Konjac petroleum ether extract inhibits triple-negative breast cancer cell migration and invasion by attenuating
Yian Chen1, Qinghong Yu1, Haining Ding1
1The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Background And Aim:
This study, alongside clinical specimens, investigated the inhibitory effect of konjac petroleum ether extract on the migration, invasion, and epithelial-mesenchymal transition (EMT) of triple-negative breast cancer (TNBC) cells via the OLFML2A gene, with the objective of elucidating the potential efficacy and mechanism of action of konjac petroleum ether extract.
Experimental Procedure:
Histopathological examination of OLFML2A was performed on TNBC tumor specimens (n = 8). mRNA and protein levels of OLFML2A and EMT markers (E-cadherin, N-cadherin, vimentin, elastin) were analyzed via qPCR and Western blot. OLFML2A-knockout MDA-MB-231 cells were treated with gradient concentrations of konjac petroleum ether extract. Cell migration (wound healing assay), adhesion, and invasion (Transwell assay) were evaluated, and EMT marker expression was further examined using qPCR, Western blot, and immunofluorescence (n = 3).
Results:
In TNBC patients with high OLFML2A expression, reduced E-cadherin and increased N-cadherin, vimentin, and elastin were observed, while low OLFML2A cases exhibited no significant EMT changes. In MDA-MB-231 cells, OLFML2A knockdown significantly reduced migration and invasion while upregulating E-cadherin and downregulating mesenchymal markers, phenocopying the effects of konjac petroleum ether extract treatment. Konjac extract inhibited cell proliferation with an IC50 of 220 μg/mL at 48 h. The extract inhibited migration and invasion in a dose-dependent manner, with significant effects observed at 200 μg/mL, though potential contributions from cytotoxicity at 300 μg/mL cannot be entirely excluded.
Conclusion:
The research findings suggest that konjac petroleum ether extract inhibits TNBC cells migration and invasion by modulating OLFML2A to inhibit EMT. These findings highlight its potential as a candidate for further investigation for preventing TNBC metastasis, though the contribution of cytotoxicity at higher concentrations warrants further investigation.
Insights
Konjac extract inhibits triple-negative breast cancer (TNBC) cell migration and invasion by modulating OLFML2A to suppress epithelial-mesenchymal transition (EMT). This suggests konjac extract
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Triple-negative breast cancer (TNBC) is an aggressive subtype with limited treatment options.
- Epithelial-mesenchymal transition (EMT) is a key process in cancer metastasis.
- The OLFML2A gene's role in TNBC progression is under investigation.
Purpose of the Study:
- To investigate the inhibitory effect of konjac petroleum ether extract on TNBC cell migration, invasion, and EMT.
- To elucidate the mechanism of action involving the OLFML2A gene.
- To assess the potential of konjac extract as a therapeutic agent for TNBC.
Main Methods:
- Analysis of OLFML2A expression and EMT markers in TNBC patient specimens.
- Gene knockdown of OLFML2A in MDA-MB-231 cells.
- Treatment of OLFML2A-knockdown cells with konjac petroleum ether extract.
- Evaluation of cell migration, invasion, adhesion, and EMT marker expression using qPCR, Western blot, and immunofluorescence.
Main Results:
- High OLFML2A expression correlated with reduced E-cadherin and increased N-cadherin, vimentin, and elastin in TNBC patients.
- OLFML2A knockdown in MDA-MB-231 cells reduced migration and invasion, upregulating E-cadherin and downregulating mesenchymal markers.
- Konjac extract inhibited TNBC cell proliferation (IC50 = 220 μg/mL at 48h) and dose-dependently inhibited migration and invasion.
- Konjac extract mimicked the effects of OLFML2A knockdown on EMT markers.
Conclusions:
- Konjac petroleum ether extract inhibits TNBC cell migration and invasion by modulating OLFML2A to inhibit EMT.
- These findings suggest konjac extract's potential for preventing TNBC metastasis.
- Further investigation is needed to understand the contribution of cytotoxicity at higher concentrations.
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