Cell Adhesion & Migration最新文献

Peripheral nerve injury repair has always been a research concern of scientists. At the tissue level, axonal regeneration has become a research spotlight in peripheral nerve repair. Through transplantation of autologous nerve grafts or other emerging biomaterials functional recovery after facial nerve injury is not ideal in clinical scenarios. Great strides have been made to improve facial nerve repair at the micro-cellular level. Physical stimulation techniques can trigger Schwann cells (SCs) to migrate and differentiate into cells required for peripheral nerve repair. Classified by the sources of physical stimulations, SCs repair peripheral nerves through galvanotaxis, magnetotaxis and durotaxis. This article summarized the activation, directional migration and differentiation of SCs induced by physical stimulations, thus providing new ideas for the research of peripheral nerve repair.

This study investigated the role of long-chain acyl-CoA dehydrogenase (ACADL) in lung adenocarcinoma (LUAD). ACADL was significantly downregulated in human LUAD tissues compared to normal lung tissues. In vitro, ectopic expression of ACADL in murine LLC cells decreased cell viability, migration, and invasion, while ACADL knockdown exhibited the opposite effect. In vivo, ACADL overexpression impeded tumor growth and metastasis. Mechanistically, ACADL hindered tumor progression by inducing cell cycle arrest, promoting apoptosis, and suppressing the epithelial-mesenchymal transition (EMT) process. These findings suggest ACADL acts as a tumor suppressor in LUAD progression.

Claudins (CLDNs), as the key components of tight junctions, have been implicated as key factors in carcinogenesis and metastasis. A total of 1720 publications on CLDNs in the field of cancer were published from January 2005 to December 2022. The United States dominates the research on CLDNs in cancer, followed by China. China Medical University is the most productive, and Johns Hopkins University has the most citations. Morin PJ is credited with initiating research on CLDNs in cancer. CLDN18, the intestinal barrier, and the intestinal microbiota are the focus and hotspots in this field. The mechanism of CLDN-mediated metastasis still needs further investigation, and the development of CLDN-targeted therapies also needs to be explored in the future.

A single cell or cell population exhibits the fundamental phenomenon of cell migration during developmental processes or disease progression. Vast literature suggests that, in vitro 2-dimensional or 3-dimensional cell migration assay is one of the most commonly used assays in cancer, wound healing research, and developmental biology research. The data obtained from this assay are often analyzed using various proprietary or open-source programs. Proprietary software are costly and not always accessible to everyone. Whereas the open-source programs are free, easy to access, and user friendly. However, not all researchers are aware of these open-source programs. Despite the increasing availability of these programs, many researchers still rely on proprietary software, due to a lack of comparative analyses and practical guidance on their implementation. Hence, this review aims to provide insights into these open-source tools and serves as a practical guide to both biologists and computational researchers for their specific analytical needs.

Background: Research on the function of HGH1 in breast cancer remains lacking.

Methods: TCGAand GEO (GSE45827) datasets investigated discrepancies in HGH1 expression in BC. An aggregate of 106 clinical samples were gathered through immunohistochemistry, KM curves were drawn for prognostic analysis, and the function of HGH1 of BC was predicted. Finally, the effects of HGH1 knockdown on MDA-MB-231 and MCF-7 BC cells were verified via CCK8, invasion, wound healing and colony formation assays.

Results: HGH1 is highly expressed in BC and is linked to unfavorable prognosis. HGH1 overexpression is connected to keratinization and the cell cycle and is closely related to ER and PR expression and tumor stage in BC patients. Knocking down HGH1 in BC cells inhibited the viability, invasion and migration.

Conclusion: Knockdown of HGH1 in breast cancer cell lines can inhibit the viability, invasion and migration of tumor cells.

Adhesion molecules are proteins expressed at the surface of various cell types. Their main contribution to immunity is to allow the infiltration of immune cells in an inflamed site. In cancer, adhesion molecules have been shown to promote tumor dissemination favoring the development of metastasis. While adhesion molecule inhibition approaches were unsuccessful for cancer control, their importance for the generation of an immune response alone or in combination with immunotherapies has gained interest over the past years. Currently, the balance of adhesion molecules for tumor promotion/inhibition is unclear. Here we review the role of selectins, intercellular adhesion molecules (ICAM) and vascular cell adhesion molecules (VCAM) from the perspective of the dual contribution of adhesion molecules in tumor progression and immunity.

Tektins, a family of microtubule-stabilizing proteins, are critical for cilia and flagella assembly in mammals. They maintain doublet microtubule stability and ciliary/flagellar motility. Loss of Tekt1-5 causes microtubule instability, impaired motility, and diseases like infertility, retinal degeneration, Mainzer-Saldino syndrome, and diabetic nephropathy. Pathophysiological stimuli regulate Tektin expression through transcriptional, posttranscriptional, translational, and posttranslational modifications. This review summarizes the latest findings on Tektin functions and their role in diseases.

The accumulation of lipid droplets (LDs) enhancing nasopharyngeal carcinoma (NPC) cell migration. We reveals that CDP-diacylglycerol synthase 1 (CDS1), an inhibitor of LDs formation, is significantly downregulated in NPC. Restoring CDS1 expression suppresses NPC cell growth, colony formation, tumorigenesis, migration, and invasion. The anti-cancer effect of CDS1 is attributed to its role in decreasing the intracellular LDs. Moreover, CDS1 promotes activation of the NF-κB signaling pathway, resulting in elevated levels of inflammatory cytokines within NPC cells. This is likely to enhance the immunogenicity of these cells, thereby reducing tumor volume in the in vivo model. These findings establish CDS1 as a novel suppressor of NPC by modulating LDs levels, suggesting potential therapeutic avenues aimed at limiting LDs accumulation.

This study examines Holocytochrome c synthase (HCCS) expression in lung adenocarcinoma (LUAD) and its impact on the tumor immune environment. By analyzing multiple tumor databases, the research highlights HCCS expression patterns across various cancer types, focusing on its correlation with M2-type macrophages, which aid tumor progression. Findings show that high HCCS expressionin LUAD is associated with increased M2-type macrophages, and variations in HCCS levels influence immune cell infiltration and cancer therapy responsiveness. It suggests that HCCS significantly shapes the immune landscape within tumors, promoting growth and spread, and underscores its potential as a therapeutic target in LUAD and other cancers with similar expression profiles.

The research endeavors to expound the role of ORM1 in bladder cancer (BCa) and the implied response mechanism. RT-qPCR and Western blotting examined ORM1 and S100A12 expression. Functional experiments assessed the cellular phenotypes. HDOCK and Co-IP confirmed the interaction of ORM1 and S100A12. Western blotting tested apoptosis- and ERK signaling-associated proteins. ORM1 and S100A12 were abundant in the BCa cells. ORM1 or S100A12 loss impaired cell proliferation, migration, and invasion, and aggravated cell apoptosis. ORM1 interacted with S100A12. ORM1 knockdown down-regulated S100A12 expression and inactivated ERK signaling.S100A12 overexpression or ERK activator reversed the impacts of ORM1 interference on ERK signaling and BCa cells. ORM1 mightdrive BCa via binding to S100A12 and activating ERK signaling.