Cell Adhesion & Migration最新文献

Preeclampsia (PE) is a severe pregnancy complication with unclear molecular mechanisms. Our research investigated the effect of UNC5C-AS1 on human umbilical vein endothelial cell (HUVEC) function in PE. UNC5C-AS1 was downregulated in PE placentas. Upregulating UNC5C-AS1 promoted HUVEC migration, invasion, tube formation, and the expression of vascular permeability factors, while UNC5C-AS1 silencing exhibited an opposite effect. UNC5C-AS1 directly targeted the miR148a3p/EMP1 axis. MiR-148a-3p was up-regulated and EMP1 was downregulated in PE. The regulatory effects of UNC5C-AS1 overexpression on HUVEC functions were reversed by miR-148a-3p mimics, and this reversal was subsequently rescued by EMP1 upregulation. UNC5C-AS1 overexpression ameliorated tissue damage in the PE mouse model. UNC5C-AS1 alleviated the PE-associated injury and modulated HUVEC function by targeting miR-148a-3p/EMP1 axis.

In the tumor microenvironment, tissue-resident macrophages (TRMs) promote malignant tumor progression, yet their tissue-specific heterogeneity and complex functions bring research challenges. This study analyzes the research status and trends of TRMs in oncology. Via VOSviewer, CiteSpace, R software and WoSCC, a visual bibliometric network was built for quantitative analysis, with future research directions explored in depth. The US leads in publications and academic influence, and the University of Washington tops in paper output. Research focuses on TRMs' origin, classification and tumor microenvironment functions; microglia and Kupffer cells are the most studied subsets. Current research centers on pathway exploration, immunotherapy and single-cell sequencing. This study summarizes TRMs' research status, hotspots and trends in oncology, providing valuable insights for relevant collaborators and institutions.

Lactoferrin (LTF) has gained attention as a potential anti-cancer biomarker, but its role in left-sided colon cancer (LCC) remains poorly understood. This study explores the function of LTF in LCC and its underlying mechanisms. LTF expression was significantly elevated in tumor tissues compared to normal tissues (59.67-fold increase, p < .001). LTF overexpression significantly enhanced LCC cell proliferation, migration, and invasion (p < .01), while suppressing apoptosis (p < .05). In contrast, LTF knockdown markedly inhibited these oncogenic behaviors. Western blot analysis demonstrated that LTF overexpression led to increased phosphorylation of PI3K and Akt proteins (p < .01), suggesting activation of the PI3K/AKT signaling pathway, while LTF knockdown resulted in decreased phosphorylation levels (p < .01). This study identifies LTF as a promoter of LCC development via activation of the PI3K/AKT pathway, suggesting LTF as a promising therapeutic target. Further research is warranted to evaluate its clinical potential in LCC treatment.

EPB41L1-5 is known to maintain cell morphology and signal transduction, with evidence suggesting it can inhibit tumor progression. However, its role in kidney renal clear cell carcinoma (KIRC) is not fully understood. This study evaluated EPB41L1-5's prognostic value in KIRC using bioinformatics methods and validation through qPCR, immunohistochemistry, and cell functional experiments. The results demonstrated a decreased expression of EPB41L in KIRC tissue compared to normal renal tissue, correlating with lower survival rates. Low EPB41L expression was also associated with overall survival in KIRC. Additionally, EPB41L was found to be involved in extracellular matrix regulation, G protein-coupled receptor ligand binding, and multiple immune cell infiltrations. In addition, their elevated methylation levels are associated with poor prognosis in KIRC patients. Overall, EPB41L family is a potential molecular marker for predicting KIRC prognosis, offering insights for therapeutic development.

This study investigated the role of COPB2 in gastric cancer (GC) pathogenesis. Analysis of TCGA datasets and tissue microarrays revealed its upregulation in GC tissues compared to normal adjacent tissues, which was correlated with advanced tumor stage and lymphatic invasion and demonstrated significant diagnostic value (AUC = 0.895 and 0.851). Functional assays using lentiviral-mediated silencing in GC cells showed that COPB2 knockdown suppressed cell proliferation and migration, induced G0/G1-phase arrest, and promoted apoptosis. Mechanistic investigations through microarray, KEGG, and IPA analyses indicated that COPB2 dysregulation inactivated the PI3K/AKT and NF-κB signaling pathways. This led to the downregulation of key oncogenic effectors including Slug, FN1, CDH2, F2RL1, CDK6, CCND1, MMP9, CDKN2A, and SQSTM1, while upregulating tumor suppressors CDKN1B, CDKN1A, and DDIT3. In conclusion, COPB2 acts as an oncogene in GC, driving tumor progression through modulation of the cell cycle and key signaling pathways, highlighting its potential as a therapeutic target.

