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Published on: June 9, 2023
The LQB-223 Compound Modulates Antiapoptotic Proteins and Impairs Breast Cancer Cell Growth and Migration
Lauana Greicy Tonon Lemos1, Gabriel Mello da Cunha Longo2, Bruna Dos Santos Mendonça3,4
1Laboratório de Hemato-Oncologia Celular e Molecular, Programa de Hemato-Oncologia Molecular, Instituto Nacional do Câncer (INCA). Praça da Cruz Vermelha, 23, 6 andar, Rio de Janeiro (RJ) 20230 130, Brazil. lauanalemos@gmail.com.
Abstract:
Drug resistance represents a major issue in treating breast cancer, despite the identification of novel therapeutic strategies, biomarkers, and subgroups. We have previously identified the LQB-223, 11a-N-Tosyl-5-deoxi-pterocarpan, as a promising compound in sensitizing doxorubicin-resistant breast cancer cells, with little toxicity to non-neoplastic cells. Here, we investigated the mechanisms underlying LQB-223 antitumor effects in 2D and 3D models of breast cancer. MCF-7 and MDA-MB-231 cells had migration and motility profile assessed by wound-healing and phagokinetic track motility assays, respectively. Cytotoxicity in 3D conformation was evaluated by measuring spheroid size and performing acid phosphatase and gelatin migration assays. Protein expression was analyzed by immunoblotting. Our results show that LQB-223, but not doxorubicin treatment, suppressed the migratory and motility capacity of breast cancer cells. In 3D conformation, LQB-223 remarkably decreased cell viability, as well as reduced 3D culture size and migration. Mechanistically, LQB-223-mediated anticancer effects involved decreased proteins levels of XIAP, c-IAP1, and Mcl-1 chemoresistance-related proteins, but not survivin. Survivin knockdown partially potentiated LQB-223-induced cytotoxicity. Additionally, cell treatment with LQB-223 resulted in changes in the mRNA levels of epithelial-mesenchymal transition markers, suggesting that it might modulate cell plasticity. Our data demonstrate that LQB-223 impairs 3D culture growth and migration in 2D and 3D models of breast cancer exhibiting different phenotypes.
Insights
The compound LQB-223 effectively inhibits breast cancer cell migration and growth in 2D and 3D models. It reduces chemoresistance proteins and may modulate cell plasticity, offering a potential new strategy against drug-resistant breast cancer.
Area of Science:
- Oncology
- Pharmacology
Background:
- Drug resistance is a significant challenge in breast cancer treatment.
- Novel therapeutic strategies are crucial for overcoming resistance.
- LQB-223 has shown promise in sensitizing doxorubicin-resistant breast cancer cells.
Purpose of the Study:
- To investigate the antitumor mechanisms of LQB-223 in 2D and 3D breast cancer models.
- To assess LQB-223's effects on cell migration, motility, and viability.
- To elucidate the molecular pathways involved in LQB-223's anticancer activity.
Main Methods:
- Utilized wound-healing and phagokinetic track motility assays for 2D models.
- Assessed cytotoxicity, spheroid size, and migration in 3D cultures.
- Analyzed protein expression via immunoblotting and mRNA levels of epithelial-mesenchymal transition markers.
Main Results:
- LQB-223 suppressed breast cancer cell migration and motility in 2D models.
- LQB-223 significantly reduced cell viability, spheroid size, and migration in 3D cultures.
- Mechanisms involved decreased levels of XIAP, c-IAP1, and Mcl-1, with potential modulation of epithelial-mesenchymal transition.
Conclusions:
- LQB-223 demonstrates potent antitumor effects by impairing growth and migration in diverse breast cancer models.
- The compound targets key chemoresistance proteins and may influence cell plasticity.
- LQB-223 represents a promising therapeutic candidate for drug-resistant breast cancer.
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