NF-κB plays a pivotal role in oncogenesis. This transcription factor is best known for promoting cancer cell survival and tumour-driving inflammation. However, several lines of evidence support a crucial role for NF-κB in governing energy homeostasis and mediating cancer metabolic reprogramming. Mitochondria are central players in many metabolic processes altered in cancer. Beyond their bioenergetic activity, several facets of mitochondria biology, including mitochondrial dynamics and oxidative stress, promote and sustain malignant transformation. Recent reports revealed an intimate connection between NF-κB pathway and the oncogenic mitochondrial functions. NF-κB can impact mitochondrial respiration and mitochondrial dynamics, and, reciprocally, mitochondria can sense stress signals and convert them into cell biological responses leading to NF-κB activation. In this review we discuss their emerging reciprocal regulation and the significance of this interplay for anticancer therapy.
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http://dx.doi.org/10.1016/j.semcdb.2019.05.021 | DOI Listing |
Neurochem Int
January 2025
Department of Environmental and Occupational Health, School of Public Health, Guangdong Medical University, Dongguan, 523808, PR China; Dongguan Key Laboratory of Environmental Medicine, School of Public Health, Guangdong Medical University, Dongguan, 523808, PR China. Electronic address:
Neurodegenerative diseases are a group of diseases that pose a serious threat to human health, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD) and Amyotrophic Lateral Sclerosis (ALS). In recent years, it has been found that mitochondrial remodeling plays an important role in the onset and progression of neurodegenerative diseases. Mitochondrial remodeling refers to the dynamic regulatory process of mitochondrial morphology, number and function, which can affect neuronal cell function and survival by regulating mechanisms such as mitochondrial fusion, division, clearance and biosynthesis.
View Article and Find Full Text PDFInt J Biol Macromol
January 2025
College of Chemistry and Life Science, Beijing University of Technology, Beijing 100124, China; Beijing Institute of Radiation Medicine, Beijing 100850, China; School of Pharmacy, Guangdong Pharmaceutical University, Guangzhou 510006, China. Electronic address:
Neuroinflammation is a key driver of neurological disorders. Evodiamine (EVO), an alkaloid from the traditional Chinese herb Evodia rutaecarpa, possesses potent biological activities, notably anticancer and anti-inflammatory effects. This study investigates EVO's potential to attenuate LPS-induced neuroinflammation, focusing on identifying its therapeutic targets and mechanisms of action.
View Article and Find Full Text PDFNeuro Oncol
January 2025
Department of Pathology, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada.
Adv Mater
January 2025
Príncipe Felipe Research Center, Polymer Therapeutics Lab., Valencia, 46012, Spain.
Mitochondria play critical roles in regulating cell fate, with dysfunction correlating with the development of multiple diseases, emphasizing the need for engineered nanomedicines that cross biological barriers. Said nanomedicines often target fluctuating mitochondrial properties and/or present inefficient/insufficient cytosolic delivery (resulting in poor overall activity), while many require complex synthetic procedures involving targeting residues (hindering clinical translation). The synthesis/characterization of polypeptide-based cell penetrating diblock copolymers of poly-L-ornithine (PLO) and polyproline (PLP) (PLO-PLP, n:m ratio 1:3) are described as mitochondria-targeting nanocarriers.
View Article and Find Full Text PDFCancers (Basel)
January 2025
Department of Radiotherapy, Universitair Ziekenhuis Brussel, Vrije Universiteit Brussel, 1090 Brussels, Belgium.
FLASH radiotherapy (FLASH RT) is an innovative modality in cancer treatment that delivers ultrahigh dose rates (UHDRs), distinguishing it from conventional radiotherapy (CRT). FLASH RT has demonstrated the potential to enhance the therapeutic window by reducing radiation-induced damage to normal tissues while maintaining tumor control, a phenomenon termed the FLASH effect. Despite promising outcomes, the precise mechanisms underlying the FLASH effect remain elusive and are a focal point of current research.
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