ABSTRACT
Objective: To assess the clinical efficacy of thoracoscopic surgery with the da Vinci surgical system versus video-assisted thoracoscopic surgery (VATS) for lung cancer. Methods: From August 2019 to December 2020, 193 patients with lung cancer assessed for eligibility scheduled for surgery in our hospital were recruited and assigned at a ratio of 1 : 1 to receive VATS (control group) or thoracoscopic surgery with the da Vinci surgical system (research group). The primary measurement is the clinical efficacy of the two surgical modalities. Results: The baseline features of the research group were comparable with those of the control group (P > 0.05). Besides, the two groups showed similar tumor types, tumor locations, and clinicopathological staging (P > 0.05). Da Vinci surgical system-assisted thoracoscopic surgery had short operative time, less intraoperative blood loss, better lymph node dissection, and lower intraoperative conversion rates compared to VATS. Compared with the control group, the research group had significantly higher postoperative forced expiratory volume in one second (FEV1), forced vital capacity (FVC), maximal voluntary ventilation (MVV), the functional assessment of cancer therapy-general module (FACT-G) of the FACT-lung (FACT-L) Chinese version V4.0, lung cancer-specific module scores, and total scores (P < 0.05). The research group showed better postoperative drainage volume, shorter intubation duration, and length of hospital stay and a lower incidence of complications versus the control group (P < 0.05). The da Vinci surgical system reduced the probability of intraoperative mistakes and better ensured a safe and satisfactory surgery. Conclusion: The thoracoscopic surgery with the da Vinci surgical system better reduces intraoperative and postoperative bleeding, shortens drainage and intubation duration, enhances the lung function and survival quality of patients, and lowers the risk of surgical mistakes to ensure surgical safety versus VATS.
ABSTRACT
Nicotine has been found to induce the proliferation of lung cancer cells through tumor invasion and to confer resistance to apoptosis. Periostin is abnormally highly expressed in lung cancer and is correlated with angiogenesis, invasion and metastasis. Here, we investigated the roles of periostin in the lung cancer cell proliferation, drug resistance, invasion and epithelial-mesenchymal transition (EMT) induced by nicotine. The periostin gene was silenced using small interfering RNA (siRNA) in A549 non-small cell lung cancer (NSCLC) cells. The cells were transfected with control or periostin siRNA plasmids. Periostin mRNA was evaluated by quantitative reverse transcription-polymerase chain reaction (RT-PCR). Cell proliferation was detected using the MTT assay and cell apoptosis was detected by Annexin V-FITC and propidium iodide (PI) double staining. Tumor invasion was detected by the Boyden chamber invasion assay. Western blotting was performed to detect the expression of the EMT marker Snail. Our results revealed that stably periostin-silenced cells were acquired by G418 screening, and the periostin mRNA expression levels of which were decreased by nearly 80%. Periostin-silenced A549 cells exhibited reduced cell proliferation, elevated sensitivity to chemotherapy with cisplatin, decreased cell invasion and Snail expression (P<0.05). Nicotine upregulated the periostin protein levels in the A549 cells and this upregulation was not blocked by the generalized nicotinic acetylcholine receptor (nAChR) antagonist, hexamethonium. In conclusion, periostin is one of the targets regulated by nicotine in lung cancer cells and is involved in the cancer cell growth, drug resistance, invasion and EMT induced by nicotine.
