miR-124-3p has been implicated in a variety of cancers. The purpose of the present study was to investigate the expression, prognostic roles and functions of miR-124-3p in gastric cancer. Functional studies indicated that ectopic overexpression of miR-124-3p in gastric cancer cells suppressed cell viability and plate colony formation in vitro and tumor growth in vivo. In situ hybridization analysis demonstrated that decreased expression of miR-124-3p was associated with clinical stage and lymph node metastasis, as well as shorter overall survival and disease-free survival rates. Furthermore, it was observed that miR-124-3p repressed the carcinogenesis of gastric cancer by targeting Ras-related C3 botulinum toxin substrate 1 (Rac1) and specificity protein 1 (SP1). Collectively, these results indicate a potential underlying mechanism for the regulation of gastric cancer by miR-124-3p involving targeting of Rac1 and SP1. Thus, miR-124-3p may be an independent indicator of survival and treatment strategy for patients with gastric cancer.
The present study aimed to explore how histone deacetylases (HDAC3) regulated the resistance to cisplatin by inhibiting the transcription of lncRNA-LOC101928316 (LOC101928316) in gastric cancer (GC). We revealed that HDAC3 expression in cisplatin-resistant cell lines was significantly higher than that of GC parental cell lines. Besides, knockdown of HDAC3 inhibited the cell activity, cell invasion, and migration but promoted the apoptosis of GC cisplatin-resistant cell lines. To our surprise, silencing HDAC3 inhibited the transcription of LOC101928316 by promoting the level of acetylation of H3K4 on the LOC101928316 promoter, thus promoting the LOC101 expression in GC cisplatin-resistant cell lines. Together, the overexpression of HDAC3 mediated LOC101928316 to promote GC resistance to cisplatin by activating the PI3K-Akt-mTOR pathway. Therefore, HDAC3 may serve as a potential target of cisplatin resistance in GC.
We are reporting a case of toxic epidermal necrosis induced by herbal
medicine in a 54-year-old woman who had been diagnosed with primary
Sjogren’s syndrome for nine years and had discontinued all conventional
therapies for at least one year. Approximately two weeks prior to her
current admission, she developed crops of petechiae and purpuric macules
on her lower extremities, which are typical symptoms of
hypergammaglobulinemic purpura of Waldenström, and began taking herbal
medicine. The following day, she presented to us with a high fever and
new, generalized erythematous rashes over her face and trunk. She was
ultimately diagnosed with toxic epidermal necrosis induced by the herbal
medicine.
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