Reprogramming of astrocytes and glioma cells into neurons for central nervous system repair and glioblastoma therapy.

Central nervous system (CNS) damage is usually irreversible owing to the limited regenerative capability of neurons. Following CNS injury, astrocytes are reactively activated and are the key cells involved in post-injury repair mechanisms. Consequently, research on the reprogramming of reactive astrocytes into neurons could provide new directions for the restoration of neural function after CNS injury and in the promotion of recovery in various neurodegenerative diseases.

Role of histone modifications in neurogenesis and neurodegenerative disease development.

Progressive neuronal dysfunction and death are key features of neurodegenerative diseases; therefore, promoting neurogenesis in neurodegenerative diseases is crucial. With advancements in proteomics and high-throughput sequencing technology, it has been demonstrated that histone post-transcriptional modifications (PTMs) are often altered during neurogenesis when the brain is affected by disease or external stimuli and that the degree of histone modification is closely associated with the development of neurodegenerative diseases. This review aimed to show the regulatory role of histone modifications in neurogenesis and neurodegenerative diseases by discussing the changing patterns and functional significance of histone modifications, including histone methylation, acetylation, ubiquitination, phosphorylation, and lactylation.

PTBP1 as a potential regulator of disease.

Polypyrimidine tract-binding protein 1 (PTBP1) is a member of the heterogeneous nuclear ribonucleoprotein (hnRNP) family, which plays a key role in alternative splicing of precursor mRNA and RNA metabolism. PTBP1 is universally expressed in various tissues and binds to multiple downstream transcripts to interfere with physiological and pathological processes such as the tumor growth, body metabolism, cardiovascular homeostasis, and central nervous system damage, showing great prospects in many fields. The function of PTBP1 involves the regulation and interaction of various upstream molecules, including circular RNAs (circRNAs), microRNAs (miRNAs) and long non-coding RNAs (lncRNAs).

Aptamer-Protein Interactions: From Regulation to Biomolecular Detection.

Serving as the basis of cell life, interactions between nucleic acids and proteins play essential roles in fundamental cellular processes. Aptamers are unique single-stranded oligonucleotides generated by in vitro evolution methods, possessing the ability to interact with proteins specifically. Altering the structure of aptamers will largely modulate their interactions with proteins and further affect related cellular behaviors.

Health systems efficiency in China and ASEAN, 2015-2020: a DEA-Tobit and SFA analysis application.

Objective: To evaluate the health systems efficiency in China and Association of Southeast Asian Nations (ASEAN) countries from 2015 to 2020.

Design: Health efficiency analysis using data envelopment analysis (DEA) and stochastic frontier approach analysis.

Setting: Health systems in China and ASEAN countries.

Nucleic Acid Probes for Single-Molecule Localization Imaging of Cellular Biomolecules.

Endogenous biomolecules in cells are the basis of all life activities. Directly visualizing the structural characteristics and dynamic behaviors of cellular biomolecules is significant for understanding the molecular mechanisms in various biological processes. Single-molecule localization microscopy (SMLM) can circumvent the optical diffraction limit, achieving analysis of the fine structures and biological processes in living cells with nanoscale resolution.

In Situ Visualization of Epidermal Growth Factor Receptor Nuclear Translocation with Circular Bivalent Aptamer.

Epidermal growth factor receptor (EGFR) nuclear translocation correlates with the abnormal proliferation, migration, and anti-apoptosis of tumor cells. Monitoring EGFR nuclear translocation provides insights into the molecular mechanisms underlying cancers. EGFR nuclear translocation includes two processes, EGFR phosphorylation and phosphorylated EGFR translocation to the nucleus.

High FHL2 mRNA expression and its prognostic value in lung cancer.

Background: Lung cancer is the most frequent cancer globally with a high number of cancer-related deaths. The 4-and-a-half LIM domain protein 2 (FHL2) is an oncogenic gene, which promotes the proliferation, invasion, and metastasis of cancer cells. In this study, we aimed to demonstrate that lung cancer patients with high FHL2 expression have worse overall survival (OS) and relapse-free survival (RFS).

CLDN6 inhibits breast cancer cell malignant behavior by suppressing ERK signaling.

Claudin 6 (CLDN6) is an important component of tight junctions. Through the PDZ binding motif, CLDN6 binds to a variety of signaling proteins that contain the PDZ domain to regulate different signaling pathways, and plays an important role in the occurrence and development of tumors. Our previous work showed that CLDN6 was expressed at low levels in breast cancer cells, and overexpression of CLDN6 inhibited breast cancer cell proliferation, migration and invasion.

CLDN6 Suppresses c-MYC-Mediated Aerobic Glycolysis to Inhibit Proliferation by TAZ in Breast Cancer.

Claudin 6 (CLDN6) was found to be a breast cancer suppressor gene, which is lowly expressed in breast cancer and inhibits breast cancer cell proliferation upon overexpression. However, the mechanism by which CLDN6 inhibits breast cancer proliferation is unclear. Here, we investigated this issue and elucidated the molecular mechanisms by which CLDN6 inhibits breast cancer proliferation.

The Expression of CLDN6 in Hepatocellular Carcinoma Tissue and the Effects of CLDN6 on Biological Phenotypes of Hepatocellular Carcinoma Cells.

CLDN6, a member of claudin (CLDN) family, was found to be a breast cancer suppressor gene in our early experiments. However, CLDN6 was highly expressed in human hepatocellular carcinoma (hHCC) (TCGA database), and the role of CLDN6 in hHCC is still unclear. To investigate the expression of CLDN6, immunohistochemical staining was performed in hHCC tissues.

Metabolic crosstalk in the tumor microenvironment regulates antitumor immunosuppression and immunotherapy resisitance.

The successful treatment of human cancers by immunotherapy has been made possible by breakthroughs in the discovery of immune checkpoint regulators, including CTLA-4 and PD-1/PD-L1. However, the immunosuppressive effect of the tumor microenvironment still represents an important bottleneck that limits the success of immunotherapeutic approaches. The tumor microenvironment influences the metabolic crosstalk between tumor cells and tumor-infiltrating immune cells, creating competition for the utilization of nutrients and promoting immunosuppression.