Purpose: Neutral cholesterol ester hydrolase 1 (NCEH1), a key enzyme in cellular lipid metabolism, is associated with cancer progression. Its molecular functions in breast cancer remain poorly understood.

Methods: This study evaluated the expression of NCEH1 in breast cancer patients using multiple databases. Functionally, the effects of NCEH1 silencing or overexpression on breast cancer cell growth and motility were investigated. RNA-seq was employed to identify downstream target genes and signalling pathways.

Results: The expression of NCEH1 in breast cancer tissues and cells was significantly higher than that in normal tissues and cells. Silencing NCEH1 suppressed breast cancer cell proliferation and migration. Mechanistically, NCEH1 regulated Neuropilin-1 (NRP1) expression, and both promoted malignant phenotypes in breast cancer by activating the TNF-α/NF-κB signalling pathway.

Conclusion: Our findings demonstrate that NCEH1 accelerates breast cancer progression by modulating NRP1 and activating the TNF-α/NF-κB signalling pathway. Collectively, NCEH1 represents a potential novel biomarker and therapeutic target for breast cancer.

Na+/H+ exchanger 1 (Nhe1) is a crucial regulator of pH homeostasis and the present study demonstrates that Nhe1 is required for directional sensing in vegetative Dictyostelium cell migration. nhe1 null cells exhibited severe defects in directional sensing and migration in response to folate gradients and applied electric fields.Specifically, nhe1 null cells failed to exhibit proper translocation of phosphatidylinositol (3,4,5)-trisphosphate (PIP3) to the cell cortex and showed abnormal intracellular calcium signaling upon folate stimulation. Additionally, cells lacking Nhe1 exhibited a reduced capacity to engulf bacteria and latex beads. In contrast, nhe1 null cells in the developed stage displayed a defect in cAMP-directed chemotaxis, but normal translocation kinetics of PIP3 to the cell cortex upon cAMP stimulation.

Sheep ovarian granulosa cells (GCs) play a unique role in the ovary. Damage to GCs can affect the normal development of oocytes. The oxidative stress model was constructed by H₂O₂to study the biological changes. Specifically, pathological characteristic was assessed by immunohistochemistry (IHC), while signaling pathway was studied using western blot, quantitative RT-PCR, and immunofluorescence. Theresults showed that the oxidative damage model was successfully constructed by 200 μmol/LH₂O₂ for 12 h. NAC can protect the proliferation of GCs under H₂O₂-induced oxidative stress and reduce apoptosis. It can also promote the secretion of E₂ and P₄ by GCs and reduce the inflammatory response of GCs. NAC can enhance the expression of NRF2, PI3K and Akt. These findings suggest that NAC alleviates H₂O₂-induced oxidative stress injury through NRF2/PI3K/AKT signaling pathways. Provide ideas for studying the poor quality of mammalian oocytes.

MiR-646, a small non-coding RNA, poorly expressed in a variety of tumors. This study aimed to clarify the role of miR-646 and its underlying mechanisms in glioblastoma (GBM). In our study, we found that miR-646 mRNA levels were lower in tumor tissues than in non-cancer tissues. The ability of glioma cells to proliferate, invade, and migrate is diminished by miR-646 overexpression in vitro and in vivo. Mechanistically, miR-646 targeted sequestosome 1 (p62) in the 3'UTR and affected the Keap1/Nrf2 pathway, thus attenuating the expression of the HO-1 gene. In conclusion, this study provided a novel finding that miR-646 tampered with gliomagenesis by regulating the p62/Keap1/Nrf2 axis, which provides a potential target for GBM therapy.

Gliomas are aggressive brain tumors whose infiltrative growth is mediated by intercellular crosstalk. Exosomes, small extracellular vesicles, play a key role in cell-cell communication but are difficult to visualize using conventional microscopy. Performing immunostaining for CD63, a known exosome marker, and using STED microscopy, we demonstrate exosome secretion in primary glioma cells. Applying mathematical deconvolution, we enhance the contrast and resolution for in-depth analysis of STED images. We identify CD63-positive cellular footprints and exosome deposits in the extracellular space. Quantitative analysis shows CD63-positive exosomes ranging 36.55-157.06 nm in size. CD63/actin co-staining demonstrates different actin polymerization states associated with exosomes. In conclusion, STED microscopy coupled with immunostaining allows exosome primary characterization at the single-vesicle level in the cellular spatial context.