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Background Adenomyoepithelioma (AME) of the breast is a rare subtype of breast tumor. Most of AMEs reported are solid, however, cystic or prominent cystic changes are extremely rare. Case presentation A 51-year-old woman presented a lump in the upper outer quadrant of right breast, and it was accompanied by continuous breast pain and bilateral axillary itching for more than 2 months. There were no other symptoms found. Preoperative mammography and ultrasound examination were performed. Mammography showed a noncalcified lobulated mass, and it was considered to be a benign cyst with septum on ultrasound, but ductal carcinoma of breast, adenoid cystic carcinoma could not be excluded. At first, AME was not considered preoperatively, because the imaging features of this rare tumor may vary widely, which may result in an incorrect diagnosis. But eventually, AME was diagnosed by postoperative pathology and immunohistochemistry. Conclusion We herein present a rare case of breast AME with prominent cystic changes. AME has no-specific imaging features, but the benign or malignant nature of the lesion might be suspected on imaging.

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The study aimed to identify TUG1 as an essential regulator of apoptosis in HT22 (mouse hippocampal neuronal cells) by direct interaction with the RNA-binding protein HuR. In order to study the role of TUG1 in the context of ischemia, we used mouse hippocampal neuronal cells treated with oxyglucose deprivation to establish an in-vitro ischemia model. A bioinformatic analysis and formaldehyde RNA immunoprecipitation (fRIP) were used to investigate the biological functions. A Western blot assay and reverse transcription polymerase chain reaction were used to explore the expression of the molecules involved. A cell proliferation and cytotoxicity assay was performed to detect neuronal apoptosis. TUG1 exhibits a localization-specific expression pattern in HT22 cells under OGD treatment. The bioinformatics analysis showed a strong correlation between the TUG1 and HuR as predicted, and this interaction was subsequently confirmed by fRIP-qPCR. We found that HuR was translocated from the nucleus to the cytoplasm after ischemia treatment and subsequently targeted and stabilized COX-2 mRNA, which led to elevated COX-2 mRNA levels and apoptosis of the HT22 cells. Furthermore, nuclear-specific disruption of TUG1 prevented the translocation of HuR to the cytoplasm and decreased COX-2 mRNA expression, resulting in increased cell viability and partially reversed apoptosis. In conclusion, it was demonstrated that TUG1 accelerates the process of apoptosis by promoting the transfer of HuR to the cytoplasm and stabilizing COX-2 mRNA. These results provide useful information concerning a therapeutic target for ischemic stroke.