ArticleProceedings of the National Academy of Sciences of the United States of America2021
Ki-67 regulates global gene expression and promotes sequential stages of carcinogenesis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 120 citations in OpenAlex.
- Ki-67 regulates heterochromatin organization in neurons and forms condensates with heterochromatic components.Nature communications · 2026Article
- Association of hormone receptor-based pathological features with prognosis in high-grade serous ovarian carcinoma: a retrospective cohort study and nomogram construction.Journal of ovarian research · 2026Article
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- Ki-67 shapes the nucleolus by anchoring chromatin via its amphiphilic properties.The EMBO journal · 2026Article
- Therapeutic targeting of RAGE/STAT3 signaling abrogates S100A7-driven breast tumorigenicity and immune suppression.Breast cancer research : BCR · 2026Article
- Bioactive Natural Compounds in Triple-Negative Breast Cancer: Molecular Targets and Therapeutic Perspectives.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Vascular invasion-associated gene expression is detectable in pre-surgical biopsies of stage I lung adenocarcinoma.Nature communications · 2026Article
- ROS-Fueled Allies: STAT3, PKM2, and HIF-1α Influencing Energy Metabolism in Hormone-Independent Cancers.International journal of molecular sciences · 2026Article
- Establishment of an immortalized porcine erythroid progenitor cell line using species-adapted papillomavirus oncogenes.Frontiers in bioengineering and biotechnology · 2026Article
- The miR-16-1-3p passenger strand exhibits functional activity and suppresses malignant phenotypes in osteosarcoma.Frontiers in genetics · 2026Article
- From incidentaloma to actionable insight: a clinical-molecular-imaging framework for risk-stratified management of testicular microlithiasis.Frontiers in endocrinology · 2026Review
- Preoperative prediction of breast cancer Ki-67 status via multimodal ultrasound-clinical nomogram: a single-center study.Translational cancer research · 2025Article
- Comments on: CT-based intratumoral and peritumoral radiomics to predict the treatment response to hepatic arterial infusion chemotherapy plus lenvatinib and PD-1 in high-risk hepatocellular carcinoma cases: a multi-center study.Hepatology international · 2025Article
- Microplastics' Impact on the Development of AOM/DSS-Induced Colitis-Associated Colorectal Cancer in Mice.International journal of molecular sciences · 2025Article
- A specific tsRNA in serum from patients with nasopharyngeal carcinoma: 5'tiRNA-32-ValAAC-2 mediates malignance of nasopharyngeal carcinoma cells.Frontiers of medicine · 2025Article
- Pharmacological reduction of neutrophil infiltration reducesbioRxiv : the preprint server for biology · 2025Article
- The MAO-B Inhibitor Selegiline Reduces the Viability of Different Prostate Cancer Cell Lines and Enhances the Effects of Anti-Androgen and Cytostatic Agents.Pharmacology research & perspectives · 2025Article
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- B1 corrected T1 mapping in the differentiation and prediction of breast cancer.Scientific reports · 2025Article
- The intervention of NLRP3 inflammasome inhibitor: oridonin against azoxymethane and dextran sulfate sodium-induced colitis-associated colorectal cancer in male BALB/c mice.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ki-67 is a nuclear protein that is expressed in all proliferating vertebrate cells. Here, we demonstrate that, although Ki-67 is not required for cell proliferation, its genetic ablation inhibits each step of tumor initiation, growth, and metastasis. Mice lacking Ki-67 are resistant to chemical or genetic induction of intestinal tumorigenesis. In established cancer cells, Ki-67 knockout causes global transcriptome remodeling that alters the epithelial-mesenchymal balance and suppresses stem cell characteristics. When grafted into mice, tumor growth is slowed, and metastasis is abrogated, despite normal cell proliferation rates. Yet, Ki-67 loss also down-regulates major histocompatibility complex class I antigen presentation and, in the 4T1 syngeneic model of mammary carcinoma, leads to an immune-suppressive environment that prevents the early phase of tumor regression. Finally, genes involved in xenobiotic metabolism are down-regulated, and cells are sensitized to various drug classes. Our results suggest that Ki-67 enables transcriptional programs required for cellular adaptation to the environment. This facilitates multiple steps of carcinogenesis and drug resistance, yet may render cancer cells more susceptible to antitumor immune responses.
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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.