Journal of Zhejiang University SCIENCE B最新文献

Numerous studies have demonstrated that the high expression of CXC motif chemokine ligand 16 (CXCL16) in cancer correlates with poor prognosis, as well as tumor cell proliferation, migration, and invasion. While CXCL16 can serve as a tumor biomarker, the underlying mechanism in modulating head and neck squamous cell carcinoma (HNSCC) remains unclear. In this study, the aimed was to investigate the CXCL16 expression in HNSCC and to uncover the potential underlying mechanism. Hereby, we determined the high expression of CXCL16 in The Cancer Genome Atlas (TCGA) database, as well as in tissue samples from patients with HNSCC at our central hospital and from HNSCC cell lines. The results showed that CXCL16 knockdown inhibited the proliferation, migration, and invasion of HNSCC cells. Mechanistically, transcriptome sequencing revealed that CXCL16 may affect HNSCC cell growth by regulating the antioxidant pathway of glutathione peroxidase 1 (GPX1). The reactive oxygen species (ROS) levels were elevated in small interfering CXCL16 (si-CXCL16) cells, which may contribute to the inhibition of cell proliferation, migration, and invasion. Moreover, treatment of cells with the GPX1 inhibitor eldecalcitol (ED-71) revealed that HNSCC cell growth was significantly inhibited in the synergistic group of si-CXCL16 and GPX1 inhibitor compared to the si-CXCL16 group. In conclusion, CXCL16 contributed to the development of HNSCC cells by modulating the GPX1-mediated antioxidant pathway. Thus, targeting cellular CXCL16 expression seems to be a promising strategy for treating HNSCC.

Oligodendrocytes are the myelinating cells of the central nervous system. Brain injury and neurodegenerative disease often lead to oligodendrocyte death and subsequent demyelination-related pathological changes, resulting in neurological defects and cognitive impairment (Spaas et al., 2021; Zhang J et al., 2022). Multiple sclerosis (MS) is a major demyelinating disease of the central nervous system. The pathology of MS is characterized by the loss of myelin, oligodendrocytes, and axons in the brain, brain stem, and spinal cord, as well as by white matter lesions (Lassmann et al., 2007). Unfortunately, no definitive cure for MS has been developed. Immunomodulatory and anti-inflammatory drugs are effective in the relapsing-remitting phase of MS because they reduce the frequency of relapses and the formation of inflammatory lesions; however, they do not alter the course of progressive MS and are insufficient to cure chronic neurological dysfunction (Xiao et al., 2015; Zhang et al., 2021). The treatment outcome is even worse for MS patients with primary and secondary progressions. Mesenchymal stem cells (MSCs) are stromal cells that can self-renew and exhibit multilineage differentiation. MSCs are easy to expand in vitro and exhibit low immunogenicity, no tumorigenic risks, and ethical controversies, making them a promising candidate for regenerative medicine (Zhang L et al., 2022; Xu et al., 2023). Many studies have confirmed the neural differentiation potential of MSCs under certain conditions, making them a prime candidate for treating neurodegenerative diseases (Jang et al., 2010; Yan et al., 2013). The present study investigated the effects of cranial bone-marrow mesenchymal stem cells (cBMMSCs) and oligodendrocyte-specific protein 2-positive (Olig2⁺) single-colony-derived cBMMSC (sc-cBMMSC), isolated in our previous work (Yang et al., 2022), in a central nervous system demyelination mouse model.

Neurodegenerative diseases (NDDs), mainly including Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), and Alzheimer's disease (AD), are sporadic and rare genetic disorders of the central nervous system. A key feature of these conditions is the slow accumulation of misfolded protein deposits in brain neurons, the excessive aggregation of which leads to neurotoxicity and further disorders of the nervous system.

Oligodendrocytes are the myelinating cells of the central nervous system. Brain injury and neurodegenerative disease often lead to oligodendrocyte death and subsequent demyelination-related pathological changes, resulting in neurological defects and cognitive impairment (Spaas et al., 2021; Zhang J et al., 2022). Multiple sclerosis (MS) is a major demyelinating disease of the central nervous system. The pathology of MS is characterized by the loss of myelin, oligodendrocytes, and axons in the brain, brain stem, and spinal cord, as well as by white matter lesions (Lassmann et al., 2007). Unfortunately, no definitive cure for MS has been developed. Immunomodulatory and anti-inflammatory drugs are effective in the relapsing-remitting phase of MS because they reduce the frequency of relapses and the formation of inflammatory lesions; however, they do not alter the course of progressive MS and are insufficient to cure chronic neurological dysfunction (Xiao et al., 2015; Zhang et al., 2021). The treatment outcome is even worse for MS patients with primary and secondary progressions. Mesenchymal stem cells (MSCs) are stromal cells that can self-renew and exhibit multilineage differentiation. MSCs are easy to expand in vitro and exhibit low immunogenicity, no tumorigenic risks, and ethical controversies, making them a promising candidate for regenerative medicine (Zhang L et al., 2022; Xu et al., 2023). Many studies have confirmed the neural differentiation potential of MSCs under certain conditions, making them a prime candidate for treating neurodegenerative diseases (Jang et al., 2010; Yan et al., 2013). The present study investigated the effects of cranial bone-marrow mesenchymal stem cells (cBMMSCs) and oligodendrocyte-specific protein 2-positive (Olig2+) single-colony-derived cBMMSC (sc-cBMMSC), isolated in our previous work (Yang et al., 2022), in a central nervous system demyelination mouse model.

