ArticleInternational journal of molecular sciences2014
Paclitaxel induces apoptosis in breast cancer cells through different calcium--regulating mechanisms depending on external calcium conditions.
Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 57 citations in OpenAlex.
- Chemotherapy-induced peripheral neuropathy in patients with breast cancer treated with taxanes (Review).Oncology letters · 2025Review
- A novel taxane SB-T-101141 triggers a noncanonical ferroptosis to overcome Paclitaxel resistance of breast cancer via iron homeostasis-related KHSRP.Cell death & disease · 2025Article
- Article
- Implantable Polymer Scaffolds Loaded with Paclitaxel-Cyclodextrin Complexes for Post-Breast Cancer Tissue Reconstruction.Polymers · 2025Article
- Article
- Deguelin Restores Paclitaxel Sensitivity in Paclitaxel-Resistant Ovarian Cancer Cells via Inhibition of the EGFR Signaling Pathway.Cancer management and research · 2024Article
- Monitoring the Intracellular pH and Metabolic State of Cancer Cells in Response to Chemotherapy Using a Combination of Phosphorescence Lifetime Imaging Microscopy and Fluorescence Lifetime Imaging Microscopy.International journal of molecular sciences · 2023Article
- Taxanes in the Treatment of Head and Neck Squamous Cell Carcinoma.Biomedicines · 2023Review
- MiR-138-5p improves the chemosensitivity of MDA-MB-231 breast cancer cell line to paclitaxel.Molecular biology reports · 2023Article
- Rutin and Hesperidin Revoke the Hepatotoxicity Induced by Paclitaxel in Male Wistar RatsEvidence-based complementary and alternative medicine : eCAM · 2023Article
- Amplified CaInternational journal of cancer · 2022Article
- Roles of calpain in the apoptosis of Eimeria tenella host cells at the middle and late developmental stages.Parasitology research · 2022Article
- Identification of phenolics from miracle berry (Frontiers in nutrition · 2022Article
- Carbonic anhydrase 12 gene silencing reverses the sensitivity of paclitaxel in drug-resistant breast cancer cells.Bioengineered · 2021Article
- Role of JNK activation in paclitaxel-induced apoptosis in human head and neck squamous cell carcinoma.Oncology letters · 2021Article
- Tracing of intracellular pH in cancer cells in response to Taxol treatment.Cell cycle (Georgetown, Tex.) · 2021Article
- Protective Effects of Curcumin Against Paclitaxel-Induced Spinal Cord and Sciatic Nerve Injuries in Rats.Neurochemical research · 2021Article
- Th1 cytokines in conjunction with pharmacological Akt inhibition potentiate apoptosis of breast cancer cellsOncotarget · 2020Article
- PBK attenuates paclitaxel-induced autophagic cell death by suppressing p53 in H460 non-small-cell lung cancer cells.FEBS open bio · 2020Article
- Paclitaxel's Mechanistic and Clinical Effects on Breast Cancer.Biomolecules · 2019Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previously, we reported that endoplasmic reticulum calcium stores were a direct target for paclitaxel initiation of apoptosis. Furthermore, the actions of paclitaxel attenuated Bcl-2 resistance to apoptosis through endoplasmic reticulum-mediated calcium release. To better understand the calcium-regulated mechanisms of paclitaxel-induced apoptosis in breast cancer cells, we investigated the role of extracellular calcium, specifically; whether influx of extracellular calcium contributed to and/or was necessary for paclitaxel-induced apoptosis. Our results demonstrated that paclitaxel induced extracellular calcium influx. This mobilization of extracellular calcium contributed to subsequent cytosolic calcium elevation differently, depending on dosage. Under normal extracellular calcium conditions, high dose paclitaxel induced apoptosis-promoting calcium influx, which did not occur in calcium-free conditions. In the absence of extracellular calcium an "Enhanced Calcium Efflux" mechanism in which high dose paclitaxel stimulated calcium efflux immediately, leading to dramatic cytosolic calcium decrease, was observed. In the absence of extracellular calcium, high dose paclitaxel's stimulatory effects on capacitative calcium entry and apoptosis could not be completely restored. Thus, normal extracellular calcium concentrations are critical for high dose paclitaxel-induced apoptosis. In contrast, low dose paclitaxel mirrored controls, indicating that it occurs independent of extracellular calcium. Thus, extracellular calcium conditions only affect efficacy of high dose paclitaxel-induced apoptosis.
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