ABSTRACT
@#Objective To explore the safety and feasibility of the application of video-assisted thoracic surgery (VATS) anatomic segmentectomy in single-stage bilateral thoracic surgery for the treatment of bilateral localized bronchiectasis. Methods From June 2014 to June 2018, 19 patients with bilateral localized bronchiectasis underwent single-stage bilateral thoracic surgery with VATS anatomic segmentectomy, including 11 males and 8 females aged 38.0±12.5 years. The clinical efficacy of the surgery was evaluated. Results All surgeries were successfully completed, of which 17 were bilateral VATS, 2 were unilateral VATS with the other lateral converted to thoracotomy. The average number of bilateral resected segments was 4-8 (5.9±1.2). Mean operation time was 330.0±40.0 min and mean blood loss was 150.0±60.0 mL. Mean ventilator-assisted breathing time was 6.0±1.8 h, mean duration of chest-tube placement was 4.0±1.0 d and mean hospital stay time was 14.0±1.5 d. Three patients suffered pulmonary infection and 1 patient received tracheotomy. No perioperative death occurred. Arterial oxygen pressures on postoperative day (POD) 1 (F=340.18, P<0.05) and POD 3 (F=131.26, P<0.05) were significantly lower than that before operation, arterial carbon dioxide pressures on POD 1 (F=46.62, P<0.05) and POD 3 (F=48.21, P<0.05) were significantly higher than that before operation, and pulse oximeter saturation on POD 1 was significantly lower than that before operation (F=210.82, P<0.05). The patients were followed up for one to five years without recurrence. Conclusion Application of VATS anatomic segmentectomy in single-stage bilateral thoracic surgery for the treatment of bilateral localized bronchiectasis is safe and feasible with strictly selected patients. Postoperative airway management is very important. The surgery is worthy of wide clinical practice.
ABSTRACT
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.
ABSTRACT
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.
Subject(s)
Humans , Carcinogenesis , Metabolism , Pathology , Carcinoma, Non-Small-Cell Lung , Metabolism , Pathology , Cell Line, Tumor , Lung Neoplasms , Metabolism , Pathology , Oligopeptides , Metabolism , Phosphatidylinositol 3-Kinases , Metabolism , Proto-Oncogene Proteins c-akt , Metabolism , Signal Transduction , PhysiologyABSTRACT
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.
ABSTRACT
This study examined the synergetic effect of class IA Phosphoinositide 3-kinases catalytic subunit p110β knockdown in conjunction with oxaliplatin treatment on colon cancer cells. Down-regulation of p110β by siRNA interference and oxaliplatin treatment were applied in colon cancer cell lines HT29, SW620 and HCT116. MTT assay was used to measure the inhibitory effect of p110β knockdown on the proliferation of colon cancer cell lines. SubG1 assay and Annexin-V FITC/PI double-labeling cytometry were applied to detect cell apoptosis. And cell cycle was evaluated by using PI staining and flow cytometry. The expression of caspase 3, cleaved PARP, p-Akt, T-Akt and p110β was determined by western blotting. The results suggested that down-regulation of p110β expression by siRNA obviously reduced cell number via accumulation in G(0)-G(1) phase of the cell cycle in the absence of notablely increased apoptosis in colon cancer cell lines HT29 and SW620 (S phase arrest in HCT116). Moreover, inhibition of p110β expression increased oxaliplatin-induced cell apoptosis and cell cycle arrest in HT29, HCT116 and SW620 cell lines. In addition, increases of cleaved caspase-3 and cleaved PARP induced by oxaliplatin treatment were determined by immunoblotting in p110β knockdown group compared with normal control group and wild-type group. It is concluded that down-regulated expression of p110β could inhibit colon cancer cells proliferation and result in increased chemosensitivity of colorectal cancer cells to oxaliplatin through augmentation of oxaliplatin-induced cell apoptosis and cell cycle arrest.