Neurodegenerative diseases (NDDs), mainly including Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), and Alzheimer's disease (AD), are sporadic and rare genetic disorders of the central nervous system. A key feature of these conditions is the slow accumulation of misfolded protein deposits in brain neurons, the excessive aggregation of which leads to neurotoxicity and further disorders of the nervous system.

Type 1 diabetes (T1D) is a T lymphocyte-mediated autoimmune disease caused by pancreatic β‍-cell destruction, which eventually leads to reduced insulin level and increased blood glucose level (Syed, 2022). As a multifactorial disease, T1D is characterized by a genetic predisposition associated with various environmental and cellular elements (Syed, 2022). Pancreatic β cells have long been considered the "innocent victims" in T1D pathogenesis since the pancreas is attacked by the immune cells, resulting in a process known as insulitis, in which the immune cells infiltrate pancreatic islets and secrete pro-inflammatory cytokines. However, growing evidence suggests that various β‍-cell stresses, dysfunction, and death contribute to T1D pathogenesis, as it has been observed that β‍-cell dysfunction in autoantibody-positive (Aab⁺) individuals exists long before T1D diagnosis (Evans-Molina et al., 2018).

Aging and age-related ailments have emerged as critical challenges and great burdens within the global contemporary society. Addressing these concerns is an imperative task, with the aims of postponing the aging process and finding effective treatments for age-related degenerative diseases. Recent investigations have highlighted the significant roles of nicotinamide adenine dinucleotide (NAD⁺) in the realm of anti-aging. It has been empirically evidenced that supplementation with nicotinamide mononucleotide (NMN) can elevate NAD⁺ levels in the body, thereby ameliorating certain age-related degenerative diseases. The principal anti-aging mechanisms of NMN essentially lie in its impact on cellular energy metabolism, inhibition of cell apoptosis, modulation of immune function, and preservation of genomic stability, which collectively contribute to the deferral of the aging process. This paper critically reviews and evaluates existing research on the anti-aging mechanisms of NMN, elucidates the inherent limitations of current research, and proposes novel avenues for anti-aging investigations.

Breast cancer is the most common cancer in women and one of the deadliest cancers worldwide. According to the distribution of tumor tissue, breast cancer can be divided into invasive and non-invasive forms. The cancer cells in invasive breast cancer pass through the breast and through the immune system or systemic circulation to different parts of the body, forming metastatic breast cancer. Drug resistance and distant metastasis are the main causes of death from breast cancer. Research on breast cancer has attracted extensive attention from researchers. In vitro construction of tumor models by tissue engineering methods is a common tool for studying cancer mechanisms and anticancer drug screening. The tumor microenvironment consists of cancer cells and various types of stromal cells, including fibroblasts, endothelial cells, mesenchymal cells, and immune cells embedded in the extracellular matrix. The extracellular matrix contains fibrin proteins (such as types I, II, III, IV, VI, and X collagen and elastin) and glycoproteins (such as proteoglycan, laminin, and fibronectin), which are involved in cell signaling and binding of growth factors. The current traditional two-dimensional (2D) tumor models are limited by the growth environment and often cannot accurately reproduce the heterogeneity and complexity of tumor tissues in vivo. Therefore, in recent years, research on three-dimensional (3D) tumor models has gradually increased, especially 3D bioprinting models with high precision and repeatability. Compared with a 2D model, the 3D environment can better simulate the complex extracellular matrix components and structures in the tumor microenvironment. Three-dimensional models are often used as a bridge between 2D cellular level experiments and animal experiments. Acellular matrix, gelatin, sodium alginate, and other natural materials are widely used in the construction of tumor models because of their excellent biocompatibility and non-immune rejection. Here, we review various natural scaffold materials and construction methods involved in 3D tissue-engineered tumor models, as a reference for research in the field of breast cancer.

The original version of this article (Zhao et al., 2021) unfortunately contained two mistakes.

The online version of the original article can be found at https://doi.org/10.1631/jzus.B2300401.