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Emerging evidence supports a role for p38 MAPK in negative regulation of tumorigenesis. Here we show that a subtle activation of p38 MAPK is sufficient to suppress tumorigenesis as measured by the ability to form tumors when MKK6-inducible cells were explanted into nude mice. On the other hand, this activation of p38 MAPK did not necessarily cause an immediate inhibition of cell growth in vitro as measured by standard MTS assay. This data uncovers a new methodology for anti-cancer drugs screening and suggests that a substantial number of potential anti-tumor compounds, such as activators of MKK6/p38 signaling, was missed out in previous high throughput screens based on conventional growth inhibition assays.
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http://dx.doi.org/10.4161/cc.4.1.1342 | DOI Listing |
Cell Physiol Biochem
September 2025
Department of General Practice, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China, E-Mail:
Background/aims: Ubiquitin D (UBD), a member of the ubiquitin-like modifier (UBL) family, is significantly overexpressed in various cancers and is positively correlated with tumor progression. However, the role and underlying mechanisms of UBD in rheumatoid arthritis (RA) remain poorly understood. This study aimed to investigate the effects of UBD knockdown on the progression of RA.
View Article and Find Full Text PDFPhytomedicine
August 2025
Cardiology Department, Affiliated Hospital of Jiangxi University of Chinese Medicine, Nanchang, China. Electronic address:
Background: Atherosclerosis (AS) is a leading risk factor for cardiovascular diseases globally, characterised by the accumulation of lipids and cholesterol in arterial walls, causing vascular narrowing and sclerosis along with chronic inflammation; this leads to increased risk of heart disease and stroke, significantly impacting patients' health. Danxia Tiaoban Decoction (DXTB), a traditional Chinese medicine (TCM) formula, has demonstrated positive clinical effects in treating AS; however, its mechanisms of action remain unclear.
Objective: To explore the potential mechanisms of action of DXTB in treating AS through multi-omics integration and experimental validation.
Eur J Pharmacol
September 2025
General Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, PR China. Electronic address:
We previously screened a peptide PDBAG1 that remarkably inhibited triple-negative breast cancer, and found that its target was C1QBP. Recently, C1QBP has been reported as a potential tumor marker in ovarian cancer, which of the mortality rate ranks first among malignant tumors of the female reproductive tract. However, it is unclear whether and how PDBAG1 plays a regulatory role in ovarian cancer.
View Article and Find Full Text PDFBiochim Biophys Acta Rev Cancer
September 2025
Department of Neurosurgery, The First Hospital of China Medical University, Nanjing Street 155, Heping District, Shenyang 110001, PR China. Electronic address:
The complement system, a cornerstone of innate immunity, plays pivotal roles in both defense and pathology, particularly through its anaphylatoxins, C3a and C5a. These small peptides, generated during complement activation, not only mediate pro-inflammatory responses but also contribute to the progression of various cancers by modulating the tumor microenvironment (TME). Anaphylatoxins influence tumor cell proliferation, epithelial-mesenchymal transition, angiogenesis, immune suppression, and therapy resistance via key signaling pathways such as PI3K/AKT, MEK/ERK, and p38 MAPK.
View Article and Find Full Text PDFBiomaterials
August 2025
Department of Anesthesiology and Perioperative Medicine, The Second Affiliated Hospital of Anhui Medical University, 678 Furong Road, Hefei, 230601, China; Key Laboratory of Anesthesiology and Perioperative Medicine of Anhui Higher Education Institutes, Anhui Medical University, 678 Furong Road, Hef
Activation of p38 mitogen-activated protein kinase plays an important role in the progression of ventricular muscle inflammation after myocardial ischemia-reperfusion (MI/R). The inhibition of p38 activation in ischemic myocardium can reduce ventricular muscle remodeling post-MI. However, owing to the dynamic change of p38 in ischemic myocardium after MI, the clinical therapeutic effect of p38 inhibitors is insufficient.
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