ArticleCell death & disease2017
Wild-type and mutant p53 differentially modulate miR-124/iASPP feedback following pohotodynamic therapy in human colon cancer cell line.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Article
- Multifaceted roles of miR‑124 in cancer: Molecular mechanisms and clinical prospects (Review).International journal of oncology · 2026Review
- Comprehensive bioinformatics analysis and clinical validation of PPP1R13L in rectal adenocarcinoma.BMC cancer · 2026Article
- p53 in colorectal cancer: from a master player to a privileged therapy target.Journal of translational medicine · 2025Review
- Peptide Fractions Extracted from the Hemolymph ofInternational journal of molecular sciences · 2025Article
- Review
- iASPP suppression mediates terminal UPR and improves BRAF-inhibitor sensitivity of colon cancers.Cell death and differentiation · 2023Article
- Photodynamic Therapy for Inflammatory and Cancerous Diseases of the Intestines: Molecular Mechanisms and Prospects for Application.International journal of biological sciences · 2023Review
- The NF-κB/miR-488/ERBB2 axis modulates pancreatic cancer cell malignancy and tumor growth through cell cycle signaling.Cancer biology & therapy · 2022Article
- Emerging roles for lncRNA-NEAT1 in colorectal cancer.Cancer cell international · 2022Review
- iASPP suppresses Gp78-mediated TMCO1 degradation to maintain CaProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Combination of phototherapy with immune checkpoint blockade: Theory and practice in cancer.Frontiers in immunology · 2022Review
- Porphyrin/Chlorin Derivatives as Promising Molecules for Therapy of Colorectal Cancer.Molecules (Basel, Switzerland) · 2021Review
- In situ delivery of biobutyrate by probiotic Escherichia coli for cancer therapy.Scientific reports · 2021Article
- Inhibitor of apoptosis-stimulating p53 protein protects against inflammatory bowel disease in mice models by inhibiting the nuclear factor kappa B signaling.Clinical and experimental immunology · 2021Article
- The Relationship Between the Network of Non-coding RNAs-Molecular Targets and N6-Methyladenosine Modification in Colorectal Cancer.Frontiers in cell and developmental biology · 2021Review
- A Novel Mechanism of the c-Myc/NEAT1 Axis Mediating Colorectal Cancer Cell Response to Photodynamic Therapy Treatment.Frontiers in oncology · 2021Article
- Tumor suppressor p53 independent apoptosis in HT-29 cells by auransterol from Penicillium aurantiacobrunneum.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2020Article
- miR-124 Intensified Oxaliplatin-Based Chemotherapy by Targeting CAPN2 in Colorectal Cancer.Molecular therapy oncolytics · 2020Article
- LncGBP9/miR-34a axis drives macrophages toward a phenotype conducive for spinal cord injury repair via STAT1/STAT6 and SOCS3.Journal of neuroinflammation · 2020Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) is a most common digestive system malignant tumor. p53 mutation has essential role in cancers and is frequently observed in CRC and presents a huge challenge. p53 mutation has been reported to attenuate the inhibitory effect of photofrin-based photodynamic therapy (PDT). p53 mutation-induced gain of function brings up the dysfunction of carcinogenic factors, including miRNAs. Our research found that PDT suppressed CRC cell viability, reduced the tumor size and prolonged the survival time, all of which could be attenuated by p53 mutation or deletion. After p53 mutation or deletion, several miRNA expression levels were downregulated, among which miR-124 was the most strongly downregulated, whereas iASPP expression was upregulated. p53 binds to the promoter of miR-124 to promote its expression and then inhibited iASPP expression, so as to amplify the inhibitory effect of PDT on wild-type p53 cells. In p53-mutant or -deleted cells, this binding no longer worked to promote miR-124 expression, and iASPP expression increased, finally resulted in promoted CRC cell viability upon PDT. The interactive modulation among miR and iASPP in p53-mutant or -deleted cells may serve as a crucial pathway, which mediates therapy resistance when p53 is mutated or deleted, in the process of PDT treatment of CRC.
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