ArticleClinical and translational medicine2021
c-Myb facilitates immune escape of esophageal adenocarcinoma cells through the miR-145-5p/SPOP/PD-L1 axis.
Article in Clinical and translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 26 citations in OpenAlex.
- Not only as a Cullin3 ligase adaptor, SPOP may also act as a molecular bridge.Genes & diseases · 2027Review
- miR-486-5p suppresses autophagy in hepatocellular carcinoma via activation of the AKT/mTOR signalling pathway.Molecular biomedicine · 2026Article
- Radiation-induced MYB reduction unleashes TIM-3 expression in NK cells to attenuate antitumor immunity in colorectal cancer.Journal of translational medicine · 2026Article
- Fusobacterium nucleatum promotes tumor extravasation and metastasis in head and neck cancer via TLR4/MYB/ESPN axis.Communications biology · 2026Article
- Reduced YTHDF2 inhibits PD-L1 expression by stabilizing mCell death & disease · 2026Article
- LncRNA OTUD6B-AS1 overexpression induces parthanatos in esophageal adenocarcinoma cells by binding to miR-145-5p and promoting AIF expression.American journal of translational research · 2026Article
- Article
- Harnessing miR-145 in NSCLC: mechanistic roles, diagnostic-prognostic utility, and therapeutic potential.Cancer cell international · 2025Review
- Role of miRNA‑145‑5p in cancer (Review).Oncology reports · 2025Review
- Exosome-Derived Cargos in Immune Microenvironment in Esophageal Carcinoma: A Mini-Review.Recent patents on anti-cancer drug discovery · 2025Review
- Uncovering the role of microRNAs in esophageal cancer: from pathogenesis to clinical applications.Frontiers in pharmacology · 2025Review
- Exosomes in esophageal cancer: function and therapeutic prospects.Medical oncology (Northwood, London, England) · 2024Review
- BCLAF1 binds SPOP to stabilize PD-L1 and promotes the development and immune escape of hepatocellular carcinoma.Cellular and molecular life sciences : CMLS · 2024Article
- miRNA profiling of esophageal adenocarcinoma using transcriptome analysis.Cancer biomarkers : section A of Disease markers · 2024Article
- Characterization of PDL1 enhanced siRNA/albumin liposome for effective therapeutic function in lung cancer.Journal of cancer research and clinical oncology · 2023Article
- The prognostic and immunological role of MYB: from bladder cancer validation to pan-cancer analysis.Bioscience reports · 2023Article
- New 4,5-Diarylimidazol-2-ylidene-iodidogold(I) Complexes with High Activity against Esophageal Adenocarcinoma Cells.International journal of molecular sciences · 2023Article
- The E3 ubiquitin ligases regulate PD-1/PD-L1 protein levels in tumor microenvironment to improve immunotherapy.Frontiers in immunology · 2023Review
- Effects of PAMK on lncRNA, miRNA, and mRNA expression profiles of thymic epithelial cells.Functional & integrative genomics · 2022Article
- Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Esophageal adenocarcinoma (EAC), a subtype of esophageal carcinoma, is a severe health problem associated with high death rate and poor prognosis. Immunotherapy has proven to be effective in many solid tumors, including EAC, but immune escape blocks its effectiveness. Thus, we explored the mechanisms and functional role of c-Myb in immune escape of EAC cells. Clinical EAC tissues were collected for determining the expression of c-Myb, speckled POZ protein (SPOP), and miR-145-5p. Functional assays were then performed to detect the interactions between c-Myb and SPOP as well as between SPOP and miR-145-5p. EAC cell invasion and migration were assessed. Next, T cells were sorted and cocultured with EAC cells with different treatments followed by detection of T-cell viability. In addition, a mouse model of EAC was constructed for relevant in vivo assays. c-Myb and miR-145-5p were highly expressed and SPOP had low expressions in EAC. c-Myb activated the transcription of miR-145-5p, which in turn targeted SPOP. Further, SPOP accelerated the ubiquitination of PD-L1 to enhance its expression. Overexpression of PD-L1 suppressed T-cell functions and promoted proliferative and migrative abilities of EAC cells to induce immune escape. The above findings were also confirmed in the ECA mouse model in vivo. Our findings uncovered that c-Myb can promote the immune escape of EAC cells by favoring the transcription of miR-145-5p and inhibiting SPOP-dependent ubiquitination and degradation of PD-L1, thus, presenting new target for EAC adjunct therapy.
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