Several studies have reported that FZD2 regulates tumor biology in a complex manner. The aim of the present study was to identify the role of FZD2 in the cell growth and metastasis of salivary adenoid cystic carcinomas (SACCs). The expression of FZD2 in ACC-83 and ACC-LM cells were measured with real-time PCR. Immunohistochemical staining was used to detect the expression of FZD2 in clinical SACC samples with or without metastasis. Cell proliferation and Transwell assays were performed to explore the effects of FZD2 on cell growth and migration following the silencing of FZD2 with small interference RNAs and the overexpression of FZD2 with plasmid. Our data showed that FZD2 was downregulated in ACC-LM cells, which are an adenoid cystic carcinoma cell line with high metastatic potential, compared to ACC-83 cells, which have low metastatic potential. Additionally, the expression of FZD2 was lower in SACC tissues with metastasis compared to SACC tissues without metastasis (P<0.05). Cell proliferation and migration of ACC-83 cells were increased after the knockdown of FZD2 and decreased following overexpression of FZD2. Knockdown of FZD2 downregulated the expression of PAI-1. Our results suggest that FZD2 may be a tumor suppressor gene in SACCs that inhibits cell growth and migration.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.3892/or.2015.3811 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
High-Throughput Formation of Pre-Vascularized hiPSC-Derived Hepatobiliary Organoids on a Chip via Nonparenchymal Cell Grafting.
Adv Sci (Weinh)
January 2025
Tissue Engineering and Organ Manufacturing (TEOM) Lab, Department of Biomedical Engineering, Wuhan University TaiKang Medical School (School of Basic Medical Sciences), Wuhan, 430071, China.
Liver organoids have been increasingly adopted as a critical in vitro model to study liver development and diseases. However, the pre-vascularization of liver organoids without affecting liver parenchymal specification remains a long-lasting challenge, which is essential for their application in regenerative medicine. Here, the large-scale formation of pre-vascularized human hepatobiliary organoids (vhHBOs) is presented without affecting liver epithelial specification via a novel strategy, namely nonparenchymal cell grafting (NCG).
View Article and Find Full Text PDFMiR-128-3p promotes hyperproliferation of keratinocytes and psoriasis-like inflammation by targeting SIRT1/HIF-1α.
Arch Dermatol Res
January 2025
Department of Dermatology, Zhejiang Provincial Hospital of Dermatology, Huzhou, 313200, China.
Psoriasis is a long-lasting inflammatory skin condition characterized by excessive keratinocyte growth. Recent studies have confirmed abnormal regulation of microRNAs (miRNAs/miRs) in individuals with psoriasis. This study aimed to investigate the function and specific mechanism of action of miR-128a-3p in interleukin-22 (IL-22)-stimulated HaCaT cells.
View Article and Find Full Text PDFBerberine restrains non-small cell lung cancer cell growth, invasion and glycolysis via inactivating the SPC25/NUF2 pathway.
Naunyn Schmiedebergs Arch Pharmacol
January 2025
Department of Respiratory and Critical Care Medicine, Guangdong Provincial Hospital of Traditional Chinese Medicine, No. 111, Dade Road, Guangzhou, 510120, China.
Berberine (BBR) has been proved to inhibit the malignant progression of non-small cell lung cancer (NSCLC), but the underlying molecular mechanism still needs to be further revealed. NSCLC cells (A549 and H1299) were treated with BBR. CCK8 assay, colony formation assay, flow cytometry, TUNEL staining and transwell assay were used to examine cell proliferation, apoptosis and invasion.
View Article and Find Full Text PDFADAMDEC1 promotes the malignant progression of cholangiocarcinoma by regulating NF-κB signaling pathway.
Sci Rep
January 2025
School of Medicine, Nankai University, Tianjin, 300071, China.
Cholangiocarcinoma (CCA), a highly aggressive form of cancer, is known for its high mortality rate. A Disintegrin and Metalloprotease Domain-like Protein Decysin-1 (ADAMDEC1) can promote the development and metastasis in various tumors by degrading the extracellular matrix. However, its regulatory mechanism in CCA remains unclear.
View Article and Find Full Text PDFDifferential regulatory effects of the N-terminal region in SYK-fusion kinases reveal unique activation-inducible nuclear translocation of ITK-SYK.
Sci Rep
January 2025
Department of Laboratory Medicine, Karolinska Institutet, ANA Futura, Alfred Nobels Allé 8, Floor 8, 14152, Huddinge, Sweden.
ITK-SYK and TEL-SYK (also known as ETV6-SYK) are human tumor-causing chimeric proteins containing the kinase region of SYK, and the membrane-targeting, N-terminal, PH-TH domain-doublet of ITK or the dimerizing SAM-PNT domain of TEL, respectively. ITK-SYK causes peripheral T cell lymphoma, while TEL-SYK was reported in myelodysplastic syndrome. BTK is a kinase highly related to ITK and to further delineate the role of the N-terminus, we generated the corresponding fusion-kinase BTK-SYK.
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!