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In the field of modern biotechnology, the CRISPR/Cas system has become one of the important tools for gene editing. Especially for RNA editing, the CRISPR/Cas13 system shows great potential. Among the Cas13 family, Cas13d is considered to be the most active isoform in mammalian cells. However, Cas13d is insufficiently active in the cytosol of mammalian cells, which limits its efficiency in applications such as programmed antiviral therapy. Since most RNA viruses only replicate in the cytoplasm, the effectiveness of existing Cas13d-based antiviral methods is limited by uncontrolled leakage of nucleic acids.
A research team from Tsinghua University School of Medicine in China published a research paper titled "Nuclear RNA homeostasis promotes systems-level coordination of cell fate and senescence" in the journal Cell Stem Cell. This study demonstrates that nuclear RNA homeostasis contributes to the systemic coordination of cell fate and aging. Depletion of RNA exosomes leads to destruction of nuclear RNA, which leads to systemic functional decline, changes in cellular status, and promotes aging.
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.
Targeted therapies mediated by antibodies and chimeric antigen receptor (CAR) T cells improve survival in patients with solid tumors and hematological malignancies. Recently, in a research report titled "TRBC1-targeting antibody–drug conjugates for the treatment of T cell cancers" published in the international journal Nature, scientists from Johns Hopkins University School of Medicine and other institutions have developed a new treatment for human leukemia and lymphoma that is expected to effectively kill cancer cells in mice carrying human T-cell tumors.
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.
DNA double-strand breaks (DSBs) lead to genomic instability and are a key feature of cancer development. DSBs are mainly repaired through homologous recombination (HR) and non-homologous end joining (NHEJ).
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.
Understanding the cellular processes that underlie the development of early-stage lung adenocarcinoma (LUAD) is necessary to design interventions. Recently, in a research report titled "An atlas of epithelial cell states and plasticity in lung adenocarcinoma" published in the international magazine Nature, scientists from the University of Texas MD Anderson Cancer Center and other institutions have constructed a new map of lung cells through research. The study reveals new cellular pathways and precursors in the development of lung adenocarcinoma, and related findings may help develop new strategies to detect or block the progression of the disease at an early stage.