ArticlePloS one2011
Up-regulation of kin17 is essential for proliferation of breast cancer.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- Regulation of EMT and cholangiocarcinoma metastasis by KIN17 through the mTOR signaling pathway.Molecular and cellular biochemistry · 2026Article
- Proteomic analysis of the zone of degeneration at the mitosis-meiosis transition stage in wild-caught male catshark (Scyliorhinus canicula), correlated with an unusually high-water temperature in the English Channel.Journal of fish biology · 2026Article
- Kin17 promotes rDNA transcription, ribosomal biogenesis, and cortical lamination.EMBO reports · 2025Article
- DNA/RNA-binding protein KIN17 supports esophageal cancer progression via resolving noncanonical STING activation induced by R-loop.Signal transduction and targeted therapy · 2025Article
- KIN17 modulates the WNT/β-catenin pathway and epithelial mesenchymal transition in non-small cell lung cancer.Scientific reports · 2025Article
- Onvansertib and Navitoclax Combination as a New Therapeutic Option for Mucinous Ovarian Carcinoma.International journal of molecular sciences · 2025Article
- KIN17 functions in DNA damage repair and chemosensitivity by modulating RAD51 in hepatocellular carcinoma.Human cell · 2024Article
- Kin17 regulates proper cortical localization of Miranda in Drosophila neuroblasts by regulating Flfl expression.Cell reports · 2024Article
- Article
- Roles and regulatory mechanisms of KIN17 in cancers (Review).Oncology letters · 2023Review
- A genetic screen in C. elegans reveals roles for KIN17 and PRCC in maintaining 5' splice site identity.PLoS genetics · 2022Article
- Deficiency of kin17 Facilitates Apoptosis of Cervical Cancer Cells by Modulating Caspase 3, PARP, and Bcl-2 Family Proteins.Journal of oncology · 2022Article
- Interactome Analysis of KIN (Kin17) Shows New Functions of This Protein.Current issues in molecular biology · 2021Article
- KIN17 promotes tumor metastasis by activating EMT signaling in luminal-A breast cancer.Thoracic cancer · 2021Article
- Analysis of the association between KIN17 expression and the clinical features/prognosis of epithelial ovarian cancer, and the effects of KIN17 in SKOV3 cells.Oncology letters · 2021Article
- Kin17 facilitates thyroid cancer cell proliferation, migration, and invasion by activating p38 MAPK signaling pathway.Molecular and cellular biochemistry · 2021Article
- Kin17 knockdown suppresses the migration and invasion of cervical cancer cells through NF-κB-Snail pathway.International journal of clinical and experimental pathology · 2020Article
- Integrative genomic analysis identifies associations of molecular alterations to APOBEC and BRCA1/2 mutational signatures in breast cancer.Molecular genetics & genomic medicine · 2019Article
- Knockdown of DNA/RNA-binding protein KIN17 promotes apoptosis of triple-negative breast cancer cells.Oncology letters · 2019Article
- Upregulation of KIN17 is associated with non-small cell lung cancer invasiveness.Oncology letters · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKin17 is ubiquitously expressed at low levels in human tissue and participates in DNA replication, DNA repair and cell cycle control. Breast cancer cells are characterized by enabling replicative immortality and accumulated DNA damage. However, whether kin17 contributes to breast carcinogenesis remains unknown. METHODOLOGY/PRINCIPAL
findingsIn this study, we show for the first time that kin17 is an important molecule related to breast cancer. Our results show that kin17 expression was markedly increased in clinical breast tumors and was associated with tumor grade, Ki-67 expression, p53 mutation status and progesterone receptor expression, which were assessed in a clinicopathologic characteristics review. Knockdown of kin17 inhibited DNA replication and repair, blocked cell cycle progression and inhibited anchorage-independent growth, while increasing sensitivity to chemotherapy in breast cancer cells. Moreover, kin17 silencing decreased EGF-stimulated cell growth. Furthermore, overexpression of kin17 promoted DNA replication and cell proliferation in MCF-10A. CONCLUSIONS/SIGNIFICANCE: Our findings indicate that up-regulation of kin17 is strongly associated with cellular proliferation, DNA replication, DNA damage response and breast cancer development. The increased level of kin17 was not only a consequence of immortalization but also associated with tumorigenesis. Therefore, kin17 could be a novel therapeutic target for inhibiting cell growth in breast cancer.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.