Cited by Novel Approaches to 3D Skin Cancer Models Usability in Research

The interconnective role of the UPS and autophagy in the quality control of cancer mitochondria DOI

Wanting Xu,

Lei Dong, Jiyan Dai

et al.

Cellular and Molecular Life Sciences, Journal Year: 2025, Volume and Issue: 82(1)

Published: Jan. 12, 2025

Uncontrollable cancer cell growth is characterized by the maintenance of cellular homeostasis through continuous accumulation misfolded proteins and damaged organelles. This review delineates roles two complementary synergistic degradation systems, ubiquitin–proteasome system (UPS) autophagy-lysosome system, in organelles for intracellular recycling. We emphasize interconnected decision-making processes systems maintaining homeostasis, such as biophysical state substrates, receptor oligomerization potentials (e.g., p62), compartmentalization capacities membrane structures). Mitochondria, hubs respiration metabolism, are implicated tumorigenesis. In subsequent sections, we thoroughly examine mechanisms mitochondrial quality control (MQC) preserving human cells. Notably, explored relationships between dynamics (fusion fission) various MQC processes—including UPS, proteases, mitophagy—in context repair pathways. Finally, assessed potential targeting (including molecular chaperones, dynamics, mitophagy biogenesis) therapeutic strategies. Understanding underlying may offer novel insights future therapies. highlights UPS degrading proteins, emphasizing substrate states, oligomerization, homeostasis. Innovatively links coordination to examining interplay these pathways varying degrees damage.

Language: Английский

Citations

CRIP1 inhibits cutaneous melanoma progression through TFAM-mediated mitochondrial biogenesis DOI

Jianqiang Wu, Lixia Chen,

Pengqiang Wen

et al.

Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)

Published: Feb. 4, 2025

Language: Английский

Citations

Telomere stabilization by metformin mitigates the progression of atherosclerosis via the AMPK-dependent p-PGC-1α pathway DOI

Jin Young Sung,

Seul Gi Kim, So‐Young Park

et al.

Experimental & Molecular Medicine, Journal Year: 2024, Volume and Issue: 56(9), P. 1967 - 1979

Published: Sept. 2, 2024

Abstract Telomere dysfunction is a well-known molecular trigger of senescence and has been associated with various age-related diseases, including atherosclerosis. However, the mechanisms involved have not yet elucidated, extent to which telomeres contribute atherosclerosis unknown. Therefore, we investigated mechanism metformin-induced telomere stabilization ability metformin inhibit vascular smooth muscle cell (VSMC) caused by advanced The present study revealed that inhibited phenotypes in VSMCs. Metformin increased phosphorylation AMPK-dependent PGC-1α thus telomerase activity protein level TERT OA-treated Mechanistically, AMPK only enhanced function but also TERT, whereas knockdown accelerated development senescent VSMCs regardless treatment. Furthermore, vivo results showed attenuated formation atherosclerotic plaque markers aortas HFD-fed ApoE KO mice. Although did reduce size, it AMPK/PGC-1α/TERT signaling cascade, maintenance progression formation, Accordingly, atherosclerosis-associated vitro vivo. These observations show enhancement specific pathways during findings suggest via AMPK/p-PGC-1α pathway might provide strategy for developing therapeutics against diseases such as

Language: Английский

Citations

Molecular Insights in the Anticancer Activity of Natural Tocotrienols: Targeting Mitochondrial Metabolism and Cellular Redox Homeostasis DOI

