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hnRNPU-mediated pathogenic alternative splicing drives gastric cancer progression.
J Exp Clin Cancer Res
January 2025
Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China.
Background: Alternative splicing (AS) is a process that facilitates the differential inclusion of exonic sequences from precursor messenger RNAs, significantly enhancing the diversity of the transcriptome and proteome. In cancer, pathogenic AS events are closely related to cancer progression. This study aims to investigate the role and regulatory mechanisms of AS in gastric cancer (GC).
View Article and Find Full Text PDFFat mass and obesity-related protein contributes to the development and maintenance of bone cancer pain in rats by abrogating m6A methylation of RNA.
Mol Pain
October 2024
Department of Anesthesiology and Pain Medicine, Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang, China.
Effective prevention and treatment options for bone cancer-related pain (BCP) are lacking. In recent years, numerous studies have investigated the association between m6A epigenetic modifications and pain, revealing their significant role in pain initiation and maintenance. This study aimed to provide theoretical support for the treatment of BCP and to identify target drugs for future development.
View Article and Find Full Text PDFRepurposing auranofin and meclofenamic acid as energy-metabolism inhibitors and anti-cancer drugs.
PLoS One
September 2024
Laboratorio de Control Metabólico, Carrera de Biología de la Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Tlalnepantla, México.
Objective: Cytotoxicity of the antirheumatic drug auranofin (Aur) and the non-steroidal anti-inflammatory drug meclofenamic acid (MA) on several cancer cell lines and isolated mitochondria was examined to assess whether these drugs behave as oxidative phosphorylation inhibitors.
Methods: The effect of Aur or MA for 24 h was assayed on metastatic cancer and non-cancer cell proliferation, energy metabolism, mitophagy and metastasis; as well as on oxygen consumption rates of cancer and non-cancer mitochondria.
Results: Aur doses in the low micromolar range were required to decrease proliferation of metastatic HeLa and MDA-MB-231 cells, whereas one or two orders of magnitude higher levels were required to affect proliferation of non-cancer cells.
Detouring NSAID into Mitochondria to Induce Apoptosis in Cancer Cells.
Chem Asian J
December 2024
Department of Chemistry, Indian Institute of Technology (IIT) Gandhinagar, Palaj, Gandhinagar, Gujarat, 382355, India.
Article Synopsis
- Scientists are studying ways to hurt the powerhouses of cancer cells, called mitochondria, to help treat cancer.
- They found that certain anti-inflammatory drugs, like Meclofenamic acid and Naproxen, can be modified to better target these mitochondria.
- One specific version of Meclofenamic acid (called 8A3) was successful in killing colon cancer cells by damaging their mitochondria and triggering cell death.
Antiseizure properties of fenamate NSAIDs determined in mature human stem-cell derived neuroglial circuits.
Front Pharmacol
May 2024
Thomas J. Long School of Pharmacy, University of the Pacific, Stockton, CA, United States.
Repeated and uncontrolled seizures in epilepsy result in brain cell loss and neural inflammation. Current anticonvulsants primarily target ion channels and receptors implicated in seizure activity. Identification of neurotherapeutics that can inhibit epileptiform activity and reduce inflammation in the brain may offer significant benefits in the long-term management of epilepsy.
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