Results 91 to 100 of about 233,797 (295)
Urokinase Expression by Tumor Suppressor Protein p53 [PDF]
Lung carcinoma (H1299) cells deficient in p53 (p53(-/-)) express large amounts of urokinase-type plasminogen activator (uPA) protein and uPA mRNA, and exhibit slower degradation of uPA mRNA than that of p53-expressing nonmalignant Beas2B human airway epithelial cells. Expression of p53 protein in H1299 cells, upon transfection with p53 cDNA, suppressed
Praveenkumar, Shetty +5 more
openaire +2 more sources
CIN85 is highly expressed in osteosarcoma, particularly in metastatic lesions. Its overexpression increases cell migration and Matrigel invasion, while silencing CIN85 suppresses these behaviors. Transcriptome analysis shows that CIN85 regulates MMP2, COL3A1, and Akt/mTOR signaling. Targeting these pathways reverses CIN85‐induced motility, highlighting
Iryna Horak +10 more
wiley +1 more source
The purpose of the study was to determine the frequency of expression p53 and p16INK4a proteins and bcl2- oncoprotein in malignant skin melanoma and to determine their correlation with the proliferative index and tumor thickness.
Miloš Kostov +5 more
doaj +1 more source
An evaluation of the efficacy of adenovirus-mediated gene therapy with p53 for the treatment of cancer [PDF]
Cancer is the second leading cause of mortality in the United States today, and equally prevalent throughout the world. Traditional treatments such as chemotherapy and radiotherapy have thus far proven unable to treat the disease with high efficacy, with
Liepart IV, George Hampson
core +1 more source
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis +3 more
wiley +1 more source
p53 Genetics and Biology in Lung Carcinomas: Insights, Implications and Clinical Applications
The TP53 gene is renowned as a tumor suppressor, playing a pivotal role in overseeing the cell cycle, apoptosis, and maintaining genomic stability. Dysregulation of p53 often contributes to the initiation and progression of various cancers, including ...
Dixan A. Benitez +7 more
doaj +1 more source
Anchorage‐independent and faster growth in clonal population from UV‐irradiated NER‐deficient cells
UV‐irradiated cells expressing a DDB2 mutant protein unable to interact with PCNA (DDB2PCNA‐) form clones able to grow without anchorage. Different experimental approaches reveal heterogeneity in cell cycle regulation and drug response within these clones, emphasizing the crucial role of the DDB2‐PCNA interaction in preventing cellular transformation ...
Paola Perucca +6 more
wiley +1 more source
Protein methylation: a new mechanism of p53 tumor suppressor regulation.
The tumor suppressor p53 is the most frequently inactivated gene in human cancers. The p53 protein functions as a sequence-specific transcription factor to regulate key cellular processes, including cell-cycle arrest, DNA repair, apoptosis, and senescence in response to stress signals.
Scoumanne, A., Chen, X.
openaire +3 more sources
BCR/ABL Recruits p53 Tumor Suppressor Protein to Induce Drug Resistance [PDF]
Tumors expressing the ABL oncoproteins (BCR/ABL, TEL/ABL, v-ABL) can avoid apoptosis triggered by DNA damaging agents. The tumor suppressor protein p53 is an important activator of apoptosis in normal cells; conversely its functional loss may cause drug resistance.
Tomasz, Stoklosa +6 more
openaire +2 more sources
Chemotherapy side effects significantly impact cancer survivors' quality of life. Using protein levels in blood samples from breast cancer patients before and after 12 weeks of taxane treatment, we detected treatment‐dependent changes in calcium signaling and aging pathways associated with cancer recurrence.
Saira Munshani +6 more
wiley +1 more source

