ReviewCell biology international2022
Research progress of Bub3 gene in malignant tumors.
Review in Cell biology international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 9 citations in OpenAlex.
- BUB signaling in cancer and molecular insights into targeted therapies.Communications biology · 2026Review
- Proteomic Signatures of Vemurafenib Resistance in Canine Urothelial Carcinoma Harboring the BRAFV595E Mutation.Journal of proteome research · 2026Article
- RNA-binding protein RALYL-mediated BCL11B RNA stability promotes immune escape in small cell lung cancer through transcriptional activation of BUB3.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Pan-cancer characterization of POSTN and its clinical and microenvironmental associations in ERScientific reports · 2026Article
- NUF2 interacts with BUB3 and drives lung adenocarcinoma progression through activation of the NF-κB pathway.World journal of surgical oncology · 2026Article
- mir-188-5p emerges as an oncomir to promote chronic myeloid leukemia via upregulation of BUB3 and SUMO2.Molecular biology reports · 2025Article
- A whole-genome CRISPR screen identifies the spindle accessory checkpoint as a locus of nab-paclitaxel resistance in a pancreatic cancer cell line.Scientific reports · 2024Article
- A whole-genome CRISPR screen identifies the spindle accessory checkpoint as a locus of nab-paclitaxel resistance in pancreatic cancer cells.bioRxiv : the preprint server for biology · 2024Article
- Comprehensive analysis of BUBs gene family in lung adenocarcinoma with immunological analysis.Aging · 2023Article
- Research progress of Bub3 gene in malignant tumors.Cell biology international · 2022Review
- Identification of genetic risk loci for depression and migraine comorbidity in Han Chinese residing in Taiwan.Frontiers in psychiatry · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The spindle assembly checkpoint (SAC) is a highly conserved monitoring system that ensures a fidelity of chromosome segregation during mitosis. Bub3, a mitotic Checkpoint Protein, is a member of the Bub protein family, and an important factor in the SAC. Abnormal expression of Bub3 results in mitotic defects, defective spindle gate function, chromosomal instability and the development of aneuploidy cells. Aneuploidy is a state of abnormal karyotype that has long been considered as a marker of tumorigenesis. Karyotypic heterogeneity in tumor cells, known as "chromosomal instability" (CIN), can be used to distinguish cancerous cells from their normal tissue counterpart. In this review, we summarize the expression and clinical significance of Bub3 in a variety of tumors and suggest that it has potential in the treatment of cancer.
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.