ArticleInternational journal of oncology2023
Targeting the mitochondrial calcium uniporter inhibits cancer progression and alleviates cisplatin resistance in esophageal squamous cell carcinoma.
Article in International journal of oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Integrated Bioinformatics and Experimental Validation Reveal the Diagnostic and Prognostic Value of SMDT1 in Thyroid Carcinoma.Diagnostics (Basel, Switzerland) · 2026Article
- NOL7 Inhibits Ovarian Cancer Progression and Suppresses Angiogenesis by Stabilizing GADD45A to Deactivate STAT3.Cancer science · 2026Article
- Trichosanthin elicits antitumor activity via MICU3 mediated mitochondria calcium influx.Journal of advanced research · 2025Article
- Mitochondrial CaJournal of cellular physiology · 2025Review
- Targeting Drp1 inhibits ESCC progression via the ROS-PGC1-α-Nrf1/2 pathway.Journal of translational medicine · 2025Article
- Calcium channels as pharmacological targets for cancer therapy.Clinical and experimental medicine · 2025Review
- MCU complex: Exploring emerging targets and mechanisms of mitochondrial physiology and pathology.Journal of advanced research · 2025Review
- The IPBiochimica et biophysica acta. Molecular basis of disease · 2025Article
- An Oxidative Stress Nano-Amplifier for Improved Tumor Elimination and Combined Immunotherapy.Advanced healthcare materials · 2024Article
- Spatial and single-cell explorations uncover prognostic significance and immunological functions of mitochondrial calcium uniporter in breast cancer.Cancer cell international · 2024Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin is the standard chemotherapeutic drug used for the treatment of esophageal squamous cell carcinoma (ESCC). Acquired cisplatin resistance is the primary obstacle to prolonging patient survival time. Here, the therapeutic effects of mitochondrial calcium uniporter (MCU) inhibition on tumor growth and cisplatin resistance in ESCC were assessed. MCU was stably overexpressed or knocked down in three ESCC cell lines and three cisplatin‑resistant ESCC cell lines. Then, proliferation, migration, and mitochondrial membrane potential (MMP) were measured by colony formation, wound healing, Transwell, and JC‑1 staining assays. MCU, MICU2, MICU1, and PD‑L1 levels were detected through western blotting and immunofluorescence. ESCC and cisplatin‑resistant ESCC xenograft mouse models were established. After MCU knockdown, tumor volume was measured. The expression levels of proliferation markers (CyclinD1 and Ki‑67), MICU1/2, PD‑L1, epithelial-mesenchymal transition (EMT) markers (vimentin, β‑catenin, and E‑cadherin), and the angiogenesis marker CD34 were detected through western blotting, immunohistochemistry, or immunofluorescence. The results showed that MCU overexpression significantly promoted proliferation, migration, and MMP in ESCC cells and cisplatin‑resistant ESCC cells. However, proliferation, migration, and MMP were suppressed following MCU knockdown. In ESCC cells, MCU overexpression markedly increased MICU2, MICU1, and PD‑L1 levels, and the opposite results were observed when MCU was stably knocked down. Similarly, MCU inhibition decreased MICU2, MICU1, and PD‑L1 expression in cisplatin‑resistant ESCC cells. Moreover, MCU knockdown substantially decreased tumor growth, EMT, and angiogenesis in ESCC and cisplatin‑resistant ESCC xenograft mice. Collectively, targeting MCU may inhibit cancer progression and alleviate cisplatin resistance in ESCC.
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