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 investigate the safety and efficacy of laparoscopy-assisted D2 radical gastrectomy in the treatment of advanced gastric cancer.Methods From March 2011 to March 2016,one hundred and four cases treated with LAG for advanced gastric cancer in the general surgery department of Gaochun District People Hospital of Nanjing and the 251st Hospital of PLA were collected in the laparoscope group,104)and 101 cases undergoing gastric cancer surgery from the same period were selected as the control group(open surgery group).A retrospective analysis was performed between the two groups in operation time, intraoperative blood loss, postoperative eating time, ambulation time, exhaust time, postoperative fever, postoperative analgesic use,hospitalization time,postoperative complications,the proximal and distal margins and the number of lymph node dissection.Results The operation time was significantly longer in the LAG group than in the open surgery group(311.2 ± 28.9)min vs.(157.38 ± 11.9)min,t=2.899,P<0.01).The intraoperative blood loss in the laparoscope group was less than that in the open surgery group((100.3±12.1) ml vs.(200.6±16.3)ml,t=3.014,P<0.01).In addition,the frequency of postoperative analgesia,the first postoperative exhaust time,the first postoperative eating time and the postoperative hospital stay in the laparoscopic group were better than those in the open surgery group(P<0.05).There was no significant difference in the number of lymph node dissection and postoperative complication between the two groups(P=0.264,P=0.575).The survival analysis showed that the overall survival rate in the two groups was equivalent at 6 years after surgery(P=0.623).Conclusion Laparoscopy-assisted radical gastrectomy for advanced gastric cancer is safe and feasible,with acceptable long-term results,and shows better performance in the near future.

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