Xiang-Wei Meng

Wnt/β-catenin signaling pathway may regulate cell cycle and expression of cyclin A and cyclin E protein in hepatocellular carcinoma cells

Wnt/β-catenin signaling pathway and cell cycle play the key roles during the genesis and development of hepatocellular carcinoma (HCC). The cytoplasmic protein β-catenin is a multifunctional protein and a central molecule in the Wnt signaling pathway. Cell cycle is regulated by a a series of regulatory factors. Current researches indicated that expression of cyclin D1 and c-myc decreased after silencing β-catenin gene in HCC, but it is unclear if other cyclins are affected. To determine the relation, small interference RNA(siRNA) against β-catenin was transfected into HCC cell line HepG2, and cell cycle and cyclin A and cyclin E protein expression were detected. We demonstrated that cell cycle was arrested in G0/G1 at 72 h after the transfection and with the time passing, the cell cycle began to transfer from G0/G1 to G2/M through S and had a trend to revert at 96 h. In addition, β-catenin protein expression was decreased at both 72 and 96 h, although the level was slightly higher at 96 h than that at 72 h. However, cyclin A and cyclin E protein expression increased at 72 h and decreased at 96 h. These findings suggest that silencing β-catenin gene may induce the changes of cell cycle and cyclin A and cyclin E expression. Wnt/β-catenin signaling pathway probably takes part in the genesis and development of HCC through regulating cell cycle and the expression of cyclin A and cyclin E.

The effect of cell cycle and expression of cyclin B1 and cyclin C protein in hepatocellular carcinoma cell line HepG2 and SMMC-7721 after of silencing β-catenin gene.

BACKGROUND/AIMS Abnormalities in cell cycle regulation are reported to be strongly associated with tumorigenesis and progression of tumors. Wnt/β-catenin signaling pathway and cell cycle play key roles during the genesis and development of hepatocellular carcinoma (HCC). Current studies indicated that expressions of cyclin A, E and D1 were affected after silencing of β-catenin gene in HCC, but it is unclear if other cyclins are affected. METHODOLOGY To determine the relation, small interference RNA (siRNA) against β-catenin was transfected into HCC cell lines HepG2 and SMMC-7721, and cell cycle and cyclin B1 and cyclin C protein expression were detected. RESULTS Cell cycle was arrested in G0/G1 at 72h after transfection and the cell cycle began to transfer from G0/G1 to G2/M through S and had a trend to revert at 96h. In addition, β-catenin protein expression was decreased at both 72 and 96h, although the level was slightly higher at 96h than that at 72h. However, cyclin B1 expression decreased at 72h and increased at 96h, cyclin C expression increased at 72h and decreased at 96h. CONCLUSIONS These findings suggest that silencing β-catenin gene may induce the changes of cell cycle and cyclin B1 and cyclin C protein expression. Wnt/β-catenin signaling pathway probably takes part in the genesis and development of HCC through regulating cell cycle and the expression of cyclin B1 and cyclin C.

Differences in the expression profiles of claudin proteins in human gastric carcinoma compared with non‑neoplastic mucosa

Numerous genetic alterations associated with cancer progression have the potential to serve as biomarkers for the early diagnosis of cancer. Numerous studies have suggested that claudin proteins, which are the primary components of tight junction structures, are associated with the regulation of cell polarity and cell differentiation. To investigate the expression profiles of the tight junction proteins claudin-2, −5, −7 and −8 in gastric carcinoma, immunohistochemical analysis, western blotting and reverse transcription-quantitative polymerase chain reaction analysis was used to detect the expression profiles of these claudin proteins in gastric carcinoma tissues and in homologous non-neoplastic mucosal tissues. According to the present study, the expression levels of claudin-7 and claudin-8 were downregulated, while the expression of claudin-5 was upregulated in gastric carcinoma tissues compared with in non-neoplastic mucosal tissues. Additionally, no notable difference was observed between claudin-2 expression in gastric carcinoma tissues and non-neoplastic mucosae. Correlations between claudin-7 and −8 expression and lymphatic metastasis in gastric carcinoma tissues were additionally reported. In summary, the present study revealed the distinct expression profiles of claudin-5, −7 and −8 in non-neoplastic mucosal tissues and gastric carcinoma tissues. Furthermore, the expression of these claudin proteins was highly associated with metastatic progression and prognosis in patients with gastric carcinoma, and had predictive value for the metastasis and survival of patients with gastric carcinoma.

A Case of Primary Malignant Melanoma of the Esophagus

A 63-year-old female presented with progressive dysphagia for 1 month. CT scan of the chest demonstrated esophageal narrowing due to extrinsic compression at the lower esophageal (Fig. 1). There was no conspicuous lymphadenectasis in the superior and middle mediastinum. Endoscopy identified a large, easy bleeding pigmented polypoidal lesion with superficial anabrosis located 30–35 cm from the incisors (Fig. 2).The tumor was removed via a left thoracotomy. In gross appearance, the resected specimen measured 3.5 9 2.5 9 1.5 cm in size (Fig. 3). A definite diagnosis was made by histologic section (Fig. 4) and immunohistochemical examination with positive results of HMB45 and S100 protein. The clinical stage was finally classified as IIb (T1N1M0). After recovering from operation, the patient was sent to the oncology department to receive radiotherapy and chemotherapy. One year and five months after the surgery, an endoscopy was operated on this patient, and the result showed that there was no manifestation of tumor recurrence in the anastomotic area (Fig. 5). Discussion