Objective: To explore the effect of As₂O₃on Hedgehog pathway in chronic myeloid leukemia (CML) cells.
Methods: The apoptosis of K562 cells was detected by MTT method and flow cytometry; the expressions of PTCH and SMO protein and mRNA in Hedgehog pathway were determined by Western blot and real-time PCR, respectively. Retults: The As₂O₃ could induce the apoptosis of K562 cells with optimal concentration 2 µmol/L and optimal time 24 hours. The expressions of PTCH and SMO protein and mRNA in Hedgehog pathway of K562 cells treated with As₂O₃at optimal concentration and optimal time were down-regulated.
Conclusion: The As₂O₃can down-regulate the expression of PTCH and SMO in Hedgehog pathway.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.7534/j.issn.1009-2137.2015.04.012 | DOI Listing |
Prev Nutr Food Sci
December 2024
Department of Culinary Arts & Hotel Food Service, Yeonsung University, Gyeonggi 14011, Korea.
The inhibitory effect of L. on adipocyte differentiation can be enhanced by lactic acid bacteria (LAB) fermentation. In this study, we assessed the cellulose resolution, L.
View Article and Find Full Text PDFCancer Cell Int
January 2025
Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, NHC Key Laboratory of Hepatobiliary Cancers, Nanjing, Jiangsu, China.
Background: Hepatocellular carcinoma (HCC) continues to be a major cause of cancer-related death worldwide, primarily due to delays in diagnosis and resistance to existing treatments. Recent research has identified ATP-dependent chromatin remodeling-related genes (ACRRGs) as promising targets for therapeutic intervention across various types of cancer. This development offers potential new avenues for addressing the challenges in HCC management.
View Article and Find Full Text PDFNeurosci Lett
January 2025
Cellular and Molecular Research Center, Faculty of Medicine, Yasuj University of Medical Sciences, Yasuj, Iran. Electronic address:
The study aimed to understand the impact of the sonic-hedge signal pathway (SHH) on mouse neural stem cells. We manipulated the pathway using purmorphamine (Pur) and Gant 61 and observed the effects on cell viability, neurosphere formation, and gene expression. We found that activating the SHH pathway with Pur increased cell viability, neurosphere formation, and the expression of specific genes, promoting the differentiation of neural stem cells into mature cells.
View Article and Find Full Text PDFEur J Pharmacol
January 2025
Department of Conservative Dentistry & Endodontics, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai 600077, Tamil Nadu, India. Electronic address:
Oral squamous cell carcinoma (OSCC) remains a major cause of morbidity and mortality worldwide with high recurrence rates and resistance to conventional therapies. Recent studies have highlighted the pivotal role of oral cancer stem cells (OCSCs) in driving treatment resistance and tumor recurrence. OCSCs possess unique properties, including self-renewal, differentiation potential, and resistance to chemotherapy and radiotherapy, which contribute to their ability to survive treatment and initiate tumor relapse.
View Article and Find Full Text PDFCell Biochem Funct
January 2025
Stem Cells & Biotherapy Engineering Research Center of Henan, College of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Spinal cord injury (SCI) is a common neurological trauma that cannot be completely cured with surgical techniques and medications. In this study, we established a mouse SCI model and used an adeno-associated virus (AAV) to achieve the high expression of sonic hedgehog (Shh) at the injury site to further investigate the therapeutic effect and mechanism of Shh on SCI. The results of the present study show that Shh may promote motor function recovery.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!