ArticleCell death discovery2023
Knockdown of KIF15 suppresses proliferation of prostate cancer cells and induces apoptosis through PI3K/Akt signaling pathway.
Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 7 citations in OpenAlex.
- PI3K/AKT signaling pathway: molecular crossroads in tumorigenesis and therapeutic innovation.Signal transduction and targeted therapy · 2026Review
- KIF15 (Kinesin-12): molecular biology, physiological functions, and roles in disease.Journal of cancer research and clinical oncology · 2026Review
- Mitochondrial fission genes MTFP1/MTFP2 as predictive biomarkers in prostate cancer: a mendelian randomization study.Discover oncology · 2025Article
- Review
- The multifaceted role of KIF15 in cancer progression and therapy.Investigational new drugs · 2025Review
- Development of a prostate cancer biochemical recurrence risk signature using machine learning and motor protein-related genes.PloS one · 2025Article
- KIF15 promotes human glioblastoma progression under the synergistic transactivation of REST and P300.International journal of biological sciences · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Prostate cancer is one of the most common malignancies in men, which has been considered a public health threat. KIF15 is a kind of driver protein, and its abnormal expression is closely related to the occurrence and development of malignant tumors. The purpose of the study was to explore the significance and role of KIF15 in prostate cancer and to show some potential value for prostate cancer. Immunohistochemistry analysis showed that KIF15 was highly expressed in prostate cancer tissues, which was also positively correlated with T Infiltrate. The loss-of-function and gain-of-function assays based on prostate cancer cells indicated that the change in KIF15 expression could significantly affect cell proliferation, tumorigenesis, migration, and cell apoptosis. The inhibition of prostate cancer development by KIF15 knockdown was also assured in vivo. The Human Apoptosis Antibody Array showed that CD40L, cytoC, DR6, and p21 were up-regulated upon KIF15 knockdown, while IGF-I and Survivin were down-regulated. Moreover, the involvement of the PI3K/Akt pathway in the KIF15-mediated regulation of prostate cancer was preliminarily proved. In summary, KIF15 was identified to play an important role in the development or biological progress of prostate cancer and is considered to possess the potential to be used as a therapeutic target.
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.