Cessation of blood supply due to myocardial infarction (MI) leads to complicated pathological alteration in the affected regions. Cardiac stem cells (CSCs) migration plays a major role in promoting recovery of cardiac function and protecting cardiomyocytes in post-MI remodeling. Despite being the most abundant cell type in the mammalian heart, cardiac fibroblasts (CFs) were underestimated in the mechanism of CSCs migration. Our objective in this study is therefore to investigate the migration related factors secreted by hypoxia CFs in vitro and the degree that they contribute to CSCs migration. We found that supernatant from hypoxia induced CFs could accelerate CSCs migration. Four migration-related cytokines were reported upregulated both in mRNA and protein levels. Upon adding antagonists of these cytokines, the number of migration cells significantly declined. When the cocktail antagonists of all above four cytokines were added, the migration cells number reduced to the minimum level. Besides, MMP-9 had an important effect on triggering CSCs migration. As shown in our results, MMP-9 induced CSCs migration and the underlying mechanism might involve TNF-α signaling which induced VEGF and MMP-9 expression.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4342180 | PMC |
| http://dx.doi.org/10.1155/2015/836390 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Sertaconazole, an Imidazole Antifungal Agent, Suppresses the Stemness of Breast Cancer Cells by Inhibiting Stat3 Signaling.
In Vivo
December 2024
Graduate Program for Bio-health/Innovative Drug Development using Subtropical Bio-Resources, Jeju National University, Jeju, Republic of Korea;
Background/aim: Breast cancer stem cells (BCSCs) are a subpopulation of tumor cells that play a role in therapeutic resistance. In this study, we demonstrated that sertaconazole, an antifungal agent, displayed a potent inhibition on cancer stem cells (CSCs) and investigated the mechanism of action involved in its anti-BCSC effect.
Materials And Methods: The effect of sertaconazole on BCSCs was investigated using a mammosphere formation assay, a colony formation assay, and a cell migration assay.
FDFT1 maintains glioblastoma stem cells through activation of the Akt pathway.
Stem Cell Res Ther
December 2024
Department of Pathology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 33 Ying Feng Road, Guangzhou, 510120, China.
Background: Cancer stem cells (CSCs) have unique metabolic characteristics and are hypothesized to contribute significantly to the recurrence and drug resistance of glioblastoma multiforme (GBM). However, the reliance on mitochondrial metabolism and the underlying mechanism of glioblastoma stem cells (GSCs) remains to be elucidated.
Methods: To quantify differential mitochondrial protein expression between GSCs and differentiated cells, a mass spectrum screen was applied by the Stable Isotope Labeling with Amino Acids in Cell Culture (SILAC) technique.
is a potential therapeutic target for osteosarcoma: and evaluations using generated artificial osteosarcoma cancer stem cell‑like cells.
Oncol Rep
February 2025
Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe 650‑0017, Japan.
Cancer stem cells (CSCs) have been implicated as critical mediators in the progression, chemoresistance and metastatic capabilities of diverse malignancies, including osteosarcoma (OS). The authors have succeeded in generating CSC‑like cells (MG‑OKS) from the OS cell line MG‑63 by transducing defined factors. A significant increase in small proline‑rich protein 1A (SPRR1A) expression, a cross‑linked envelope protein in keratinocytes, was observed in MG‑OKS cells.
View Article and Find Full Text PDFNUF2 is associated with cancer stem cell characteristics and a potential drug target for prostate cancer.
Front Mol Biosci
December 2024
Department of Urology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Background: Cancer stem cells are characterized by self-renewal, clonal tumor initiation capacity, and treatment resistance, which play essential roles in the tumor progression of prostate cancer (PCa). In this study, we aim to explore the features of cancer stemness and characterize the expression of stem cell-related genes for PCa.
Methods: We downloaded RNA-seq data and related clinical information from The Cancer Genome Atlas (TCGA) database.
RANKL regulates differentially breast cancer stem cell properties through its RANK and LGR4 receptors.
Biochim Biophys Acta Mol Cell Res
December 2024
Innovation and Precision Medicine Laboratory, Instituto Nacional de Medicina Genómica, Periférico Sur No.4809, Col Arenal Tepepan, Tlalpan, Mexico City C.P. 14610, Mexico. Electronic address:
Background: Breast cancer stem cells (BCSC) are a subpopulation responsible for cancer resistance and relapse. The receptor activator of nuclear factor kappa-Β ligand (RANKL) is a cytokine capable of activating RANK and LGR4 receptors. RANKL/RANK signaling maintains the self-renewal of BCSCs, however, the effect of RANKL via LGR4 remains unclear.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!