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Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells
Published on: January 18, 2017
Indentification of breast cancer subtypes sensitive to HCQ-induced autophagy inhibition
Ping Wang1, Yangyang Du2, Jingfen Wang2
1Department I of breast, Linyi Cancer Hospital, Linyi, China.
Background:
Breast cancer is the most frequent carcinoma in females, which could be classified to 4 subtypes and the current treatment is still far from satisfactory. In this study, we explored the effects of autophagy inhibition on certain subtypes of breast cancer and the molecular mechanism underlying the different response for breast cancer subtypes initially.
Methods:
Autophagy inhibitor hydroxychloroquine (HCQ) was used to identify the sensitivity of breast cancer subtypes to autophagy inhibition in the present study. Cell proliferation and cell invasion were assessed by Cell Counting Kit-8 assay (CCK-8) and transwell assay, respectively. Immunofluorescence staining and western blotting were applied to evaluate cell autophagy. In addition, levels of Ras/Raf/ERK signaling pathway were evaluated by western blotting.
Results:
Our results showed that HCQ treatment suppressed breast cancer cell proliferation and migration in especially SUM-190 cells, which was most sensitive. Furthermore, HCQ inhibited cell autophagy in breast cancer cells by regulating levels of p62, LC3-I and LC3-II. Moreover, the expression of Ras was significant lower than other breast cancer cells. HCQ treatment markedly inhibited the activation of Ras/Raf/ERK signaling in SUM190 cells.
Conclusion:
To conclude, basal-like breast cancer represented by SUM-190 cells may be most sensitive to HCQ induced autophagy inhibition and the mechanism might be relative to Ras/Raf/ERK signaling pathway.
Insights
Hydroxychloroquine (HCQ) effectively inhibits breast cancer cell proliferation and migration, particularly in basal-like SUM-190 cells. This autophagy inhibition mechanism involves the Ras/Raf/ERK signaling pathway.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Breast cancer, a prevalent female carcinoma, exhibits diverse subtypes with currently limited treatment efficacy.
- Understanding subtype-specific responses to novel therapeutic strategies is crucial for improving patient outcomes.
Purpose of the Study:
- To investigate the impact of autophagy inhibition on different breast cancer subtypes.
- To elucidate the molecular mechanisms driving differential responses to autophagy inhibition.
Main Methods:
- Hydroxychloroquine (HCQ), an autophagy inhibitor, was employed to assess breast cancer subtype sensitivity.
- Cell proliferation, invasion, and autophagy were evaluated using CCK-8, transwell assays, immunofluorescence, and western blotting.
- The Ras/Raf/ERK signaling pathway activation was analyzed via western blotting.
Main Results:
- HCQ treatment significantly suppressed proliferation and migration, with SUM-190 cells showing the highest sensitivity.
- HCQ effectively inhibited autophagy by modulating p62 and LC3-I/II levels.
- HCQ markedly inhibited Ras/Raf/ERK signaling activation in SUM-190 cells, which exhibited lower basal Ras expression.
Conclusions:
- Basal-like breast cancer, exemplified by SUM-190 cells, demonstrates heightened sensitivity to HCQ-induced autophagy inhibition.
- The Ras/Raf/ERK signaling pathway is implicated as a key mechanism in the response of SUM-190 cells to HCQ.
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