This study examined the role of EMP-1 in tumorigenesis of non-small cell lung carcinoma (NSCLC) and the possible mechanism. Specimens were collected from 28 patients with benign lung diseases and 28 with NSCLC, and immunohistochemically detected to evaluate the correlation of EMP-1 expression to the clinical features of NSCLC. Recombinant adenovirus was constructed to over-express EMP-1 and then infect PC9 cells. Cell proliferation was measured by Ki67 staining. Western blotting was performed to examine the effect of EMP-1 on the PI3K/AKT signaling. Moreover, tumor xenografts were established by subcutaneous injection of PC9 cell suspension (about 5×10(7)/mL in 100 μL of PBS) into the right hind limbs of athymic nude mice. The results showed EMP-1 was significantly up-regulated in NSCLC patients as compared with those with benign lung diseases. Over-expression of EMP-1 promoted proliferation of PC9 cells, which coincided with the activation of the PI3K/AKT pathway. EMP-1 promoted the growth of xenografts of PC9 cells in athymic nude mice. It was concluded that EMP-1 expression may contribute to the development and progress of NSCLC by activating PI3K/AKT pathway.

Objective To explore the function of p53 on regulating the expression of miR-148b in lung cancer cell line PC-9 and its corresponding molecular mechanism and the impact on cell proliferation. Methods Transient transfection of p53 eukaryotic expressing plasmids into lung cancer cell line PC-9 was performed to establish a cell model over-expressing p53. RT-PCR was used to explicit the impact of p53 on the expression of miR-148b. A reporter vector containing miR-148b promoter was used to investigate the function of p53 on regulating the transcription of miR-148b. Low-expressing miR-148b by transfecting its specific inhibitors , a CCK-8 assay was performed to explore the influence of miR-148b on the lung cancer cell proliferation inhibited by p53. Results Over-expression of p53 promoted miR-148b expression in lung cancer cell line PC-9. P53 could increase the luciferase activity driven by miR-148b promoters. Knockdown of miR-148b attenuated the impact of p53 on inhibiting the proliferation of PC-9 cells. Conclusion P53 inhibits the proliferation of lung cancer cell line PC-9 partially depending on miR-148b.

Objective To compare the clinical efficacy of laparoscopic wedge resection and open wedge resection in the treatment of gastrointestinal stromal tumor. Methods Fifty?five patients with gastrointestinal stromal tumor who underwent laparoscopic wedge resection and 61 cases underwent open wedge resection in Tongji Hospital from January 2009 to December 2014 were included into this study. The perioperative, surgical operative and postoperative data of the patients were documented and analyzed. Results The operation time of laparoscopic group was significantly shorter than that of the open group [(108.2±27.2) min versus (139.9±75.3) min, P=0.021], the amount of intraoperative blood loss was overtly reduced in the laparoscopic group [(57.1±48.7) ml versus (100.6±45.8) ml, P=0.011], the time to postoperative exhaust or defecation was (2.2±1.4) d in the laparoscopic group and (3.5±1.8) d in the open group (P=0.028), and the length of hospital stay was (5.7±1.3) d versus (6.9±2.1) d (P=0.044). There were intraoperative complication in one case and postoperative complications in 5 cases, while neither tumor rupture nor obvious perioperative complication was observed in the laparoscopic group. During the period of follow?up ( mean, 15.3 months) , only one case of replase occurred in the laparoscopic group while four cases of relapse were observed in the open group. Conclusions With experienced skills and to strictly comply with the surgical indications, laparoscopic wedge resection is prior to tranditional open wedge resection for the treatment of gastrointestinal stromal tumor. The laparoscopic wedge resection can achieve the standard of R0 resection, keep the resected tumor with an intact capsule, reduce the operating time and operative trauma, promote the postoperative recovery and get a better prognosis. Therefore, it is a feasible, safe, minimally invasive surgical procedure associated with a rapid postoperative recovery.

Objective To compare the clinical efficacy of laparoscopic wedge resection and open wedge resection in the treatment of gastrointestinal stromal tumor. Methods Fifty?five patients with gastrointestinal stromal tumor who underwent laparoscopic wedge resection and 61 cases underwent open wedge resection in Tongji Hospital from January 2009 to December 2014 were included into this study. The perioperative, surgical operative and postoperative data of the patients were documented and analyzed. Results The operation time of laparoscopic group was significantly shorter than that of the open group [(108.2±27.2) min versus (139.9±75.3) min, P=0.021], the amount of intraoperative blood loss was overtly reduced in the laparoscopic group [(57.1±48.7) ml versus (100.6±45.8) ml, P=0.011], the time to postoperative exhaust or defecation was (2.2±1.4) d in the laparoscopic group and (3.5±1.8) d in the open group (P=0.028), and the length of hospital stay was (5.7±1.3) d versus (6.9±2.1) d (P=0.044). There were intraoperative complication in one case and postoperative complications in 5 cases, while neither tumor rupture nor obvious perioperative complication was observed in the laparoscopic group. During the period of follow?up ( mean, 15.3 months) , only one case of replase occurred in the laparoscopic group while four cases of relapse were observed in the open group. Conclusions With experienced skills and to strictly comply with the surgical indications, laparoscopic wedge resection is prior to tranditional open wedge resection for the treatment of gastrointestinal stromal tumor. The laparoscopic wedge resection can achieve the standard of R0 resection, keep the resected tumor with an intact capsule, reduce the operating time and operative trauma, promote the postoperative recovery and get a better prognosis. Therefore, it is a feasible, safe, minimally invasive surgical procedure associated with a rapid postoperative recovery.

This study examined the role of EMP-1 in tumorigenesis of non-small cell lung carcinoma (NSCLC) and the possible mechanism. Specimens were collected from 28 patients with benign lung diseases and 28 with NSCLC, and immunohistochemically detected to evaluate the correlation of EMP-1 expression to the clinical features of NSCLC. Recombinant adenovirus was constructed to over-express EMP-1 and then infect PC9 cells. Cell proliferation was measured by Ki67 staining. Western blotting was performed to examine the effect of EMP-1 on the PI3K/AKT signaling. Moreover, tumor xenografts were established by subcutaneous injection of PC9 cell suspension (about 5×10(7)/mL in 100 μL of PBS) into the right hind limbs of athymic nude mice. The results showed EMP-1 was significantly up-regulated in NSCLC patients as compared with those with benign lung diseases. Over-expression of EMP-1 promoted proliferation of PC9 cells, which coincided with the activation of the PI3K/AKT pathway. EMP-1 promoted the growth of xenografts of PC9 cells in athymic nude mice. It was concluded that EMP-1 expression may contribute to the development and progress of NSCLC by activating PI3K/AKT pathway.
Carcinogenesis ; metabolism ; pathology ; Carcinoma, Non-Small-Cell Lung ; metabolism ; pathology ; Cell Line, Tumor ; Humans ; Lung Neoplasms ; metabolism ; pathology ; Oligopeptides ; metabolism ; Phosphatidylinositol 3-Kinases ; metabolism ; Proto-Oncogene Proteins c-akt ; metabolism ; Signal Transduction ; physiology