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Updated: Aug 15, 2025

Real-Time Quantitative Measurement of Tumor Cell Migration and Invasion Following Synthetic mRNA Transfection
Published on: June 23, 2023
LQB-118 Suppresses Migration and Invasion of Prostate Cancer Cells by Modulating the Akt/GSK3β Pathway and MMP-9/Reck
Thiago Martino1, Graziele Freitas DE Bem2, Shirley Vania Moura Santos1
1LIA-BPPN, Department of Biochemistry, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Background/Aim:
Prostate cancer (PCa) is one of the most common malignancies in adult men. LQB-118 is a pterocarpanquinone with antitumor activity toward prostate cancer cells. It inhibits cell proliferation by down-regulating cyclins D1 and B1 and up-regulating p21. However, the effects of LQB-118 on PCa cell migration are still unclear. Herein, the LQB-118 effects on PCa metastatic cell migration/invasion and its mechanism of action were evaluated.
Materials And Methods:
PC3 cells were treated with LQB-118 or Paclitaxel (PTX), and cell migration (wound healing and Boyden chamber assays) and invasion (matrigel assay) were determined. The LQB-118 mechanisms were evaluated by αVβIII protein expression (flow cytometry), protein phosphorylation (Western blot), and mRNA expression (qPCR).
Results:
LQB-118 impaired PCa cell migration and invasion, down-regulated Akt phosphorylation, and also reduced GSK3β phosphorylation, through a FAK-independent pathway. Also, it was observed that LQB-118 controlled the invasiveness behavior by reducing matrix metalloproteinase-9 (MMP-9) and up-regulating reversion-inducing cysteine rich protein with Kazal motifs (Reck) mRNA levels. Interestingly, LQB-118 increased integrin αvβIII expression, but this effect was not related to its activation, since the cell adhesion ability was reduced after LQB-118 treatment.
Conclusion:
These data highlight novel LQB-118 mechanisms in prostate cancer cells. LQB-118 acts as a negative regulator of the Akt/GSK3 signaling pathway and can modulate PCa cell proliferation, death, and migration/invasion. The results also support the use of LQB-118 for the treatment of metastatic PCa, alone or combined with another chemotherapeutic agent, due to its demonstrated pleiotropic activities.
Insights
LQB-118, a novel compound, inhibits prostate cancer (PCa) cell migration and invasion. It targets the Akt/GSK3 signaling pathway, offering potential for treating metastatic PCa.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Prostate cancer (PCa) is a prevalent malignancy in men.
- LQB-118, a pterocarpanquinone, exhibits antitumor properties against PCa cells.
- Previous studies showed LQB-118 inhibits proliferation; its effect on migration was unknown.
Purpose of the Study:
- To evaluate the effects of LQB-118 on prostate cancer cell migration and invasion.
- To elucidate the underlying mechanisms of LQB-118's action on PCa metastasis.
Main Methods:
- PC3 cells were treated with LQB-118 or Paclitaxel.
- Cell migration and invasion assays (wound healing, Boyden chamber, Matrigel) were performed.
- Mechanisms were assessed via flow cytometry, Western blot, and qPCR for protein expression, phosphorylation, and mRNA levels.
Main Results:
- LQB-118 significantly impaired PCa cell migration and invasion.
- It down-regulated Akt and GSK3β phosphorylation via a FAK-independent pathway.
- LQB-118 modulated MMP-9 and Reck mRNA levels, and affected integrin αvβIII expression without increasing cell adhesion.
Conclusions:
- LQB-118 negatively regulates the Akt/GSK3 signaling pathway in prostate cancer cells.
- It modulates PCa cell proliferation, death, and metastasis.
- LQB-118 demonstrates pleiotropic activities, supporting its potential use in treating metastatic PCa.
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