• Adenovirus Service • AAV Service • Lentivirus Service • Retrovirus Service
Recently, a research team from China published a research paper in the journal Science Advances titled: Cryo-shocked tumor cells deliver CRISPR-Cas9 for lung cancer regression by synthetic lethality. This study developed a cell delivery vector that efficiently delivers the CRISPR-Cas9 gene editing system to the lungs.
DNA methyltransferase inhibitors (DNMTi, DNA methyltransferase inhibitor) have limited efficacy in solid tumors. Colon cancer cells exposed to DNMTi accumulate lysine-27 trimethylation on histone H3 (H3K27me3). Recently, in a research report titled "Select EZH2 inhibitors enhance viral mimicry effects of DNMT inhibition through a mechanism involving NFAT:AP-1 signaling" published in the international magazine Science Advances, scientists from the Van Andel Institute and other institutions in the United States have discovered through research that two drugs that can cause malignant cells to behave like viruses may help treat colorectal cancer and other solid tumors in humans.
Recently, researchers at Johns Hopkins University in the United States discovered that lymphocyte activation gene-3 (Lag-3) in neurons is a specific receptor for tau PFF in the brain and can promote the spread of tau PFF between neurons. In addition, they observed that Lag-3 knockout in neurons significantly reduced the endocytosis of tau PFF and reduced its spread between neurons. Researchers also observed a similar phenomenon in conditional knockout mice of Lag-3 neurons. This result also means that Lag-3 may be used as a potential therapeutic target for AD and related tauopathies. Relevant research was published in Advanced Science.
Some anti-cancer therapies not only target tumor cells but also affect healthy cells in the body. If the effect on healthy cells is too strong, the use of this anti-cancer therapy may be limited.
Glioblastoma multiforme is a common malignant tumor of the central nervous system and one of the diseases that seriously threatens human health. Due to the rapid proliferation, migration, and invasion of glioma cells, as well as their ability to stimulate angiogenesis, gliomas grow in an aggressive and expansile manner and subsequently progress to higher grades. The current standard treatment for patients with glioma is surgical resection, followed by radiation therapy and adjuvant chemotherapy.
Every hug, every handshake, every deft movement requires tactile perception, so it is important to understand the molecular basis behind the occurrence of touch. Until now, researchers knew that an ion channel called Piezo2 was required for touch perception, but it became clear that the protein alone did not explain the body's entire touch perception.
Recently, researchers from Shanghai Jiao Tong University in China published a paper titled "Base editing effectively prevents early-onset severe cardiomyopathy in Mybpc3 mutant mice" in the journal Cell Research. This study developed an effective, PAM sequence-extended dual AAV vector-delivered adenine base editor-SpRY-ABE8e, which can effectively and precisely correct Mybpc3 gene mutations in mouse models, thereby preventing cardiac hypertrophy and dysfunction in mouse models. These trial results demonstrate the great potential of base editing as a new treatment modality for inherited cardiomyopathies and lay the foundation for future clinical applications.
The mitochondrial genome (mtDNA) encodes the basic mechanisms of oxidative phosphorylation and metabolic homeostasis. The mtDNA of tumor cells is one of the most mutation-prone regions in cancer genomes. However, there is still some controversy in the scientific community whether these mutations will affect the biological characteristics of tumors.
Modulating tumor PD-L1 expression is critical to improve researchers' understanding of tumor immune evasion and improve current anti-tumor immunotherapies. Recently, in a research report titled "CRISPR screening identifies the deubiquitylase ATXN3 as a PD-L1–positive regulator for tumor immune evasion" published in the international journal Journal of Clinical Investigation, scientists from Northwestern University and other institutions have identified a previously unknown tumor immune escape regulator through research, which may be expected to help improve the efficacy of current and future anti-tumor immunotherapies.
Recently, researchers from the University of Cambridge published a research paper titled "Arachidonic acid inhibition of the NLRP3 inflammasome is a mechanism to explain the anti-inflammatory effects of fasting" in Cell Reports. The study uncovers how fasting helps prevent inflammation. Fasting can increase the level of arachidonic acid in the blood, and arachidonic acid can reduce the activity of the NLRP3 inflammasome, thereby inhibiting inflammation. The findings also help explain some of the beneficial health effects of drugs like aspirin.
