Background & Aims: Ulceration of intestinal mucosa is rapidly followed by enterocyte migration via restitution. The aim of this study was to investigate signaling mechanisms of epidermal growth factor (EGF) receptor-stimulated monolayer restitution in a mouse intestinal epithelial cell line.
Methods: EGF-stimulated cell migration was determined using a wound model in the presence of agonists and/or antagonists of tyrosine kinase, phospholipase C, phosphatidylinositol 3-kinase, or protein kinase C. The tyrosine phosphorylation state of the EGF receptor, phosphatidylinositol phospholipase C gamma1 (PLCgamma1), focal adhesion kinase, and cellular lysates was determined by immunodetection.
Results: EGF stimulated cell migration twofold at 4, 8, and 24 hours. Inhibition of EGF receptor tyrosine kinase activity, phospholipase C, or phosphatidylinositol 3-kinase attenuated EGF-induced intestinal cell migration. Pretreatment of cells with phorbol 12-myristate 13-acetate, known to down-regulate protein kinase C expression, blocked EGF-induced cell migration. Increased tyrosine phosphorylation of the EGF receptor and PLCgamma1 was detected within 5 minutes after wounding.
Conclusions: EGF-stimulated intestinal cell migration requires intact EGF receptor tyrosine kinase, phospholipase, and protein kinase C activities. PLCgamma1 may be a key regulatory molecule in the initial EGF receptor signal transduction pathway of EGF-stimulated cell migration.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/s0016-5085(98)70532-3 | DOI Listing |
J Transl Med
January 2025
Department of Gynecology, The Fourth Hospital of Hebei Medical University, No.12 Jiankang Road, Shijiazhuang, 050000, Hebei, China.
Background: Immune cells within tumor tissues play important roles in remodeling the tumor microenvironment, thus affecting tumor progression and the therapeutic response. The current study was designed to identify key markers of plasma cells and explore their role in high-grade serous ovarian cancer (HGSOC).
Methods: We utilized single-cell sequencing data from the Gene Expression Omnibus (GEO) database to identify key immune cell types within HGSOC tissues and to extract related markers via the Seurat package.
Mol Cancer
January 2025
Department of Radiation Oncology, Peking University Third Hospital, Beijing, 100191, China.
Background: Sorafenib, an FDA-approved drug for advanced hepatocellular carcinoma (HCC), faces resistance issues, partly due to myeloid-derived suppressor cells (MDSCs) that enhance immunosuppression in the tumor microenvironment (TME).
Methods: Various murine HCC cell lines and MDSCs were used in a series of in vitro and in vivo experiments. These included subcutaneous tumor models, cell viability assays, flow cytometry, immunohistochemistry, and RNA sequencing.
J Nanobiotechnology
January 2025
School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei, China.
Esophageal cancer (EC) is one of the most common highly malignant tumors of the digestive system, with a poor prognosis under current treatment regimens. Nucleolin (NCL) is overexpressed in many tumors, and drugs specifically targeting NCL may offer a promising strategy for treating esophageal cancer. Here, we designed and prepared a novel aptamer-conjugated drug targeting NCL by AS1411 aptamer-human serum albumin (HSA)-the apoprotein of lidamycin (LDP)-active enediyne chromophore (AE), in order to achieve targeted treatment of esophageal cancer.
View Article and Find Full Text PDFCell Div
January 2025
Department of Nuclear Medicine, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South university/Hunan Cancer Hospital, No. 283 Tongzipo Road, Yuelu District, Changsha, 410013, Hunan, P.R. China.
Background: Zinc finger protein 169 (ZNF169) plays a key role in cancer development. However, the specific role of ZNF169 in the tumorigenesis of thyroid carcinoma (THCA) remains poorly understood.
Methods: The expression of ZNF169 was measured using immunohistochemistry, RT-qPCR, and western blot.
J Neuroinflammation
January 2025
Department of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Background: The retinal degenerative diseases retinitis pigmentosa (RP) and atrophic age- related macular degeneration (AMD) are characterized by vision loss from photoreceptor (PR) degeneration. Unfortunately, current treatments for these diseases are limited at best. Genetic and other preclinical evidence suggest a relationship between retinal degeneration and inflammation.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!