ArticleCell death & disease2021
B7-H3 suppresses doxorubicin-induced senescence-like growth arrest in colorectal cancer through the AKT/TM4SF1/SIRT1 pathway.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- The Relationship Between Immunogenic Cell Death and Cellular Senescence in Cancer Immunotherapy.Life (Basel, Switzerland) · 2026Review
- The Red AlgaCurrent issues in molecular biology · 2026Article
- A cascade via CD276/PI3K/SIRT1/E-Cad in overcoming contact inhibition of proliferation in hepatocellular carcinoma cells.Molecular and clinical oncology · 2026Article
- Therapy-induced senescent cancer cells as bidirectional regulators of antitumor immunity and resistance in the tumor microenvironment.Cell death & disease · 2026Review
- C5aR1 and cGAS/STING and their possible involvement in radiosensitivity of colorectal cancer.iScience · 2026Review
- Disruption of ATP Synthase Spatiotemporal Organization, CaAging cell · 2026Article
- YBX1 Enhances the Stability of TM4SF1 in an mCombinatorial chemistry & high throughput screening · 2026Article
- NSUN5 Mediates Resistance to Doxorubicin via Up-regulation of DNA Damage Repair Proteins BRCA2 and BRIP1 in Colorectal Cancer.The American journal of pathology · 2025Article
- Review
- Identification of CCNB1 as a biomarker for cellular senescence in hepatocellular carcinoma: a bioinformatics and experimental validation study.Discover oncology · 2025Article
- Transcriptomic profile of RNA pseudouridine modification as a biomarker for cellular senescence associated with survival outcomes in colorectal cancer.BMC biology · 2025Article
- Research progress of B7-H3 in malignant tumors.Frontiers in immunology · 2025Review
- Cellular senescence in colorectal cancer: its occurrence, effect and therapy.Frontiers in oncology · 2025Review
- The role of SIRT1 in the development of gastrointestinal tumors.Frontiers in cell and developmental biology · 2025Review
- miR-29 is an important driver of aging-related phenotypes.Communications biology · 2024Article
- B7-H3 at the crossroads between tumor plasticity and colorectal cancer progression: a potential target for therapeutic intervention.Cancer metastasis reviews · 2024Review
- METTL3 promotes cellular senescence of colorectal cancer via modulation of CDKN2B transcription and mRNA stability.Oncogene · 2024Article
- Review
- Non-immune functions of B7-H3: bridging tumor cells and the tumor vasculature.Frontiers in oncology · 2024Review
- B7H3 increases ferroptosis resistance by inhibiting cholesterol metabolism in colorectal cancer.Cancer science · 2023Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence suggests that cellular senescence induced by chemotherapy has been recognized as a new weapon for cancer therapy. This study aimed to research novel functions of B7-H3 in cellular senescence induced by a low dose of doxorubicin (DOX) in colorectal cancer (CRC). Here, our results demonstrated that B7-H3 knockdown promoted, while B7-H3 overexpression inhibited, DOX-induced cellular senescence. B7-H3 knockdown dramatically enhanced the growth arrest of CRC cells after low-dose DOX treatment, but B7-H3 overexpression had the opposite effect. By RNA-seq analysis and western blot, we showed that B7-H3 prevented cellular senescence and growth arrest through the AKT/TM4SF1/SIRT1 pathway. Blocking the AKT/TM4SF1/SIRT1 pathway dramatically reversed B7-H3-induced resistance to cellular senescence. More importantly, B7-H3 inhibited DOX-induced cellular senescence of CRC cells in vivo. Therefore, targeting B7-H3 or the B7-H3/AKT/TM4SF1/SIRT1 pathway might be a new strategy for promoting cellular senescence-like growth arrest during drug treatment in CRC.
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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.