Results 61 to 70 of about 16,586,228 (338)
Molecular Oncology, EarlyView.TOMM20 increases cancer aggressiveness by maintaining a reduced state with increased NADH and NADPH levels, oxidative phosphorylation (OXPHOS), and apoptosis resistance while reducing reactive oxygen species (ROS) levels. Conversely, CRISPR‐Cas9 knockdown of TOMM20 alters these cancer‐aggressive traits.
Ranakul Islam +9 more
wiley +1 more source
Journal of the American Society of Nephrology, 2018 Background Ischemia-reperfusion injury (IRI) is a major risk factor for chronic renal failure. Here, we characterize the different modes of programmed cell death in the tubular and microvascular compartments during the various stages of IRI-induced AKI ...
Bing Yang +9 more
semanticscholar +1 more source
Molecular Oncology, EarlyView.This study investigates an alternative approach to reactivating the oncosuppressor p53 in cancer. A short peptide targeting the association of the two p53 inhibitors, MDM2 and MDM4, induces an otherwise therapeutically active p53 with unique features that promote cell death and potentially reduce toxicity towards proliferating nontumor cells.
Sonia Valentini +10 more
wiley +1 more source
Cleaved Caspase-3 transcriptionally regulates angiogenesis promoting chemotherapy resistance.
Cancer Research, 2019 Caspases are well-known for their role in apoptosis. Recently, non-apoptotic roles of caspases have been identified, however, these non-canonical roles are not well-documented and the mechanisms involved are not fully understood.
Antoine Bernard +15 more
semanticscholar +1 more source
Coxsackievirus B3-induced apoptosis and Caspase-3 [PDF]
Cell Research, 2003 Cell death can be classified into two categories: apoptosis and necrosis. Apoptotic pathway can be either caspase-dependent or caspase-independent. Caspase-independent cytopathic effect (CPE) has been described. In order to evaluate the pattern of HeLa cell death induced by Coxsackievirus B3 (CVB3) and whether apoptosis involves caspase activation, we ...
Jianping Yuan +6 more
openaire +3 more sources
Molecular Oncology, EarlyView.Nuclear prothymosin α inhibits epithelial‐mesenchymal transition (EMT) in lung cancer by increasing Smad7 acetylation and competing with Smad2 for binding to SNAI1, TWIST1, and ZEB1 promoters. In early‐stage cancer, ProT suppresses TGF‐β‐induced EMT, while its loss in the nucleus in late‐stage cancer leads to enhanced EMT and poor prognosis.
Liyun Chen +12 more
wiley +1 more source
Determination of ADP/ATP translocase isoform ratios in malignancy and cellular senescence
Molecular Oncology, EarlyView.The individual functions of three isoforms exchanging ADP and ATP (ADP/ATP translocases; ANTs) on the mitochondrial membrane remain unclear. We developed a method for quantitatively differentiating highly similar human ANT1, ANT2, and ANT3 using parallel reaction monitoring. This method allowed us to assess changes in translocase levels during cellular
Zuzana Liblova +18 more
wiley +1 more source
CASPASE DEPENDENT APOPTOSIS INDUCED BY CLADRIBINE IN THE ESTROGEN RECEPTOR NEGATIVE BREAST CANCER CELL LINE, MDA-MB468 [PDF]
Journal of Sciences, Islamic Republic of Iran, 2003 The purpose of the present study is to investigate the cytotoxicity/apoptotic effect of 2-chloro-2′-deoxyadenosine, cladribine, (2-CdA) in the human breast cancer cell line, MDA-MB468 (estrogen receptor negative, ER−). MTT [3-(4,5-dimethyl-2-thiazolyl)-2,
F. Karami-Tehrani
doaj
Frontiers in Pharmacology, 2018 Cytotoxic chemotherapy, still the most widely adopted anticancer treatment, aims at eliminating cancer cells inducing apoptosis with DNA damaging agents, exploiting the differential replication rate of cancer vs.
Emanuele Bruni +5 more
doaj +1 more source
TRPM8 levels determine tumor vulnerability to channel agonists
Molecular Oncology, EarlyView.TRPM8 is a Ca2+ permissive channel. Regardless of the amount of its transcript, high levels of TRPM8 protein mark different tumors, including prostate, breast, colorectal, and lung carcinomas. Targeting TRPM8 with channel agonists stimulates inward calcium currents followed by emptying of cytosolic Ca2+ stores in cancer cells.
Alessandro Alaimo +18 more
wiley +1 more source