCSK1) in T cells and programmed death-ligand 1 (CD274) in cancer cells. They observed the recovery of IL-2 expression in Jurkat cells, with increased recovery noted in a co-culture sample. This study suggests a novel strategy to reactivate T cells.
Wound-healing involves a sequence of events, such as inflammation, proliferation, and migration of different cell types like fibroblasts. Zinc Finger CCCH-type with G-Patch Domain Containing Protein (ZGPAT), encodes a protein that has its main role as a transcription repressor by binding to a specific DNA sequence. The aim of the study was to find out whether inhibiting ZGPAT will expedite the wound healing process by accelerating cell migration. This treatment strategy can provide a key to the development of wound healing strategies in medicine and cellular biology.
Treatments inhibiting Notch signaling pathways have been explored by researchers as a new approach for the treatment of glioblastoma tumors, which is a fast-growing and aggressive brain tumor. Recently, retinoic acid (RA) therapy, which inhibits Notch signaling, has shown a promising effect on inhibiting glioblastoma progression. RA, which is a metabolite of vitamin A, is very important in embryonic cellular development, which includes the regulation of multiple developmental processes, such as brain neurogenesis. However, high doses of RA treatment caused many side effects such as headaches, nausea, redness around the injection site, or allergic reactions. Therefore, we hypothesized that a combination treatment of RA and siRNA targeting NOTCH1 (siNOTCH1), the essential gene that activates Notch signaling, would effectively inhibit brain cancer cell proliferation. The aim of the study was to determine whether inhibiting NOTCH1 would inhibit the growth of brain cancer cells by cell viability assay. We found that the combination treatment of siNOTCH1 and RA in low concentration effectively decreased the NOTCH1 expression level compared to the individual treatments. However, the combination treatment condition significantly decreased the number of live brain cancer cells only at a low concentration of RA. We anticipate that this novel combination treatment can provide a solution to the side effects of chemotherapy.
Cellular senescence plays a key role in aging cells and is attributed to a number of disease and pathology. These authors find that genetic editing of both RPS6KB1 and PPARGC1A revitalizes a human skin fibroblast cell line.
In this study, the authors investigated the time-dependent cytokine secretion ability of phyto-hemagglutinin (PHA)-activated T cells derived from human peripheral (PB) and cord blood (CB). They hypothesized that the anti-inflammatory cytokine, IL-10, and pro-inflammatory cytokine, TNFα, levels would be higher in PHA-activated T cells obtained from PB as compared to the levels obtained from CB and would decrease over time. Upon PHA-activation, the IL-10 levels were relatively high while the TNFα levels decreased, making these findings applicable in therapeutic treatments e.g., rheumatoid arthritis, psoriasis, and organ transplantation.
A central challenge of cancer therapy is identifying treatments that will effectively target cancer cells while minimizing effects on healthy cells. To identify potential targets for treating a multiple myeloma, a frequently incurable cancer, Kochenderfer and Kochenderfer analyze RNA sequencing data from the Cancer Cell Line Encyclopedia to find genes with high expression in multiple myeloma cells and low expression in normal tissues
Cancer is often caused by improper function of a few proteins, and sometimes it takes only a few proteins to malfunction to cause drastic changes in cells. Here the authors look at the genes that were mutated in patients with a type of pancreatic cancer to identify proteins that are important in causing cancer. They also determined which proteins currently lack effective treatment, and suggest that certain proteins (named KRAS, CDKN2A, and RBBP8) are the most important candidates for developing drugs to treat pancreatic cancer.
In this study, Imani et al. investigate whether a new proprietary herbal formulation, HF1, can inhibit expression of immune suppressor protein PD-L1. PD-L1 is a transmembrane protein that can be expressed by cancer cells to assist in their ability to avoid attacks from the immune system. Work from this study demonstrates that HF1 treatment can reduce expression of PD-L1 in cultured cancer cells, implicating HF1 as a potential new cancer therapy.
Here, the authors chose to investigate the efficacy of zinc oxide nanoparticles (ZnO NPs) and cisplatin or zinc ions in inducing cancer apoptosis. While both treatments were found to reduce the proliferation of lung cancer cells, the authors suggest that further studies to identify the mechanism are necessary.
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