ArticleOncology letters2017
Upregulation of KIN17 is associated with non-small cell lung cancer invasiveness.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Regulation of EMT and cholangiocarcinoma metastasis by KIN17 through the mTOR signaling pathway.Molecular and cellular biochemistry · 2026Article
- KIN17 facilitates the initiation and progression of renal tumor progression through the PI3K-AKT-mTOR pathway.Scientific reports · 2026Article
- 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
- 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
- Drug delivery approaches for HuR-targeted therapy for lung cancer.Advanced drug delivery reviews · 2022Review
- 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
- Biophysical characterization and molecular phylogeny of human KIN protein.European biophysics journal : EBJ · 2019Article
- Knockdown of DNA/RNA-binding protein KIN17 promotes apoptosis of triple-negative breast cancer cells.Oncology letters · 2019Article
- Inhibition of cell migration and invasion and promotion of cell apoptosis by overexpression of programmed cell death 4 (PDCD4) in cervical cancer Siha cells.International journal of clinical and experimental pathology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kin17 DNA and RNA binding protein (Kin17) is a highly conserved protein that participates in DNA replication, DNA repair and cell cycle progression. Recently, the tumor-promoting function of Kin17 has been demonstrated and increasingly studied. In the present study, the role of Kin17 in the invasion and metastasis of non-small cells lung cancer (NSCLC) was investigated. Elevated Kin17 mRNA and protein expression was identified in a total of 97 NSCLC and benign lung lesion tissue specimens. Kin17 overexpression was significantly correlated with high tumor grade and lymph node metastasis, indicating poor patient prognosis. Scratch and Transwell assays demonstrated that the knockdown of KIN17 inhibited the ability of NSCLC cells to migrate and invade. Furthermore, reverse transcription-quantitative polymerase chain reaction and western blot analyses confirmed that knockdown of KIN17 decreased the expression of matrix metalloproteinase 7, epidermal growth factor receptor and v-myc avian myelocytomatosis viral oncogene homolog. The results of the present study indicate that Kin17 is markedly overexpressed in NSCLC tissues compared with benign lung lesion and peritumoral tissue. The upregulation of KIN17 may serve an important role in the metastasis of NSCLC cells. These results indicate that Kin17 is a novel diagnostic and prognostic biomarker of NSCLC, in addition to being a potential therapeutic target for the treatment of patients with NSCLC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.