Eriocalyxin B induces apoptosis in human triple negative breast cancer cells via inhibiting STAT3 activation and
Ammara Riaz1, Azhar Rasul1, Ghulam Hussain2
1Department of Zoology, Government College University Faisalabad, Punjab Pakistan.
Abstract:
Eriocalyxin B (EriB), a potent ent-kaurene extracted from Isodon eriocalyx, has turned up as novel anti-cancer agent during recent years against a range of cancer types. TNBC (Triple negative breast cancer) is highly aggressive breast cancer, which is resistant towards current therapeutics due to absence of drug targets. Here, we have probed the molecular mechanism of EriB-induced apoptosis in TNBC (MDA-MB231) cells to check whether its anticancer activity is mediated by modulation of STAT3 and NF-ϰB. EriB induced apoptosis in MDA-MB231 cells via inhibiting NF-ϰBp65, STAT3 phosphorylation, increasing Bax/Bcl-2 ratio, MMP dissipation, and activation of caspase-3. These results provide a rationale for further in vivo investigations on EriB, which might also prove to be a potential drug candidate for developing novel therapeutics against TNBC.
Insights
Eriocalyxin B (EriB) shows promise as an anti-cancer agent, effectively inducing apoptosis in triple-negative breast cancer (TNBC) cells by targeting key signaling pathways like STAT3 and NF-κB.
Area of Science:
- Biochemistry
- Molecular Biology
- Pharmacology
Background:
- Triple-negative breast cancer (TNBC) is an aggressive subtype resistant to current therapies due to a lack of specific drug targets.
- Eriocalyxin B (EriB), an ent-kaurene from Isodon eriocalyx, has emerged as a potential anti-cancer agent against various cancer types.
Purpose of the Study:
- To investigate the molecular mechanisms underlying EriB-induced apoptosis in TNBC cells.
- To determine if EriB's anti-cancer activity involves the modulation of STAT3 and NF-κB signaling pathways.
Main Methods:
- Treatment of MDA-MB-231 TNBC cells with EriB.
- Analysis of apoptosis-related markers including NF-κBp65, STAT3 phosphorylation, Bax/Bcl-2 ratio, mitochondrial membrane potential (MMP), and caspase-3 activation.
Main Results:
- EriB treatment induced apoptosis in MDA-MB-231 cells.
- EriB inhibited NF-κBp65 and STAT3 phosphorylation.
- EriB increased the Bax/Bcl-2 ratio, dissipated MMP, and activated caspase-3.
Conclusions:
- EriB effectively induces apoptosis in TNBC cells through the inhibition of NF-κB and STAT3 signaling.
- EriB demonstrates potential as a therapeutic candidate for TNBC, warranting further in vivo investigation.
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