ArticleCell cycle (Georgetown, Tex.)
miR-140-3p/usp36 axis mediates ubiquitination to regulate PKM2 and suppressed the malignant biological behavior of breast cancer through Warburg effect.
Article in Cell cycle (Georgetown, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Lactylation-mitochondria axis in chronic kidney disease: metabolic reprogramming, epigenetic dysregulation, and therapeutic potential.Molecular and cellular biochemistry · 2026Review
- Pyruvate kinase M2 in Alzheimer's disease: from dysregulation to therapeutic inhibition.Brain communications · 2026Review
- Oxidative stress reactivates androgen receptor signaling via USP36 to drive castration resistance in prostate cancer.Scientific reports · 2025Article
- Deubiquitinating enzyme USP42 promotes breast cancer progression by inhibiting JNK/p38-mediated apoptosis.Scientific reports · 2025Article
- The Emerging Role of Ubiquitin-Specific Protease 36 (USP36) in Cancer and Beyond.Biomolecules · 2024Review
- A promising target for breast cancer: B7-H3.BMC cancer · 2024Review
- SUMOylation regulation of ribosome biogenesis: Emerging roles for USP36.Frontiers in RNA research · 2024Article
- The Ubiquitin-Proteasome System in Tumor Metabolism.Cancers · 2023Review
- The Ubiquitin-specific Protease USP36 Associates with the Microprocessor Complex and Regulates miRNA Biogenesis by SUMOylating DGCR8.Cancer research communications · 2023Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer is a phenomenon in which breast epithelial cells proliferate out of control under the action of various carcinogenic factors. However, the role of USP36 in breast cancer is unknown. We analyzed the expression of USP36 in breast cancer and its association with poor prognosis in breast cancer patients. The effect of USP36 on malignant biological behavior of breast cancer was verified by cell functional experiments. The upstream regulatory mechanism of USP36 was analyzed by Western blot and quantitative RT-qPCR. The influence of USP36 on the Warburg effect of breast cancer was analyzed by detecting the metabolism of cellular energy substances. We found that USP36 is highly expressed in breast tumor tissues and breast cancer cell lines. High expression of USP36 predicts poor prognosis in patients with breast cancer. Effectively reducing the expression of USP36 can significantly inhibit the proliferation, invasion and migration of breast cancer cells, and promote the apoptosis of breast cancer cells. Meanwhile, inhibiting the expression of USP36 can significantly inhibit the production of ATP, lactate, pyruvate and glucose uptake in breast cancer cells. miR-140-3p is an upstream regulator of USP36, which can partially reverse the regulatory effect of USP36 on breast cancer cells. Importantly, USP36 regulates the expression of PKM2 through ubiquitination, which plays a role in regulating the Warburg effect. We confirmed that miR-140-3p regulates the expression of USP36, which mediates ubiquitination and regulates the expression of PKM2, and regulates the malignant biological behavior of breast cancer through the energy metabolism process.
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