Publications by authors named "Cheng-Kuei Wu"
Replication stress converts the stalled forks into reversed forks, which is an important protection mechanism to prevent fork degradation and collapse into poisonous DNA double-strand breaks (DSBs). Paradoxically, the mechanism also acts in cancer cells to contribute to chemoresistance against various DNA-damaging agents. PARP1 binds to and is activated by stalled forks to facilitate fork reversal.
View Article and Find Full Text PDFBone morphogenetic protein 2 (BMP2) is highly overexpressed in human non-small cell lung cancer (NSCLC) and correlates with tumor stage and metastatic burden. Although several lines of evidence suggest that BMP2 promotes cell migration and invasiveness in vitro, the in vivo role of BMP2 in the metastasis of lung adenocarcinoma cells remains less well understood. Here, we revealed that BMP2 is highly overexpressed in lung adenocarcinoma patients with lymph node metastasis compared with patients without lymph node metastasis.
View Article and Find Full Text PDFHuman HLTF participates in the lesion-bypass mechanism through the fork reversal structure, known as template switching of post-replication repair. However, the mechanism by which HLTF promotes the replication progression and fork stability of damaged forks remains unclear. Here, we identify a novel protein-protein interaction between HLTF and PARP1.
View Article and Find Full Text PDFArticle Synopsis
- The study focuses on the Fanconi anemia pathway and how TIP60, an acetyltransferase, is linked to DNA repair, especially in repairing interstrand crosslinks (ICLs) caused by the cancer drug cisplatin.
- Researchers found that nasopharyngeal carcinoma cells resistant to cisplatin exhibited higher levels of TIP60, which binds to and activates genes like FANCD2 and BRCA1 that are crucial for DNA repair.
- The depletion of TIP60 impairs homologous recombination efficiency and leads to an increase in DNA damage, highlighting its role in maintaining genomic stability and promoting resistance to cisplatin treatment.
Article Synopsis
- Cisplatin, a common chemotherapy drug for cancer, creates crosslinks in DNA that can lead to drug resistance, particularly in nasopharyngeal carcinoma (NPC) cells.
- Chronic exposure to cisplatin increases homologous recombination (HR), enabling NPC cells to become resistant through a high frequency of sister chromatid exchanges and elevated expression of certain DNA repair genes.
- By targeting genes involved in HR, template switching (TS), or the Fanconi anemia (FA) pathway, researchers can potentially overcome cisplatin resistance in cancer treatment.