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Function: _error_handler
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Transforming growth factor (TGF)‑β1 is highly expressed in bladder transitional cell carcinoma (TCC) and is positively associated with tumor grade. TGF‑β1 signaling promotes cell metastasis by inducing epithelial‑mesenchymal transition (EMT), however, the underlying mechanisms are not fully understood. Our previous study demonstrated the anti‑metastatic effects of silibinin, a natural flavonoid derived from milk thistle, against TCC. The present study investigated the effects of silibinin on TGF‑β1‑induced EMT in TCC, focusing on the role of prostaglandin‑endoperoxide synthase 2 (COX‑2). Cell migration was determined by a wound healing assay and Transwell migration assay, and cell invasion was investigated using a Transwell invasion assay. Cell morphology was observed using an inverted microscope. Cell viability was evaluated by an MTT and cell counting assays. EMT markers were detected by reverse transcription‑quantitative polymerase chain reaction and western blotting. Specific small interfering RNA was used to knockdown COX‑2 gene expression. TGF‑β1 promoted cell migration and invasion, induced EMT and upregulated the expression of COX‑2. COX‑2 knockdown attenuated TGF‑β1‑induced EMT, indicating that COX‑2 upregulation was essential for TGF‑β1‑induced EMT. Silibinin attenuated TGF‑β1‑induced migration and invasion by inhibiting EMT, and was associated with COX‑2 downregulation. TGF‑β1‑induced COX‑2 upregulation, which was inhibited by silibinin. In addition, TGF‑β1‑induced EMT was further inhibited when silibinin treatment was combined with COX‑2‑knockdown. The results suggested that silibinin may be a potential future treatment for metastatic TCC.
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http://dx.doi.org/10.3892/or.2018.6728 | DOI Listing |
Cancer Cell Int
December 2024
Institute for Excellence in Clinical Medicine of Kunshan First People's Hospital, Soochow University, Suzhou, China.
Gliomas are the most common tumors of the central nervous system, with glioblastoma (GBM) being particularly aggressive and fatal. Current treatments for GBM, including surgery and chemotherapy, are limited by tumor aggressiveness and the blood-brain barrier. Therefore, understanding the molecular mechanisms driving GBM growth is essential.
View Article and Find Full Text PDFGut Microbes
December 2025
Department of Gastroenterology and Hepatology, General Hospital, Tianjin Medical University, National Key Clinical Specialty, Tianjin Institute of Digestive Diseases, Tianjin Key Laboratory of Digestive Diseases, Tianjin, China.
The initiation and progression of colorectal cancer (CRC) are intimately associated with genetic, environmental and biological factors. (DSV), a sulfate-reducing bacterium, has been found excessive growth in CRC patients, suggesting a potential role in carcinogenesis. However, the precise mechanisms underlying this association remain incompletely understood.
View Article and Find Full Text PDFEnzyme Microb Technol
December 2024
Department of Biotechnology, Lorena School of Engineering, University of São Paulo, Lorena, SP, Brazil. Electronic address:
β-glucosidases (BGLs) are key enzymes in the depolymerization of cellulosic biomass, catalyzing the conversion of cello-oligosaccharides into glucose. This conversion is pivotal for enhancing the production of second-generation ethanol or other value-added products in biorefineries. However, the process is often cost-prohibitive due to the high enzyme loadings required.
View Article and Find Full Text PDFKaohsiung J Med Sci
December 2024
Hunan University of Medicine, Huaihua, Hunan Province, People's Republic of China.
Epithelial-mesenchymal transition (EMT) is a critical stage in the metastasis of gastric cancer (GC). Further clarification of the EMT process in GC is still needed. This study examined the effects of the NEDD4L/BICC1 axis on GC proliferation and the EMT process.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
January 2025
Department of Anorectal, Affiliated Hospital of Jiaxing University, The Second Hospital of Jiaxing, Jiaxing City, Zhejiang Province, China.
The underlying regulating mechanisms of miR-105-5p/PTEN in colon cancer (CC) progression are still unknown. MiR-105-5p and PTEN expressions were determined using RT-PCR. PTEN protein levels were examined by western blot.
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