Renal cell carcinoma (RCC) is the most common renal tumour in adults. Altered levels of secondary messengers, that is, intracellular calcium and cyclic AMP (cAMP), have been implicated in the pathogenesis of various malignancies. In the present study, we measured levels of intracellular calcium and cAMP in RCC. The intracellular calcium level was significantly reduced, whereas the cAMP level was significantly augmented in RCC as compared with adjacent grossly normal renal parenchyma.
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http://dx.doi.org/10.1002/cbf.2913 | DOI Listing |
Nat Commun
January 2025
Center for Integrative Genomics, University of Lausanne, Faculty of Biology and Medicine, Lausanne, Switzerland.
The energetic demands of proliferating cells during tumorigenesis require close coordination between the cell cycle and metabolism. While CDK4 is known for its role in cell proliferation, its metabolic function in cancer, particularly in triple-negative breast cancer (TNBC), remains unclear. Our study, using genetic and pharmacological approaches, reveals that CDK4 inactivation only modestly impacts TNBC cell proliferation and tumor formation.
View Article and Find Full Text PDFInt J Biochem Cell Biol
January 2025
Symbiosis Centre for Stem Cell Research, Symbiosis School of Biological Sciences, Lavale, Pune, India. Electronic address:
Mesenchymal stromal cells (MSCs) isolated from tissues such as bone marrow, cord, cord blood, etc., are frequently used as feeder layers to expand hematopoietic stem/ progenitor cells (HSCs/HSPCs) in vitro. They are also co-infused with the HSCs to improve the efficacy of transplantation.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Texas Tech University Health Sciences Center, Lubbock, TX, USA.
Background: The present study delves into the intricate molecular connections between ischemic stroke (IS) and Alzheimer's disease (AD) through an analysis of mitochondrial microRNA (miRNA) patterns. By exploring their shared signatures in the context of IS and AD, our aim is to unravel potential common pathways, understand shared molecular mechanisms, explore diagnostic and therapeutic opportunities, gain a comprehensive understanding of neurodegeneration, and advance the field of biomarker research.
Method: To explore these intriguing questions, mitochondria were isolated from postmortem brains of individuals with IS, AD, and healthy controls (n=10 each).
Alzheimers Dement
December 2024
Department of Psychiatry, University of Cambridge, Cambridge, UK.
Background: Combinations of blood-based biomarkers have been used to detect Alzheimer's disease (AD). While these markers provide information about neuropathology, they fail to integrate the cellular dysfunction, such as disease-associated defects in lysosomal ion homeostasis. To understand cellular dysfunction in AD and its relation to the pathophysiology of the disease, we developed a multi-modal biomarker diagnostic platform that incorporates lysosomal ionic pH and Ca and plasma levels of Amyloid beta (Aβ), Amyloid beta (Aβ), phosphorylated Tau181 (pTau181), Neurofilament light (NfL) and Glial fibrillary acidic protein (GFAP).
View Article and Find Full Text PDFBackground: While the formation of β-amyloid plaques and neurofibrillary "tau" tangles are considered hallmarks of AD pathology, therapeutic targeting of these pathways has been unsuccessful, highlighting the necessity to define the underlying molecular mechanisms driving AD progression. Previous studies from our lab demonstrated that mitochondrial calcium (Ca) overload through neuronal ablation of the mitochondrial Na/Ca exchanger (NCLX) is sufficient to trigger 'AD-like' pathology, including mitochondrial dysfunction, amyloid deposition and tau pathology, and cognitive decline. In addition, we found significant proteomic remodeling of components of the mitochondrial calcium uniporter channel (mtCU), the primary mediator of Ca uptake, in frontal cortex samples isolated post-mortem from patients diagnosed with non-familial/sporadic AD.
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