ObjectiveTo explore the influence mechanism of proliferation and invasion in colon cancer cell after silence of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) gene. MethodsRT-PCR or Western blot method was used to detect the expression of PTEN mRNA or protein among four colon cancer cell lines (HT-29, WiDr, CaCo-2, and Colo320 cell lines). small interfering RNA (siRNA) was used to synthetize PTEN siRNA and transfect it into colon cancer cells. The expression of PTEN protein after transfecting was detected by Western blot. WsT-1 and invasion assay were used to examine the effects of PTEN siRNA silence on proliferation and invasion in colon cancer cells. ResultsPTEN mRNA and protein were expressed in all the four colon cancer cell lines. After PTEN siRNA transfected into the colon cancer cells, the expressions of PTEN proteins were inhibited in all the four colon cancer cell lines (P < 0.01), and the proliferation and invasion of colon cancer cells were enhanced significantly (P < 0.01). ConclusionsPTEN siRNA play an important role in metastasis process of colon cancer via enhanced its proliferation and invasion. Therefore, the understanding biologic mechanisms for regulation of PTEN might enable better molecular target therapy of treating the colon cancer patients with metastasis.
Objective To improve the knowledge of pulmonary artery sarcoma ( PAS) and early diagnosis.Methods The clinical data of 8 patients with PAS confirmed by biopsy from April 2001 to April 2012 in Beijing Anzhen Hospital were retrospectively analyzed. Results There were 5 males and 3 females, with mean age of 46. 75 ±11. 47 years [ range: 32-67 years] . The main clinical manifestations were chest tightness, shortness of breath, intermittent syncope, heart palpitations at exertion, etc. Laboratory examinations showed the patients with PAS have no obvious hypoxemia and most of them have normal D-dimer level. Echocardiography revealed pulmonary hypertension, right ventricular enlargement, and echo of massive lumps in main pulmonary truck. Lower limb veins were normal in color doppler ultrasonography. Chest X-ray revealed prominent pulmonary artery segment, full segment of the right pulmonary artery, an increased hilum and pleural effusion. CT pulmonary angiography showed expansion of pulmonary artery, large filling defect in main pulmonary truck and left or right pulmonary artery, combined with pericardial effusion, pleural effusion. Lung ventilation/perfusion imaging did not match, showing radioactive sparse and defects in multiple lung segments and subsegments, involved 3 to 13 lung segments. Pulmonary angiography showed filling defects in the main pulmonary artery, left or right pulmonary artery. 8 patients were confirmed pathologically after operation. Pathological results showed leiomyosarcoma differentiation in 3 cases, undifferentiated sarcoma in2 cases, and undefined pathological type in 3 cases. All 8 patients were misdiagnosed as pulmonary embolism before surgery. The average days of misdiagnosis were 85. 6 ±21. 5 days. 7 cases were given simple surgical resection, one case underwent surgical resection combined with radiotherapy and chemotherapy. 7 cases were relieved and discharged, and one case died. Conclusion PAS is a rare disease clinically and is easily misdiagnosed as pulmonary embolism. Clinicians should enhance the recognition in order to diagnose early and treat comprehensively.