Background
More and more evidences demonstrate that circular RNAs (circNRAs) can encode protein. As a circRNA with translation capabilities, outcomes of circβ‐catenin in non‐small cell lung cancer (NSCLC) still need to be explored.
Method
The research methods of circβ‐catenin in the article include qRT‐PCR, wound healing assay, CCK‐8, colony formation, and Transwell assay. Western blotting and immunofluorescence were provided to detect protein expression levels and peptide encoded by circβ‐catenin, respectively.
Results
A prominently higher circβ‐catenin expression was found in NSCLC tissues. Silencing of circβ‐catenin was able to inhibit NSCLC cell migrating, invasive, and proliferative phenotypes. Overexpression of circβ‐catenin could enhance the migrating, invasive, and proliferative phenotypes of NSCLC cells. Importantly, circβ‐catenin was found to encode a peptide in NSCLC cells. Silencing or overexpression of circβ‐catenin could reduce or increase β‐catenin protein expression via suppressing the degradation of β‐catenin.
Conclusion
Circβ‐catenin could promote NSCLC cell malignant phenotypes via peptide‐regulated β‐catenin pathway. Our study provided a new understanding for the mechanisms of NSCLC.
Purpose
Zinc oxide nanoparticles (ZnONPs) are one of the most important nanomaterials that are widely used in the food, cosmetic and medical industries. Humans are often exposed to ZnONPs via inhalation, and they may reach the brain where neurotoxic effects could occur via systemic distribution. However, the mechanisms underlying how ZnONPs produce neurotoxic effects in the brain remain unclear. In this study, we aimed to investigate the novel mechanism involved in ZnONPs-induced neurotoxicity.
Methods and Results
We demonstrated for the first time that pulmonary exposure to ZnONPs by intratracheal instillation could trigger ferroptosis, a new form of cell death, in the neuronal cells of mouse cerebral cortex. A similar phenomenon was also observed in cultured neuron-like PC-12 cell line. By using a specific inhibitor of ferroptosis ferrostatin-1 (Fer-1), our results showed that inhibition of ferroptosis by Fer-1 could significantly alleviate the ZnONPs-induced neuronal cell death both in vivo and in vitro. Mechanistic investigation revealed that ZnONPs selectively activated the JNK pathway and thus resulted in the ferroptotic phenotypes, JNK inhibitor SP600125 could reverse lipid peroxidation upregulation and ferroptotic cell death induced by ZnONPs in PC-12 cells.
Conclusion
Taken together, this study not only demonstrates that pulmonary exposure of ZnONPs can induce JNK-involved ferroptotic cell death in mouse cortex and PC-12 cells, but also provides a clue that inhibition of ferroptosis by specific agents or drugs may serve as a feasible approach for reducing the untreatable neurotoxicity induced by ZnONPs.
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