Osteosarcoma is characterized by high propensity for metastasis, especially to the lung, which is the main cause of death. Peroxiredoxin-1 (PRDX1) plays significant roles in multiple processes of initiation and progression of tumorogenesis. However, whether PRDX1 participates in metastasis of osteosarcoma remains unknown. Here, we demonstrate that PRDX1 overexpressed in osteosarcoma tissues comparing to adjacent non-tumor tissues. Two independent cohorts of patients showed high level of PRDX1 correlated with clinicopathological features such as larger tumor size and advanced tumor metastasis stage. While patients with high PRDX1 level have poor prognosis. Notably, expression level of PRDX1 especially increased in lung lesion of osteosarcoma patients, indicating that PRDX1 may promote lung metastasis. Ectopic expression of PRDX1 promotes osteosarcoma cell migration and metastasis and , whereas knockdown of PRDX1 expression suppresses cell metastatic behaviors such as invasion and migration. Furthermore, we found that PRDX1 promotes cells metastasis through enhancing Akt/mTOR signal pathway. Taken together, our findings prove the important role of PRDX1 in the molecular etiology of osteosarcoma and suggest that PRDX1 may be a novel prognostic biomarker and therapeutic target for osteosarcoma.
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http://dx.doi.org/10.18632/oncotarget.23662 | DOI Listing |
iScience
December 2024
Department of Biological Sciences and Biotechnology, Chungbuk National University, Cheongju, Chungbuk, Republic of Korea.
Peroxiredoxin 1 (PRDX1), an intracellular antioxidant enzyme, has emerged as a regulator of inflammatory responses via Toll-like receptor 4 (TLR4) signaling. Despite this, the mechanistic details of the PRDX1-TLR4 axis and its impact on osteoclast differentiation remain elusive. Here, we show that PRDX1 suppresses RANKL-induced osteoclast differentiation.
View Article and Find Full Text PDFZhongguo Zhong Yao Za Zhi
November 2024
Department of Pharmacy, Zhongshan Hospital, Fudan University Shanghai 200032, China.
This study explored the generation site and regulation mechanism of reactive oxygen species(ROS) in the apoptosis of colorectal cancer cells induced by furanodienone(Fur). RKO cells were treated with 200 μmol·L~(-1) of Fur, and the changes in intracellular nicotinamide adenine dinucleotide phosphate oxidase(NOX) activity were detected by the NOX activity detection method. The control group, Fur group, diphenyleneiodonium(DPI) inhibitor group for general NOX, mitochondrial-targeted antioxidant(MitoTEMPO) group, Fur+DPI group, Fur+MitoTEMPO group, and H_2O_2 positive control group were set up.
View Article and Find Full Text PDFToxicol In Vitro
December 2024
Laboratorio de Investigación en Patología Experimental, Hospital Infantil de México Federico Gómez, Avenida Dr. Márquez 162, Colonia Doctores, Cuauhtémoc, 06720 Ciudad de México, Mexico. Electronic address:
Benzo[ghi] perylene (b[ghi]p) is classified as non-carcinogenic to humans, and there are currently no occupational exposure models available to identify its effects. The aim of this work was to evaluate the effect of b[ghi]p on the lysosomes of NL-20 cells (a human bronchial cell line) exposed to 4.5 μM for 3 h.
View Article and Find Full Text PDFPLoS One
December 2024
Cancer Biology and Therapeutics Laboratory, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland.
Background: The Androgen Receptor (AR) pathway is crucial in driving the progression of prostate cancer (PCa) to an advanced state. Despite the introduction of second-generation AR antagonists, such as enzalutamide, majority of patients develop resistance. Several mechanisms of resistance have been identified, including the constitutive activation of the AR pathway, the emergence of AR spliced variants, and the influence of other signalling pathways.
View Article and Find Full Text PDFEnviron Toxicol
November 2024
Molecular Toxicology Laboratory, Department of Biotechnology, Bharathiar University, Coimbatore, India.
Fluoride (F) is a major groundwater contaminant spread across the world. In excess concentrations, F can be detrimental to living beings. F exposure is linked to cellular redox dyshomeostasis, leading to oxidative stress-mediated pathologies including heart dysfunction.
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