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| http://dx.doi.org/10.1097/MPA.0000000000001672 | DOI Listing |
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ZNF703 promotes Triple-Negative breast cancer cell progression and in combination with STK11 predicts disease recurrence (ZS -TNBC Model).
Gene
January 2025
Department of Nursing, The Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, China. Electronic address:
Background: It is largely unidentified concerning the underlying genetic causes responsible for triple-negative breast cancers (TNBC), with unpredictable disease recurrence. This study aimed to examine the role of ZNF703 (Zinc finger 703) in the malignant behaviors of TNBC and its role in predicting disease-free survival (DFS).
Methods: After downregulation of ZNF703 with short interfering RNA (siRNA), we examined the proliferation of TNBC cell line MDA-MB-231 by sulforhodamine B (SRB) assay, the invasion of cells by a transwell invasion model, and the migration of cells by the monolayer wound-healing experiment.
Objectives: To explore the landscape of BRCA1/2 mutations in gastric cancer patients.
Methods: Next-generation sequencing (NGS), Sanger sequencing, reverse transcription quantitative polymerase chain reaction (RT-qPCR), Immunohistochemistry, The Cancer Genome Atlas (TCGA), gnomAD, and DAVID.
Results: With 95% of bases boasting a phred score surpassing 30 and a minimum coverage depth of 500X, our NGS approach ensures high-quality data acquisition.
Synergistic Anticancer Efficacy of Curcumin and Doxorubicin Combination Treatment Inducing S-phase Cell Cycle Arrest in Triple-Negative Breast Cancer Cells: An In Vitro Study.
Cureus
December 2024
Department of Biochemistry, Era's Lucknow Medical College and Hospital, Era University, Lucknow, IND.
Background: Curcumin (Cur) is a polyphenol phyto-compound found in turmeric () that inhibits tumorigenesis by introducing apoptosis and restricting cell survival and proliferation. This in vitro research article focuses on the pharmacodynamic interactions of Cur combined with the commercial drug doxorubicin (Doxo) to enhance the cytotoxicity of Doxo at lower doses against triple-negative breast cancer cells (MDA-MB-231) with the chemo-protective effect against normal HEK293 cells. In this study, we observed the dose-dependent cytotoxicity, increased reactive oxygen species (ROS) generation, and increased chromatin condensation in combination doses compared to single doses.
View Article and Find Full Text PDFDynamic control of RNA-DNA hybrid formation orchestrates DNA2 activation at stalled forks by RNAPII and DDX39A.
Mol Cell
December 2024
Department of Gynecology, The Second Affiliated Hospital, Zhejiang University School of Medicine, 310058 Hangzhou, China; Department of Cell Biology, Zhejiang University School of Medicine, 310058 Hangzhou, China. Electronic address:
Stalled replication forks, susceptible to nucleolytic threats, necessitate protective mechanisms involving pivotal factors such as the tumor suppressors BRCA1 and BRCA2. Here, we demonstrate that, upon replication stress, RNA polymerase II (RNAPII) is recruited to stalled forks, actively promoting the transient formation of RNA-DNA hybrids. These hybrids act as safeguards, preventing premature engagement by the DNA2 nuclease and uncontrolled DNA2-mediated degradation of nascent DNA.
View Article and Find Full Text PDFPNKP safeguards stalled replication forks from nuclease-dependent degradation during replication stress.
Cell Rep
December 2024
Department of Oncology, Faculty of Medicine & Dentistry, University of Alberta, 11560 University Avenue, Edmonton, AB T6G 1Z2, Canada; Biophysics Department, Faculty of Science, Cairo University, Giza 12613, Egypt. Electronic address:
Uncontrolled degradation and collapse of stalled replication forks (RFs) are primary sources of genomic instability, yet the molecular mechanisms for protecting forks from degradation/collapse remain to be fully elaborated. Here, we show that polynucleotide kinase-phosphatase (PNKP) localizes at stalled forks and protects stalled forks from excessive degradation. The loss of PNKP results in nucleolytic degradation of nascent DNA at stalled RFs.
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