Results 101 to 110 of about 1,210,728 (258)
Molecular Oncology, EarlyView.TGF‐β has a complex role in cancer, exhibiting both tumor‐suppressive and tumor‐promoting properties. Using a series of differentiated tumoroids, derived from different stages and mutational background of colorectal cancer patients, we replicate this duality of TGF‐β in vitro. Notably, the atypical but highly aggressive KRASQ22K mutation rendered early‐
Theresia Mair +17 more
wiley +1 more source
Molecular Oncology, EarlyView.Chronic TGF‐β exposure drives epithelial HCC cells from a senescent state to a TGF‐β resistant mesenchymal phenotype. This transition is characterized by the loss of Smad3‐mediated signaling, escape from senescence, enhanced invasiveness and metastatic potential, and upregulation of key resistance modulators such as MARK1 and GRM8, ultimately promoting
Minenur Kalyoncu +11 more
wiley +1 more source
Interplay of integrins and selectins in metastasis
Molecular Oncology, EarlyView.Here we review the role of integrins and their interplay with selectins in metastasis. The efficacy of integrin‐targeted therapies may be reduced in tumors where metastasis relies heavily on selectins. In certain tumors, integrins and selectins exhibit a synergistic interaction during intraperitoneal dissemination.
Diana Maltseva +2 more
wiley +1 more source
Molecular Oncology, EarlyView.B‐cell chronic lymphocytic leukemia (B‐CLL) and monoclonal B‐cell lymphocytosis (MBL) show altered proteomes and phosphoproteomes, analyzed using mass spectrometry, protein microarrays, and western blotting. Identifying 2970 proteins and 316 phosphoproteins, including 55 novel phosphopeptides, we reveal BCR and NF‐kβ/STAT3 signaling in disease ...
Paula Díez +17 more
wiley +1 more source
Ubiquitination of transcription factors in cancer: unveiling therapeutic potential
Molecular Oncology, EarlyView.In cancer, dysregulated ubiquitination of transcription factors contributes to the uncontrolled growth and survival characteristics of tumors. Tumor suppressors are degraded by aberrant ubiquitination, or oncogenic transcription factors gain stability through ubiquitination, thereby promoting tumorigenesis.
Dongha Kim, Hye Jin Nam, Sung Hee Baek
wiley +1 more source
Targeted protein degradation in oncology: novel therapeutic opportunity for solid tumours?
Molecular Oncology, EarlyView.Current anticancer therapies are limited by the occurrence of resistance and undruggability of most proteins. Targeted protein degraders are novel, promising agents that trigger the selective degradation of previously undruggable proteins through the recruitment of the ubiquitin–proteasome machinery. Their mechanism of action raises exciting challenges,
Noé Herbel, Sophie Postel‐Vinay
wiley +1 more source
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
Molecular Oncology, EarlyView.Breast cancer metastasis is associated with myeloid cell dysregulation and the lung‐specific accumulation of tumor‐supportive Gr1+ cells. Gr1+ cells support metastasis, in part, through a CHI3L1‐mediated mechanism, which can be targeted and inhibited with cargo‐free, polymeric nanoparticles.
Jeffrey A. Ma +9 more
wiley +1 more source
CINs of the cytoplasm: dissecting dsRNA signaling in chromosomal instability
Molecular Oncology, EarlyView.Micronuclei, formed during cell division in chromosomal instability settings, rupture and lead to the accumulation of immunogenic double‐stranded RNA in the cytoplasm, activating MAVS‐dependent interferon signaling and innate antitumor immunity.
Aglaia Skolariki +2 more
wiley +1 more source