Cell Biochemistry and Function最新文献

The biosynthesis of silver nanoparticles (AgNPs) using cyanobacteria has gained significant attention due to its cost-effective and eco-friendly advantages in green synthesis. Additionally, biogenic AgNPs show great potential for biological applications, particularly in combating infections caused by drug-resistant bacteria and fungi. This study synthesized using the cyanobacterium Oscillatoria salina (Os-AgNPs). The Os-AgNPs were characterized by a UV-vis spectral absorption peak at 447 nm, and their functional groups were identified through X-ray diffraction analysis, revealing a crystal structure with a 2θ value of 38°. Transmission electron microscopy (TEM) analysis showed an average nanoparticle size of 9.81 nm. The Os-AgNPs demonstrated remarkable antioxidant, antibacterial, and antifungal properties. Their antibacterial activity was tested against multidrug-resistant (MDR) Gram-positive bacteria, including Staphylococcus aureus, Streptococcus pyogenes, and Enterococcus faecalis, as well as Gram-negative bacteria such as Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa, all isolated from clinical samples. The inhibition zones for bacterial strains ranged from 15 to 20 mm, as measured by the agar-well diffusion method. Similarly, the Os-AgNPs exhibited antifungal activity, with 20–30 mm inhibition zones against pathogenic fungi Trichophyton rubrum and Candida tropicalis. Additionally, the antiproliferative effects of the Os-AgNPs were evaluated on human cancer cell lines, including HeLa (cervical adenocarcinoma) and MD-AMB-231 (breast adenocarcinoma). In vivo toxicity studies were conducted using Swiss mouse models to assess the cytotoxic effects. Overall, the results suggest that Os-AgNPs, biosynthesized using O. salina, hold promise as potential antimicrobial and anticancer agents for pharmaceutical applications.

With the rapid development of gene editing technology, its application in breast cancer has gradually become the focus of research. This article reviews the application of gene editing technology in the treatment of breast cancer, and discusses its challenges and future development directions. The key application areas of gene editing technology in the treatment of breast cancer will be outlined, including the discovery of new therapeutic targets and the development of drugs related to the pathway. Gene editing technology has played an important role in the discovery of new therapeutic targets. Through the use of gene editing technology, breast cancer-related genes are systematically edited to regulate key regulatory factors on related pathways or key tumor suppressor genes such as FOXC1 and BRCA, and the results are analyzed in cell or animal experiments, and the target is obtained from the experimental results, which provides important clues for the development of new drugs. This approach provides an innovative way to find more effective treatment strategies and inhibit tumor growth. In addition, gene editing technology has also promoted the personalization of breast cancer treatment. By analyzing a patient's genomic information, researchers can pinpoint key genetic mutations in a patient's tumor and design personalized treatments. This personalized treatment approach is expected to improve the therapeutic effect and reduce adverse reactions. Finally, the application of gene editing technology also provides support for the development of breast cancer immunotherapy. By editing immune cells to make them more potent against tumors, researchers are trying to develop more effective immunotherapies to bring new treatment options to breast cancer patients.

The study of the mechanism of oligoasthenospermia, which is a major cause of male infertility, has been the focus of research in the field of male reproduction. TAp73, a member of the p53 family of oncogenes, is endowed with tumor-suppressing activity due to its structural and functional homology with p53. It has been found that TAp73, plays a key role in spermatogenesis and maintaining male reproduction. When TAp73 is low-expressed or absent, the process of spermatogenesis is severely impaired, and mice deficient in TAp73 exhibit spermatogonial DNA damage, disturbed apical cytoplasmic specialization, and spermatocyte malformations resulting in reduced male fertility. Nevertheless, when TAp73 is overexpressed, it not only drives exogenous death receptors to regulate germ cell apoptosis, but also interacts with its various substrate proteins to promote the translocation of cytoplasmic Bax proteins to the mitochondria, resulting in the upregulation of the Bax/Bcl-2 ratio on the mitochondrial membrane and triggering a series of mitochondrial apoptotic effects. In this article, we will analyze the mechanism of TAp73 and sperm apoptosis, and elaborate the mechanism of TAp73 upregulation, exogenous apoptosis pathway and mitochondrial apoptosis pathway to systematically explain that the process of apoptosis induced by high expression of TAp73 is not fixed and single, but is interconnected, so as to provide a basis for the treatment of oligoasthenospermia and the research and development of new drugs using TAp73 as a target.

Body wall of sea cucumber Bohadschia bivittate contains a protein consisting of highly insoluble collagen fibers. We aimed to evaluate the biocompatibility and cytotoxicity of nonirradiated or γ-irradiated pepsin soluble collagen (PSC) extracted from Bohadschia bivittata on human periodontal ligament fibroblasts cells. The MTT assay showed significant increase in the cell viability values indicating that PSC is noncytotoxic. Further, nonirradiated PSC showed higher cell viabilities values than γ-irradiated PSC at all concentration, especially at an optimal dilution of 25% (p < 0.05). This exploratory study suggests that PSC from Bohadschia bivittata could be utilized as a novel biomaterial in periodontal regenerative therapies.

N⁶-methylenadenosine (m⁶A) modification, the most abundant epitranscriptomic modification in eukaryotic mRNAs, has been shown to play crucial roles in regulating various aspects of mRNA metabolism and functions. In this study, we applied the Cre-Loxp conditional knockout system to investigate the role of the core components of the m⁶A methyltransferase complex, METTL14 and METTL3, in retinal development. Our results showed that the double absence of Mettl14 and Mettl3 caused structural disturbance in the retina and prolonged the proliferation activity of retinal progenitor cells. Interestingly, the deletion of Mettl14 and Mettl3 did not affect the generation of various retinal cells, but severely disrupted their distribution. In addition, double deletion of Mettl14 together with Mettl3 caused a stronger phenotype than did single deletion of Mettl14. In conclusion, our study demonstrated that Mettl14 and Mettl3 work cooperatively to regulate retinal development.

Spinal cord injury (SCI) is a common neurological trauma that cannot be completely cured with surgical techniques and medications. In this study, we established a mouse SCI model and used an adeno-associated virus (AAV) to achieve the high expression of sonic hedgehog (Shh) at the injury site to further investigate the therapeutic effect and mechanism of Shh on SCI. The results of the present study show that Shh may promote motor function recovery. The present findings demonstrate the protective effect of Shh overexpression in SCI by regulating the proliferation and apoptosis of nerve cells at the site of SCI. Shh promotes the proliferation of early microglia, inhibits the proliferation of early astrocytes, and promotes the formation of neurons at the site of injury. In addition, Shh may inhibit apoptosis at the SCI site. The mechanism by which Shh regulates nerve cells at the site of SCI may involve glioma-associated oncogene 1 (Gli1). The present research indicates that Gli1 regulates the transforming growth factor-β (TGF-β) signaling pathway, inhibiting the classic TGF-β1/Smad signaling pathway and activating the TGF-β1/extracellular regulated protein kinase (ERK) signaling pathway. Collectively, these findings suggest that Shh is a regulatory molecule involved in nerve cell proliferation and apoptosis. High Shh expression can accelerate motor function recovery after SCI, indicating that it may be a promising therapeutic approach for SCI.