Fluorescent carbon nanodot-based rapid cell nucleus staining and application for diagnosis.

Cell nucleus status decides the activities of corresponding cells, making its rapid and effective staining important for revealing the actual condition of biological environment in life science and related fields. In this study, fast staining of cell nucleus is realized by fluorescent carbon nanodots (CDs). The staining mechanism is due to the positively charged CD surface-induced cell membrane penetration, which facilitates the CD-nucleus binding via electrostatic attraction. The size of cell nucleus is easily measured with fluorescence imaging technique. In addition, the CD-based cell nucleus stain is applied for discriminating the normal and cancer cells by determining the cell-to-nucleus ratio with fluorescence images.

Arid2-IR downregulates miR-132-3p through methylation to promote LPS-induced ALI in pneumonia.

OBJECTIVE: Arid2-IR is a long non-coding RNA (lncRNA) that promotes renal injury, while its role in lipopolysaccharides (LPS)-induced acute lung injury (ALI) is unknown. Our preliminary sequencing analysis revealed an inverse correlation of Arid2-IR and miR-132-3p, which is known to suppress LPS-induced ALI. Therefore, Arid2-IR and miR-132-3p may interact with each other to participate in LPS-induced ALI in pneumonia. This study aimed to investigate the interaction between Arid2-IR and miR-132-3p in ALI induced by pneumonia. MATERIALS AND METHODS: Plasma samples were obtained from patients with pneumonia (n = 98) and healthy controls (n = 98) to detect the expression of circulating Arid2-IR and miR-132-3p. The correlation between them was analyzed using Pearson's correlation coefficient. The crosstalk between them in human bronchial epithelial cells (HBEpC) was analyzed through overexpression assay. MSP was applied to determine the methylation of the miR-132-3p gene. Cell viability was evaluated by 2,5-diphenyl-2H-tetrazolium bromide assay. RESULTS: Arid2-IR was highly upregulated in pneumonia group, while the expression levels of miR-132-3p decreased in pneumonia group compared to that in the controls. Arid2-IR and miR-132-3p were inversely correlated across patient samples. Overexpression of Arid2-IR decreased the expression levels of miR-132-3p in HBEpCs and increased the methylation of miR-132-3p gene. Arid2-IR suppressed the role of miR-132-3p in increasing the viability of HBEpCs induced by LPS. DISCUSSION AND CONCLUSION: Arid2-IR is upregulated in pneumonia and may downregulate miR-132-3p by increasing its methylation to decrease cell viability, thereby promoting LPS-induced ALI in pneumonia.

Extracellular Vesicles Promote the Formation of Pre-Metastasis Niche in Gastric Cancer.

Globally, gastric cancer (GC) ranks fourth in the incidence of malignant tumors. The early clinical manifestations of GC lack specificity. Most patients are already at an advanced stage when they are first diagnosed, and their late progression is mainly due to peritoneal metastasis. A pre-metastatic microenvironment is formed, before the macroscopic tumor metastasis. Extracellular vesicles (EVs) are nanovesicles released by cells into body fluids. Recent studies have shown that EVs can affect the tumor microenvironment by carrying cargos to participate in cell-to-cell communication. EVs derived from GC cells mediate the regulation of the pre-metastasis niche and act as a coordinator between tumor cells and normal stroma, immune cells, inflammatory cells, and tumor fibroblasts to promote tumor growth and metastasis. This review highlights the regulatory role of EVs in the pre-metastatic niche of GC and mulls EVs as a potential biomarker for liquid biopsy.

Honokiol induces ferroptosis in colon cancer cells by regulating GPX4 activity.

Colon cancer (CC) is a prevalent malignancy worldwide. Approaches to specifically induce tumor cell death have historically been a popular research topic. Honokiol (HNK), which exhibits highly efficient and specific anticancer effects, is a biphenolic compound found in Magnolia grandiflora. In the present study, we aim to study the effect of HNK on CC cells and elucidate the potential underlying mechanisms. Seven CC cell lines (RKO, HCT116, SW48, HT29, LS174T, HCT8, and SW480) were used. Cells were exposed to HNK and subjected to a series of assays to evaluate characteristics such as cellular activity, reactive oxygen species (ROS) levels and ferroptosis-related protein expression levels. Lentiviral transduction was also used to verify molecular mechanisms in vivo and in vitro. We here observed that HNK reduced the viability of CC cell lines by increasing ROS and Fe2+ levels. Transmission electron microscopy revealed HNK-induced changes in mitochondrial morphology. HNK decreased the activity of Glutathione Peroxidase 4 (GPX4) but did not affect system Xc-. Thus, our datas indicated that HNK can induce ferroptosis in CC cells by reducing the activity of GPX4. As a potential therapeutic drug, HNK showed good anticancer effects through diverse signal transduction mechanisms and multiple pathways.

Modeling paraquat-induced lung fibrosis in C. elegans reveals KRIT1 as a key regulator of collagen gene transcription.

Paraquat poisoning causes lung fibrosis, which often results in long-term pulmonary dysfunction. Lung fibrosis has been attributed to collagens accumulation, but the underlying regulatory pathway remains unclear. Here we use the genetically tractable C. elegans as a model to study collagen gene transcription in response to paraquat. We find that paraquat robustly up-regulates collagen gene transcription, which is dependent on KRI-1, a poorly studied protein homologous to human KRIT1/CCM1. KRI-1 knockdown prevents paraquat from activating the oxidative stress response transcription factor SKN-1/Nrf2, resulting in reduced collagen transcription and increased paraquat sensitivity. Using human lung fibroblasts (MRC-5), we confirm that both KRIT1 and Nrf2 are required for collagen transcription in response to paraquat. Nrf2 hyper-activation by KEAP1 knockdown bypasses KRIT1 to up-regulate collagen transcription. Our findings on the regulation of collagen gene transcription by paraquat could suggest potential strategies to treat pulmonary fibrosis caused by paraquat poisoning.

Clinical utility of the mood and anxiety symptom questionnaire in a chinese sample of patients with pancreatic cancer.

A review of the literature indicates a higher prevalence of depression and anxiety in patients with pancreatic carcinoma compared with nonclinical populations. The aims of this study were to evaluate the tripartite model for assessing symptoms of depression and anxiety and develop a Chinese version of the Mood and Anxiety Symptoms Questionnaire-Short Form (MASQ-SF) in patients with pancreatic cancer. The final sample consisted of 1,029 patients with pancreatic cancer. In line with our hypothesis, results of confirmatory factor analysis suggest that the three factors identified fit the hypothesized tripartite model well. The Chinese version of the MASQ-SF also exhibited high internal consistency. Reliability of the three scales was excellent with all scores greater than .79. Cronbach's alpha for the total MASQ-SF was .88. The 1-month test-retest reliability was .80. Correlation coefficients among the three subscales ranged from .36 to .75. Thus, the Chinese version of the MASQ-SF exhibited high levels of reliability and validity, indicating that the Chinese version of the MASQ-SF is appropriate for assessing symptoms of depression and anxiety in patients with pancreatic cancer. The use of this instrument may help researchers to better measure depression and anxiety in patients with pancreatic cancer and consequently develop appropriate prevention and treatment interventions.