Key result
Carvedilol inhibits trastuzumab-induced cytotoxicity in cardiomyoblasts and reverses translation protein downregulation.
Why the study?
Heart dysfunctions are the major complications of trastuzumab in patients with HER2-positive breast cancers.
Does carvedilol prevent trastuzumab-induced cytotoxicity and proteomic changes in H9c2 cardiomyoblasts?
Does carvedilol prevent trastuzumab-induced cytotoxicity and proteomic changes in H9c2 cardiomyoblasts?
Carvedilol mitigates trastuzumab-induced cardiotoxicity in H9c2 cells by reversing proteomic changes, particularly those related to translation.
Carvedilol may mitigate trastuzumab cardiotoxicity in cardiomyoblasts; hypothesis-generating for cardioprotection in HER2-positive breast cancer.
OBJECTIVE: Heart dysfunctions are the major complications of trastuzumab in patients with Human Epidermal growth factor Receptor-2 (HER2)-positive breast cancers. METHODS: In this study, the cytotoxicity of trastuzumab on H9c2 cardiomyoblasts was demonstrated, and the proteome changes of cells were investigated by a tandem mass tagging quantitative approach. The Differentially Abundant Proteins (DAPs) were identified and functionally enriched. RESULTS: We determined that carvedilol, a non-selective beta-blocker, could effectively inhibit trastuzumab toxicity when administrated in a proper dose and at the same time. The proteomics analysis of carvedilol co-treated cardiomyoblasts showed complete or partial reversion in expressional levels of trastuzumab-induced DAPs. CONCLUSION: Downregulation of proteins involved in the translation biological process is one of the most important changes induced by trastuzumab and reversed by carvedilol. These findings provide novel insights to develop new strategies for the cardiotoxicity of trastuzumab.
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Beiranvand et al. (2020) studied Trastuzumab-induced cardiotoxicity. Carvedilol vs. Trastuzumab alone was evaluated on Cytotoxicity and proteome changes. Carvedilol effectively inhibited trastuzumab-induced cytotoxicity in H9c2 cardiomyoblasts and reversed the downregulation of proteins involved in the translation biological process.
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