ArticleOncogenesis2022
ZNF655 accelerates progression of pancreatic cancer by promoting the binding of E2F1 and CDK1.
Article in Oncogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Trace Elements in the Pancreas: From Physiological Homeostasis to the Pathogenesis of Diabetes, Pancreatitis, and Cancer-A Review.Life (Basel, Switzerland) · 2026Review
- Oncogenic GPRIN1 sustains proliferation and mitochondrial homeostasis via dual‑layer CDK1-PI3K/Akt signalling in gallbladder cancer.Cell death & disease · 2026Article
- RRP9 Promotes Esophageal Squamous Cell Carcinoma Progression through E2F1 Transcriptional Regulation of CDK1.Advanced biology · 2025Article
- ZNF655 promotes tumor growth and chemoresistance by targeting MAFF-CCND1 axis in ovarian cancer.Cancer cell international · 2025Article
- The zinc finger protein560(ZNF560) functions as a novel oncogenic gene in osteosarcoma.Scientific reports · 2025Article
- From oncogenesis to prognosis: the roles of the immunoproteasome in cancer.Frontiers in immunology · 2025Review
- E2F transcription factors promote tumorigenicity in pancreatic ductal adenocarcinoma.Cancer medicine · 2024Article
- E2F1 rs3213150 polymorphism influences cytarabine sensitivity and prognosis in patients with acute myeloid leukemia.Annals of hematology · 2023Article
- Catalpol inhibits hepatic stellate cell activation by reducing the formation and changing the contents of hepatocyte-derived extracellular vesicles.Journal of cell communication and signaling · 2023Article
- Long-range RNA structures in the human transcriptome beyond evolutionarily conserved regions.PeerJ · 2023Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic cancer has an extremely terrible prognosis and is a common cause of cancer death. In this study, the clinic value, biological function and underlying mechanisms of Zinc finger protein 655 (ZNF655) in human pancreatic cancer were evaluated. The expression level of ZNF655 in pancreatic cancer was determined by immunohistochemistry (IHC) staining. The biological effects of ZNF655 in pancreatic cancer cells was investigated by loss/gain-of-function assays in vitro and in vivo. The downstream molecular mechanism of ZNF655 was explored using co-immunoprecipitation (Co-IP), dual-luciferase reporter and chromatin immunoprecipitation (Ch-IP). ZNF655 expression was significantly elevated in human pancreatic cancer and possessed clinical value in predicting poor prognosis. Functionally, ZNF655 knockdown inhibited the biological progression of pancreatic cancer cells, which was characterized by weaken proliferation, enhanced apoptosis, arrested cell cycle in G2, impeded migration, and suppressed tumor growth. Mechanistically, ZNF655 played an important role in promoting the binding of E2F transcription factor 1 (E2F1) to the cyclin-dependent kinase 1 (CDK1) promoter. Furthermore, knockdown of CDK1 alleviated the promoting effects of ZNF655 overexpression in pancreatic cancer cells. The promotive role of ZNF655 in pancreatic cancer via CDK1 was determined, which drew further interest regarding its clinical application as a promising therapeutic target.
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Registered trials
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