ABSTRACT
Primary hepatic paraganglioma (PGL) is a rare neuroendocrine tumor characterized by clinical manifestations including paroxysmal hypertension, palpitation, abdominal pain and constipation. In the present study, the case of a 21-year-old woman with pathologically confirmed hepatic PGL with megacolon following surgery is reported. The patient initially visited Beijing Tiantan Hospital (Beijing, China) for hypoferric anemia. A triple-phase CT scan of the whole abdomen showed a large hypodense mass with a solid periphery and strong arterial enhancement of the peripheral solid portion of the liver. The sigmoid colon and rectum were obviously distended, filled with gas and intestinal contents. The patient was preoperatively diagnosed with iron deficiency anemia, liver injury and megacolon and then underwent partial hepatectomy, total colectomy and enterostomy. Microscopically, the liver cells exhibited an irregular zellballen pattern. In addition, immunohistochemical staining revealed that liver cells were positive for CD56, chromogranin A, vimentin, S-100, melan-A and neuron-specific enolase. Therefore, the diagnosis of primary PGL of the liver was confirmed. These findings suggested that primary hepatic PGL should not be excluded when megacolon occurs and comprehensive imaging evaluation is of great importance for its diagnosis.
ABSTRACT
BACKGROUND: Gastric cancer is one of the most common malignant tumors of the digestive system worldwide, posing a serious danger to human health. Cyclooxygenase (COX)-2 plays an important role in the carcinogenesis and progression of gastric cancer. Acetyl-11-keto-ß-boswellic acid (AKBA) is a promising drug for cancer therapy, but its effects and mechanism of action on human gastric cancer remain unclear. AIM: To evaluate whether the phosphatase and tensin homolog (PTEN)/Akt/COX-2 signaling pathway is involved in the anti-tumor effect of AKBA in gastric cancer. METHODS: Human poorly differentiated BGC823 and moderately differentiated SGC7901 gastric cancer cells were routinely cultured in Roswell Park Memorial Institute 1640 medium supplemented with 10% fetal bovine serum and 1% penicillin/streptomycin. Gastric cancer cell proliferation was determined by methyl thiazolyl tetrazolium colorimetric assay. Apoptosis was measured by flow cytometry. Cell migration was assessed using the wound-healing assay. Expression of Bcl-2, Bax, proliferating cell nuclear antigen, PTEN, p-Akt, and COX-2 were detected by Western blot analysis. A xenograft nude mouse model of human gastric cancer was established to evaluate the anti-cancer effect of AKBA in vivo. RESULTS: AKBA significantly inhibited the proliferation of gastric cancer cells in a dose- and time-dependent manner, inhibited migration in a time-dependent manner, and induced apoptosis in a dose-dependent manner in vitro; it also inhibited tumor growth in vivo. AKBA up-regulated the expression of PTEN and Bax, and down-regulated the expression of proliferating cell nuclear antigen, Bcl-2, p-Akt, and COX-2 in a dose-dependent manner. The PTEN inhibitor bpv (Hopic) reversed the high expression of PTEN and low expression of p-Akt and COX-2 that were induced by AKBA. The Akt inhibitor MK2206 combined with AKBA down- regulated the expression of p-Akt and COX-2, and the combined effect was better than that of AKBA alone. CONCLUSION: AKBA inhibits the proliferation and migration and promotes the apoptosis of gastric cancer cells through the PTEN/Akt/COX-2 signaling pathway.
