ArticleOncology letters2018
Thapsigargin induces apoptosis of prostate cancer through cofilin-1 and paxillin.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- A novel prognostic model for lung squamous cell carcinoma based on multi-omics analysis and machine learning.PloS one · 2025Article
- Research advances in natural sesquiterpene lactones: overcoming cancer drug resistance through modulation of key signaling pathways.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Role of actin-binding proteins in prostate cancer.Frontiers in cell and developmental biology · 2024Review
- Paxillin knockout in mouse granulosa cells increases fecundity†.Biology of reproduction · 2023Article
- Physapruin A Exerts Endoplasmic Reticulum Stress to Trigger Breast Cancer Cell Apoptosis via Oxidative Stress.International journal of molecular sciences · 2023Article
- Oxidative-Stress-Mediated ER Stress Is Involved in Regulating Manoalide-Induced Antiproliferation in Oral Cancer Cells.International journal of molecular sciences · 2023Article
- Altered SERCA Expression in Breast Cancer.Medicina (Kaunas, Lithuania) · 2021Article
- Development of Potential Antitumor Agents from the Scaffolds of Plant-Derived Terpenoid Lactones.Journal of medicinal chemistry · 2020Article
- Large Scale Conversion of Trilobolide into the Payload of Mipsagargin: 8-Biomolecules · 2020Article
- Inhibiting eukaryotic ribosome biogenesis.BMC biology · 2019Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is widely considered that endoplasmic reticulum stress may rapidly induce apoptosis. The aim of the present study was to investigate the effect of thapsigargin on the induction of apoptosis in prostate cancer cells, and to explore its possible mechanism. A Cell Counting Kit-8 was selected to determine the effect of thapsigargin (0, 1, 10 and 100 nM) on the proliferation of PC3 cells. Cell proliferation of the prostate cancer cells was effectively inhibited by treatment with thapsigargin, and thapsigargin significantly increased the rate of apoptosis and caspase-3/9 activities in prostate cancer cells. The protein expression of phosphorylated (p)-RAC-α serine threonine-protein kinase, p-mechanistic target of rapamycin, F-actin and paxillin were significantly decreased, and cofilin-1 protein expression was significantly increased by treatment with thapsigargin in prostate cancer cells. Overall, the data of the present study revealed that thapsigargin induced apoptosis in prostate cancer cells through cofilin-1 and paxillin.
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Registered trials
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