Related Experiment Video
Updated: Mar 2, 2026
Methods to Classify Cytoplasmic Foci as Mammalian Stress Granules
Published on: May 12, 2017
15d-PGJ2 as an endoplasmic reticulum stress manipulator in multiple myeloma in vitro and in vivo
Marcelo Sperandio1, Ana Paula D Demasi1, Elizabeth F Martinez1
1Laboratory of Immunology and Molecular Biology, São Leopoldo Mandic Institute of Medicine & Dentistry and Research Center (SLMANDIC), Campinas, SP, Brazil.
Abstract:
Multiple myeloma (MM) is characterised by intense protein folding and, consequently endoplasmic reticulum (ER) stress. The prostaglandin 15d-PGJ2 is able to raise oxidative stress levels within the cell and potentially trigger cell death. The aim of this study was to evaluate the antineoplastic effect of 15d-PGJ2 on MM in vitro and in vivo via ER and oxidative stress pathways. MM.1R and MM.1S cell lines were treated with 15d-PGJ2 at 1-10μM and evaluated with regard to proliferation, mRNA expression of PRDX1, PRDX4, GRP78, GRP94, CHOP, BCL-2 and BAX. Stress data was validated via oxidized glutathione assays. MM.1R cells were inoculated into NOD/SCID mice, which were subsequently treated daily with 15d-PGJ2 at 4mg/kg or vehicle (control), with tumour volume being monitored for 14days. 15d-PGJ2 reduced cell proliferation, induced cell death and apoptosis at 5μM and 10μM and Stress-related genes were upregulated at the same doses. Oxidized glutathione levels were also increased. 15d-PGJ2 at 4mg/kg in vivo halted tumour growth. In conclusion, 15d-PGJ2 induced myeloma cell death via ER stress in vitro. 15d-PGJ2 in vivo also inhibited tumour growth.
Insights
The prostaglandin 15d-PGJ2 effectively combats multiple myeloma (MM) by inducing cell death through endoplasmic reticulum (ER) and oxidative stress pathways. This compound also demonstrated significant inhibition of tumor growth in vivo.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Multiple myeloma (MM) is characterized by significant protein folding, leading to endoplasmic reticulum (ER) stress.
- Prostaglandin 15d-PGJ2 is known to increase cellular oxidative stress and may induce cell death.
Purpose of the Study:
- To investigate the anti-cancer effects of 15d-PGJ2 on multiple myeloma (MM) cells.
- To explore the role of ER and oxidative stress pathways in mediating the anti-neoplastic effects of 15d-PGJ2.
Main Methods:
- MM.1R and MM.1S cell lines were treated with 15d-PGJ2 (1-10μM) to assess proliferation, apoptosis, and mRNA expression of key stress-related genes (PRDX1, PRDX4, GRP78, GRP94, CHOP, BCL-2, BAX).
- Oxidized glutathione assays were used to validate stress induction.
- In vivo studies involved inoculating MM.1R cells into NOD/SCID mice, followed by daily treatment with 15d-PGJ2 (4mg/kg) or vehicle, monitoring tumor volume for 14 days.
Main Results:
- 15d-PGJ2 significantly reduced MM cell proliferation and induced apoptosis at concentrations of 5μM and 10μM.
- Upregulation of stress-related genes and increased oxidized glutathione levels were observed at these effective doses.
- In vivo, 15d-PGJ2 administration at 4mg/kg halted tumor growth in mice.
Conclusions:
- 15d-PGJ2 effectively induces myeloma cell death through ER stress in vitro.
- 15d-PGJ2 demonstrates anti-tumor activity by inhibiting tumor growth in vivo, suggesting its potential as a therapeutic agent for multiple myeloma.
