Results 61 to 70 of about 109,926 (267)

Metabolic reprogramming in liver fibrosis

Cell Metabolism
Chronic liver diseases, primarily metabolic dysfunction-associated steatotic liver disease (MASLD), harmful use of alcohol, or viral hepatitis, may result in liver fibrosis, cirrhosis, and cancer. Hepatic fibrogenesis is a complex process with interactions between different resident and non-resident heterogeneous liver cell populations, ultimately ...
Paul Horn, Frank Tacke
openaire   +2 more sources

Dammarenediol II enhances etoposide‐induced apoptosis by targeting O‐GlcNAc transferase and Akt/GSK3β/mTOR signaling in liver cancer

Molecular Oncology, EarlyView.
Etoposide induces DNA damage, activating p53‐dependent apoptosis via caspase‐3/7, which cleaves PARP1. Dammarenediol II enhances this apoptotic pathway by suppressing O‐GlcNAc transferase activity, further decreasing O‐GlcNAcylation. The reduction in O‐GlcNAc levels boosts p53‐driven apoptosis and influences the Akt/GSK3β/mTOR signaling pathway ...
Jaehoon Lee, Byung‐Cheol Han, Gi‐Bang Koo, Jihye Park, Mijin Kwon, Young Bin Park, Jae‐Mun Choi, Seung‐Ho Lee, Sangho Roh   +8 more
wiley   +1 more source

The role of metabolic reprogramming in kidney cancer

Frontiers in Oncology
Metabolic reprogramming is a cellular process in which cells modify their metabolic patterns to meet energy requirements, promote proliferation, and enhance resistance to external stressors.
Ziyi Chen, Xiaohong Zhang, Xiaohong Zhang, Xiaohong Zhang   +3 more
doaj   +1 more source

The circadian clock CRY1 regulates pluripotent stem cell identity and somatic cell reprogramming

Cell Reports, 2023
Summary: Distinct metabolic conditions rewire circadian-clock-controlled signaling pathways leading to the de novo construction of signal transduction networks.
Shogo Sato, Tomoaki Hishida, Kenichiro Kinouchi, Fumiaki Hatanaka, Yumei Li, Quy Nguyen, Yumay Chen, Ping H. Wang, Kai Kessenbrock, Wei Li, Juan Carlos Izpisua Belmonte, Paolo Sassone-Corsi   +11 more
doaj   +1 more source

Metabolic Reprogramming in Thyroid Cancer

Endocrinology and Metabolism
Thyroid cancer is a common endocrine malignancy with increasing incidence globally. Although most cases can be treated effectively, some cases are more aggressive and have a higher risk of mortality. Inhibiting RET and BRAF kinases has emerged as a potential therapeutic strategy for the treatment of thyroid cancer, particularly in cases of advanced or ...
Sang-Hyeon Ju, Minchul Song, Joung Youl Lim, Yea Eun Kang, Hyon-Seung Yi, Minho Shong   +5 more
openaire   +3 more sources

Targeting p38α in cancer: challenges, opportunities, and emerging strategies

Molecular Oncology, EarlyView.
p38α normally regulates cellular stress responses and homeostasis and suppresses malignant transformation. In cancer, however, p38α is co‐opted to drive context‐dependent proliferation and dissemination. p38α also supports key functions in cells of the tumor microenvironment, including fibroblasts, myeloid cells, and T lymphocytes.
Angel R. Nebreda
wiley   +1 more source

Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment

Molecular Oncology, EarlyView.
This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley   +1 more source

Metabolic Reprogramming of Chemoresistant Cancer Cells and the Potential Significance of Metabolic Regulation in the Reversal of Cancer Chemoresistance

Metabolites, 2020
Metabolic reprogramming is one of the hallmarks of tumors. Alterations of cellular metabolism not only contribute to tumor development, but also mediate the resistance of tumor cells to antitumor drugs.
Xun Chen, Shangwu Chen, Dongsheng Yu
doaj   +1 more source

Network divergence analysis identifies adaptive gene modules and two orthogonal vulnerability axes in pancreatic cancer

Molecular Oncology, EarlyView.
Tumors contain diverse cellular states whose behavior is shaped by context‐dependent gene coordination. By comparing gene–gene relationships across biological contexts, we identify adaptive transcriptional modules that reorganize into distinct vulnerability axes.
Brian Nelson, Lyanne Delgado‐Coka, Natalia Marchenko, Luisa F. Escobar‐Hoyos, Kenneth R. Shroyer, Alisa Yurovsky, Trey Ideker, Gabor Balázsi, Thomas MacCarthy, Scott Powers   +9 more
wiley   +1 more source

RIPK4 function interferes with melanoma cell adhesion and metastasis

Molecular Oncology, EarlyView.
RIPK4 promotes melanoma growth and spread. RIPK4 levels increase as skin lesions progress to melanoma. CRISPR/Cas9‐mediated deletion of RIPK4 causes melanoma cells to form less compact spheroids, reduces their migratory and invasive abilities and limits tumour growth and dissemination in mouse models.
Norbert Wronski, Sławomir Lasota, Ewelina Madej, Anna A. Brożyna, Małgorzata Szczygieł, Agnieszka Harazin‐Lechowska, Jan Czerbniak, Janusz Rys, Jaroslaw Czyz, Agnieszka Wolnicka‐Glubisz   +9 more
wiley   +1 more source