Raffaella Chiaramonte,

Giulia Sauro,

Domenica Giannandrea

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(1), P. 115 - 115

Published: Jan. 20, 2025

The role of mitochondria as the electric engine cells is well established. Over past two decades, accumulating evidence has pointed out that, despite presence a highly active glycolytic pathway (Warburg effect), functional and even upregulated mitochondrial respiration occurs in cancer to meet need high energy biosynthetic demand sustain their anabolic growth. Mitochondria are also primary source intracellular ROS. Cancer maintain moderate levels ROS promote tumorigenesis, metastasis, drug resistance; indeed, once cytotoxicity threshold exceeded, trigger oxidative damage, ultimately leading cell death. Based on this, metabolic functions generation considered attractive targets synthetic natural anticancer compounds. Tocotrienols (TTs), specifically δ- γ-TT isoforms, vitamin E-derived biomolecules widely shown possess striking properties since they regulate several molecular pathways. Herein, we provide for first time an overview reprogramming redox homeostasis perturbation occurring cells, highlighting involvement TTs. This sheds light use these compounds promising preventive or therapeutic approach novel strategies.

Language: Английский

Citations

Protective effect of dapagliflozin on lipopolysaccharide-induced acute lung injury via the SIRT-1/PGC-1α pathway DOI

Mehtap Savran,

Suleyman Emre Akin,

Hasan Ekrem Çamaş

et al.

Molecular Biology Reports, Journal Year: 2025, Volume and Issue: 52(1)

Published: Jan. 29, 2025

Language: Английский

Citations

Testes-specific protease 50 heightens stem-like properties and improves mitochondrial function in colorectal cancer DOI

Feng Gao, Sichen Liu, Yue Sun

et al.

Life Sciences, Journal Year: 2025, Volume and Issue: 370, P. 123560 - 123560

Published: March 12, 2025

Language: Английский

Citations

NDUFS3 promotes proliferation via glucose metabolism reprogramming inducing AMPK phosphorylating PRPS1 to increase the purine nucleotide synthesis in melanoma DOI

Guohang Xiong, Yun Fang, Lu Jiang

et al.

Cell Death and Differentiation, Journal Year: 2025, Volume and Issue: unknown

Published: May 22, 2025

Abstract NADH dehydrogenase [ubiquinone] iron-sulfur protein 3 (NDUFS3) is the core subunit of respiratory chain complex I (CI). We found NDUFS3 were abnormally elevated in human melanoma and promoted proliferation. Furthermore, could promote oxidative phosphorylation (OXPHOS) pentose phosphate pathway (PPP), as well attenuated glycolysis. As NDUFS3-mediated metabolic changes OXPHOS glucose metabolism, cells produced more ATP, resulting inhibition AMP kinase (AMPK). AMPK induced phosphoribosyl pyrophosphate synthetase1 (PRPS1) phosphorylation, which resulted suppressed PRPS1 activity. Briefly, NDUFS3-AMPK-PRPS1 signaling axis coupled OXPHOS, purine nucleotide biosynthesis to regulate Our study highlighted an unrecognized role for melanoma, might be used a potential therapeutic target treatment this type cancer.

Language: Английский

Citations

PAX translocations remodel mitochondrial metabolism through altered leucine usage in rhabdomyosarcoma DOI

Bhargab Kalita, Gerard Martínez-Cebrián, Justina McEvoy

et al.

Cell, Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Language: Английский

Citations

Neuroprotective effect of folic acid by maintaining DNA stability and mitochondrial homeostasis through ATM/CHK2/P53/PGC-1α pathway in Alcohol-exposed mice DOI

Nan Zhang, Huaqi Zhang, Xi Liang

et al.

Food & Function, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Excessive drinking leads to alcoholic brain injury, which is characterized by neuroinflammation, cognitive decline and motor dysfunction.

Language: Английский

Citations

Pleiotropic Regulation of PGC-1α in Tumor Initiation and Progression DOI

Yan Zhang,

Huakan Zhao,

Yongsheng Li

et al.

Antioxidants and Redox Signaling, Journal Year: 2024, Volume and Issue: 41(7-9), P. 557 - 572

Published: May 21, 2024

Mitochondria are recognized as a central metabolic hub with bioenergetic, biosynthetic, and signaling functions that tightly control key cellular processes. As crucial component of mitochondrial biogenesis, peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) is involved in regulating various pathways, including energy metabolism reactive oxygen species homeostasis.

Language: Английский

Citations