Hepatoid adenocarcinoma of the stomach (HAS) is a rare form of gastric cancer that has unique clinicopathological features and an extremely poor prognosis. Here, we report on three patients with suspected gastric cancer who were referred to our hospital. Gastrointestinal fiberscopy on the three patients revealed two lesions in the antrum and a third lesion in the gastroesophageal junction. The alpha fetoprotein (AFP) serum levels were markedly elevated in all cases. At the time of diagnosis, two cases were advanced stages with lymph nodes and/or liver metastases. Two patients underwent exploratory laparotomy. A total gastrectomy was performed on the operable lesion, and an expanded gastrectomy was completed in the case with hepatic metastases. Histopathological analysis revealed that the tumors displayed two pathological changes: hepatoid-like foci and adenocarcinomatous. Furthermore, the tumor cells were immunohistochemically positive for AFP, alpha-1 antitrypsin, and alpha-1 antichymotrypsin. All three patients received chemotherapy. The follow-up duration ranged from 8-36 mo. Our experience and previous published studies have suggested that HAS is an aggressive type of adenocarcinoma. However, radical surgery and chemotherapy may positively impact clinical outcomes.
The study was aimed to investigate the role and mechanism of long non-coding RNAs (lncRNA) myocardial infarction-associated transcript (MIAT) in prostate cancer. The relationships between lncRNA MIAT and miR-361-3p, miR-361-3p and cell cycle and apoptosis regulator 2 (CCAR2) were predicted by StarBase and TargetScan, and verified by dual-luciferase reporter assay and RNA pull-down assay. Quantitative real-time PCR assay was performed to detect the mRNA expression of lncRNA MIAT, miR-361-3p, CCAR2, Bax, and Bcl-2 in the prostate cancer tissues or cells. The protein levels of CCAR2, Bax, and Bcl-2 were detected by Western blot analysis. The cell viability and apoptosis were detected by MTT assay and Flow cytometry analysis, respectively. lncRNA MIAT was upregulated, while miR-361 was downregulated in the prostate cancer tissues and Du145 cells. lncRNA MIAT negatively regulated miR-361-3p expression in Du145 cells. Downregulating lncRNA MIAT decreased the cell viability, induced the cell apoptosis, increased Bax expression, and decreased Bcl-2 expression in Du145 cells, while the effects were reversed by downregulating miR-361-3p or CCAR2 upregulation. Moreover, CCAR2 upregulation reversed the effects of miR-361-3p upregulation on Du145 cell viability and apoptosis. In conclusion, lncRNA MIAT participated in prostate cancer by regulating cell proliferation and apoptosis via miR-361-3p/CCAR2 axis.
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