Results 41 to 50 of about 8,472,955 (236)
FEBS Letters, EarlyView.This review focuses on the role of autophagy and mitophagy in maintaining pancreatic β‐cell function and homeostasis. We discuss how genetic defects affecting these pathways contribute to the development of type 1, type 2, monogenic, and gestational diabetes. We further explore their potential as therapeutic targets. Created in BioRender.
Yunkyeong Lee +2 more
wiley +1 more source
Metastatic niche shaped by host factors influences disseminated cancer cell fate
FEBS Letters, EarlyView.Metastasis is shaped not only by cancer cells but also by the environments they encounter. This review explores how factors such as aging, diet, the microbiome, lifestyle, and environmental exposures remodel organ‐specific niches in the lung, liver, bone, and brain, influencing where metastatic cells survive, remain dormant, or grow, and ultimately ...
Gwennan Delyth Ward +2 more
wiley +1 more source
Smart Medicine, 2023 TP53 mutation frequently occurs in hepatocellular carcinoma (HCC). Senescence also plays a vital role in the ongoing process of HCC. P53 is believed to regulate the advancement of senescence in HCC.
Yu‐Yan Chen +10 more
doaj +1 more source
NLRP1 inflammasome promotes senescence and senescence-associated secretory phenotype [PDF]
International audienceAbstract Background Senescence is a cellular aging-related process triggered by different stresses and characterized by the secretion of various inflammatory factors referred to as senescence-associated secretory phenotype (SASP ...
Gallardo-Orihuela, Andrea +14 more
core +1 more source
MLL1 is essential for the senescence-associated secretory phenotype [PDF]
, 2016 Oncogene-induced senescence (OIS) and therapy-induced senescence (TIS), while tumor-suppressive, also promote procarcinogenic effects by activating the DNA damage response (DDR), which in turn induces inflammation.
Shah, Parisha P. +14 more
core +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
Molecular Oncology, EarlyView.Single‐cell multi‐omics reveals epigenetic heterogeneity across therapy‐adaptive tumor states, including quiescent/dormant, drug‐tolerant persister, and EMT‐like phenotypes. By linking regulatory features with state‐associated biomarkers, these approaches inform biomarker‐guided therapeutic strategies for evolving tumors.
Hee Jung Kim +3 more
wiley +1 more source
Androgen Depletion Induces Senescence in Prostate Cancer Cells through Down-regulation of Skp2
Neoplasia: An International Journal for Oncology Research, 2011 Although the induction of senescence in cancer cells is a potent mechanism of tumor suppression, senescent cells remain metabolically active and may secrete a broad spectrum of factors that promote tumorigenicity in neighboring malignant cells.
Zuzana Pernicová +8 more
doaj +1 more source
The senescence-associated secretory phenotype as a driver of tumor growth: does G3BP1 hold the key?
, 2021 Cellular senescence is a double-edged sword that, depending on the context, acts as either a potent tumor protective mechanism or an age-related driver of diseases such as cancer.
Amr Omer +2 more
core +1 more source
CEACAM1 participation in breast cancer progression
Molecular Oncology, EarlyView.In invasive breast cancer (BC), CEACAM1 shifts from an apical to a uniform membranous/cytoplasmic pattern, or is lost, as tumors dedifferentiate, inversely tracking the Ki‐67 proliferative index. In MCF‐7 cells, only CEACAM1‐4L suppresses proliferation, repressing cell cycle and growth factor genes.
Mykola Lyndin +3 more
wiley +1 more source