ArticleCell death & disease2018
Tubeimoside I induces accumulation of impaired autophagolysosome against cervical cancer cells by both initiating autophagy and inhibiting lysosomal function.
Article in Cell death & disease, 2018. 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, 48 citations in OpenAlex.
- Structures of the neutral amino acid transporter LAT4 provide insights into antitumor effects of its inhibitor tubeimoside-1.The EMBO journal · 2026Article
- Research status and challenges of anti-tumor effects of natural saponins and their combination therapy.Journal of the Egyptian National Cancer Institute · 2026Review
- Sichuan pepper, Zanthoxylum bungeanum Maxim., suppresses human coronavirus OC43 infection by inhibiting viral entry and impairing autolysosome accumulation.Chinese medicine · 2026Article
- HDAC5 stabilization by tubeimoside I suppresses cervical cancer metastasis via inhibiting H3K27ac/KPNA2 axis.British journal of cancer · 2026Article
- Autophagy in ocular diseases: from mechanisms to therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- Single-cell analysis reveals the regulatory role of ECT2 in HPV-driven cervical carcinogenesis process.Infectious agents and cancer · 2025Article
- ARL8B regulates lysosomal function and predicts poor prognosis in hepatocellular carcinoma.Scientific reports · 2025Article
- Identification and characterization of a novel antifungal compound tubeimoside I targeting cell wall.Microbiology spectrum · 2024Article
- Molecular mechanisms of snoRNA-IL-15 crosstalk in adipocyte lipolysis and NK cell rejuvenation.Cell metabolism · 2023Article
- Tubeimoside-1 Enhances TRAIL-Induced Apoptotic Cell Death through STAMBPL1-Mediated c-FLIP Downregulation.International journal of molecular sciences · 2023Article
- Paris saponin VII, a Hippo pathway activator, induces autophagy and exhibits therapeutic potential against human breast cancer cells.Acta pharmacologica Sinica · 2022Article
- Long non-coding RNAs PGM5-AS1 upregulates Decorin (DCN) to inhibit cervical cancer progression by sponging miR-4284.Bioengineered · 2022Article
- Tubeimoside-1: A review of its antitumor effects, pharmacokinetics, toxicity, and targeting preparations.Frontiers in pharmacology · 2022Review
- Chinese endemic medicinal plantFrontiers in pharmacology · 2022Review
- Tubeimoside-1 induces TFEB-dependent lysosomal degradation of PD-L1 and promotes antitumor immunity by targeting mTOR.Acta pharmaceutica Sinica. B · 2021Article
- Article
- Identification and Validation of Autophagy-Related Gene Nomograms to Predict the Prognostic Value of Patients with Cervical Cancer.Journal of oncology · 2021Article
- Lysosomal dysfunction and autophagy blockade contribute to autophagy-related cancer suppressing peptide-induced cytotoxic death of cervical cancer cells through the AMPK/mTOR pathway.Journal of experimental & clinical cancer research : CR · 2020Article
- Article
- Tubeimoside I Inhibits Cell Proliferation and Induces a Partly Disrupted and Cytoprotective Autophagy Through Rapidly Hyperactivation of MEK1/2-ERK1/2 Cascade via Promoting PTP1B in Melanoma.Frontiers in cell and developmental biology · 2020Article
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cervical cancer is one of the most aggressive human cancers with poor prognosis due to constant chemoresistance and repeated relapse. Tubeimoside I (TBM) has been identified as a potent antitumor agent that inhibits cancer cell proliferation by triggering apoptosis and inducing cell cycle arrest. Nevertheless, the detailed mechanism remains unclear and needs to be further elucidated, especially in cervical cancer. In this study, we found that TBM could induce proliferation inhibition and cell death in cervical cancer cells both in vitro and in vivo. Further results demonstrated that treatment with TBM could induce autophagosome accumulation, which was important to TBM against cervical cancer cells. Mechanism studies showed that TBM increased autophagosome by two pathways: First, TBM could initiate autophagy by activating AMPK that would lead to stabilization of the Beclin1-Vps34 complex via dissociating Bcl-2 from Beclin1; Second, TBM could impair lysosomal cathepsin activity and block autophagic flux, leading to accumulation of impaired autophagolysosomes. In line with this, inhibition of autophagy initiation attenuated TBM-induced cell death, whereas autophagic flux inhibition could exacerbated the cytotoxic activity of TBM in cervical cancer cells. Strikingly, as a novel lethal impaired autophagolysosome inducer, TBM might enhance the therapeutic effects of chemotherapeutic drugs towards cervical cancer, such as cisplatin and paclitaxel. Together, our study provides new insights into the molecular mechanisms of TBM in the antitumor therapy, and establishes potential applications of TBM for cervical cancer treatment in clinic.
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