ArticleCancer medicine2023
ITGB3 promotes cisplatin resistance in osteosarcoma tumors.
Article in Cancer medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 17 citations in OpenAlex.
- Tumor-derived ITGB3 shapes a primed but functionally constrained NK cell state in breast cancer through HLA-E-NKG2A signaling.Molecular biology reports · 2026Article
- Gene Expression Alterations Associated With Resveratrol-Induced Antiproliferative Effects and S-Phase Cell Cycle Arrest in Osteosarcoma Cancer Cells.Journal of cellular and molecular medicine · 2026Article
- Emerging research themes in drug resistance in osteosarcoma: a 25-year bibliometric and visualized analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- The oral-gut-joint axis in osteoarthritis: a multiomics case-control study.Frontiers in cellular and infection microbiology · 2026Observational
- Targeting the METTL3/PCNA axis with STM2457 overcomes cisplatin resistance in osteosarcoma.Translational cancer research · 2025Article
- SERPINA1 drives TACE resistance in hepatocellular carcinoma by competitively binding ITGB3 to block ITCH-mediated ubiquitination and degradation.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Yin Yang 1 protein-activated N-acetyltransferase 10 drives cell malignant progression of osteosarcoma through ac4C acetylation of integrin β3.Journal of bone oncology · 2025Article
- Endometriosis: An Immunologist's Perspective.International journal of molecular sciences · 2025Review
- Enhancing radiosensitivity of osteosarcoma by ITGB3 knockdown: a mechanism linked to enhanced osteogenic differentiation status through JNK/c-JUN/RUNX2 pathway activation.Journal of experimental & clinical cancer research : CR · 2025Article
- Integrins in Cancer Drug Resistance: Molecular Mechanisms and Clinical Implications.International journal of molecular sciences · 2025Review
- Intratumor heterogeneity of EGFR expression mediates targeted therapy resistance and formation of drug tolerant microenvironment.Nature communications · 2025Article
- Identification of the biological functions and chemo-therapeutic responses of ITGB superfamily in ovarian cancer.Discover oncology · 2024Article
- Hydroxysafflor yellow A induced ferroptosis of Osteosarcoma cancer cells by HIF-1α/HK2 and SLC7A11 pathway.Oncology research · 2024Article
- ITCH-Mediated Ubiquitylation of ITGB3 Promotes Cell Proliferation and Invasion of Ectopic Endometrial Stromal Cells in Ovarian Endometriosis.Biomedicines · 2023Article
- Review
- ITGB3 promotes cisplatin resistance in osteosarcoma tumors.Cancer medicine · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveOsteosarcoma is the most malignant and common primary bone tumor with a high rate of recurrence that mainly occurs in children and young adults. Therefore, it is vital to facilitate the development of novel effective therapeutic means and improve the overall prognosis of osteosarcoma patients via a deeper understanding of the mechanisms of chemoresistance in osteosarcoma progression.
methodsIn this research, the relationship between ITGB3 and the clinical characteristics of patients was detected through analysis of publicly available clinical datasets. The expression of ITGB3 was analysis in collected human osteosarcoma tissues. In addition, the potential functions of ITGB3 in the cisplatin resistance of osteosarcoma cells were investigated in vitro and in tumor xenotransplantation. Finally, the molecular mechanism of ITGB3 in the progression and recurrence of osteosarcoma were explored via transcriptome analysis.
resultsITGB3 was identified as a potential regulator of tumorigenicity and cisplatin resistance in relapsed osteosarcoma. Furthermore, the decreased osteosarcoma cell proliferation and migration ability in ITGB3 knockout osteosarcoma cells were related to increased apoptosis and slowing cell cycle progression. In addition, ITGB3 had a positive correlation with cisplatin resistance in cells and tumor xenografts in mice. Accordingly, ITGB3 performed the functions of proliferation and cisplatin resistance in osteosarcoma through the MAPK and VEGF signaling pathways.
conclusionOur results will contribute to a better understanding of the function and mechanism of ITGB3 in osteosarcoma cisplatin resistance and provide a novel therapeutic target to decrease cisplatin resistance and tumor recurrence in osteosarcoma patients.
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.