ReviewOncology letters2023
Roles and regulatory mechanisms of KIN17 in cancers (Review).
Review in Oncology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- KIN17 facilitates the initiation and progression of renal tumor progression through the PI3K-AKT-mTOR pathway.Scientific reports · 2026Article
- Regulation of pancreatic cancer cells by suppressing KIN17 through the PI3K/AKT/mTOR signaling pathway.Oncology reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
KIN17, which is known as a DNA and RNA binding protein, is highly expressed in numerous types of human cancers and was discovered to participate in several vital cell behaviors, including DNA replication, damage repair, regulation of cell cycle and RNA processing. Furthermore, KIN17 is associated with cancer cell proliferation, migration, invasion and cell cycle regulation by regulating pathways including the p38 MAPK, NF-κB-Snail and TGF-β/Smad2 signaling pathways. In addition, knockdown of KIN17 was found to enhance the sensitivity of tumor cells to chemotherapeutic agents. Immunohistochemical analysis revealed that there were significant differences in the expression of KIN17 between cancer tissues and adjacent tissues. Both the Kaplan-Meier survival analysis and multivariate Cox regression analysis indicated that KIN17 is aberrantly high expressed in various tumor tissues and is also associated with poor prognosis in patients with various tumor types. Taken together, KIN17 has key roles in tumorigenesis and cancer development. Investigating the relationship between KIN17 and neoplasms will provide a vital theoretical basis for KIN17 to serve as a diagnostic and prognostic biomarker for cancer patients and as a potential target for cancer therapy.
Indexed as
Identifiers
What Socratic 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 Socratic graph.