Effect of Decompressive Craniectomy with Stepwise Decompression of the Intracranial Compartment on Postoperative Neurologic Function, Hemodynamics, and Glasgow Outcome Scale Score of Patients with Severe Traumatic Brain Injury.

BACKGROUND: We assess the effects of standard decompressive craniectomy with stepwise decompression of the intracranial compartment on the postoperative neurologic function, hemodynamics, and Glasgow Outcome Scale (GOS) score of patients with severe traumatic brain injury (sTBI). METHODS: One hundred sTBI patients admitted from July 2017 to February 2019 were enrolled and randomly divided into step and standard groups (n = 50) using a random number table. The standard group received traditional standard decompression during surgery, while the step group underwent multistep decompression during surgery. Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) were measured immediately after surgery (T0), 3 hours after surgery (T1), 6 hours after surgery (T2), and 12 hours after surgery (T3). The postoperative Glasgow Coma Scale (GCS) score, neurologic function deficit score, and GOS score were evaluated. RESULTS: After treatment, the excellent/good rate of neurologic function improvement and GCS and GOS scores of the step group significantly exceeded those of the standard group (p < 0.05). Compared with the standard group, the HR, SBP, DBP, and MAP decreased significantly in the step group at T1, T2, and T3 (p < 0.05). CONCLUSION: Standard decompressive craniectomy under multistep decompression can markedly improve the neurologic function, hemodynamics, and prognosis of patients.

XPA Enhances Temozolomide Resistance of Glioblastoma Cells by Promoting Nucleotide Excision Repair.

Glioblastoma is the most frequent, as well as aggressive kind of high-grade malignant glioma. Chemoresistance is posing a significant clinical barrier to the efficacy of temozolomide-based glioblastoma treatment. By suppressing xeroderma pigmentosum group A (XPA), a pivotal DNA damage recognition protein implicated in nucleotide excision repair (NER), we devised a novel method to enhance glioblastoma therapy and alleviate temozolomide resistance. On the basis of preliminary assessment, we found that XPA dramatically increased in glioblastoma compared with normal cells and contributed to temozolomide resistance. By constructing XPA stably knockdown cells, we illustrate that XPA protects glioma cells from temozolomide-triggered reproductive cell death, apoptosis, as well as DNA repair. Besides, XPA silencing remarkably enhances temozolomide efficacy in vivo. This study revealed a crucial function of XPA-dependent NER in the resistance of glioma cells to temozolomide.

CircCDC45 promotes the malignant progression of glioblastoma by modulating the miR-485-5p/CSF-1 axis.

BACKGROUND: Glioblastoma (GBM) is characterized by progressive growth and metastasis. Numerous studies claim that the deregulation of circular RNAs (circRNAs) is associated with cancer progression. However, the role of circRNAs in GBM is largely limited. The purpose of this study was to investigate the functions of circCDC45 in GBM and provide a feasible functional mechanism to support its role. METHODS: The expression of circCDC45, miR-485-5p and colony-stimulating factor 1 (CSF-1) mRNA was examined using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was assessed using cell counting kit - 8 (CCK-8) assay and colony formation assay. Cell migration and cell invasion were monitored using transwell assay. The protein levels of proliferation-related markers and CSF-1 were determined using western blot. The target relationship was predicted using bioinformatics tools and validated using dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Animal models were constructed to verify the role of circCDC45 in vivo. RESULTS: The expression of circCDC45 and CSF-1 was elevated in GBM tissues and cells, while the expression of miR-485-5p was declined. Downregulation of circCDC45 or CSF-1 blocked GBM cell proliferation, invasion and migration as well as tumor growth in vivo. In mechanism, circCDC45 positively regulated the expression of CSF-1 by targeting miR-485-5p. Inhibition of miR-485-5p reversed the biological effects caused by circCDC45 downregulation in GBM cells. CONCLUSION: CircCDC45 promoted the progression of GBM by mediating the miR-485-5p/CSF-1 axis, and circCDC45 might be a promising plasmatic biomarker for GBM diagnosis and treatment.

Hydrogen-rich saline alleviates early brain injury through regulating of ER stress and autophagy after experimental subarachnoid hemorrhage

ABSTRACT Purpose: Subarachnoid hemorrhage (SAH) is a common complication of cerebral vascular disease. Hydrogen has been reported to alleviate early brain injury (EBI) through oxidative stress injury, reactive oxygen species (ROS), and autophagy. Autophagy is a programmed cell death mechanism that plays a vital role in neuronal cell death after SAH. However, the precise role of autophagy in hydrogen-mediated neuroprotection following SAH has not been confirmed. Methods: In the present study, the objective was to investigate the neuroprotective effects and potential molecular mechanisms of hydrogen-rich saline in SAH-induced EBI by regulating neural autophagy in the C57BL/6 mice model. Mortality, neurological score, brain water content, ROS, malondialdehyde (MDA), and neuronal death were evaluated. Results: The results show that hydrogen-rich saline treatment markedly increased the survival rate and neurological score, increased neuron survival, downregulated the autophagy protein expression of Beclin-1 and LC3, and endoplasmic reticulum (ER) stress. That indicates that hydrogen-rich saline-mediated inhibition of autophagy and ER stress ameliorate neuronal death after SAH. The neuroprotective capacity of hydrogen-rich saline is partly dependent on the ROS/Nrf2/heme oxygenase-1 (HO-1) signaling pathway. Conclusions: The results of this study demonstrate that hydrogen-rich saline improves neurological outcomes in mice and reduces neuronal death by protecting against neural autophagy and ER stress.

Antitumor Effect and Toxicity of an Albumin-Paclitaxel Nanocarrier System Constructed via Controllable Alkali-Induced Conformational Changes.

Various strategies have been developed to construct albumin nanomaterials via biophysical or chemical changes. In this work, a compound comprising albumin-paclitaxel nanoparticles (NPs-PTX) with a drug loading efficiency of 21% was constructed via manipulation of alkali induced conformation changes and hydrophilic-hydrophobicity transition. The toxicity of two PTX formulations (Taxol and NPs-PTX) in human umbilical vein endothelial cells (HUVECs), RAW264.7, K562, and HepG2 cells, and rats were determined. The half maximal inhibitory concentration (IC50) of Taxol was remarkably lower than that of NPs-PTX. Both PTX formulations promoted cell apoptosis, possibly via mitochondria-dependent (intrinsic) and mitochondria-independent pathways. The effect of PTX formulations (0.5 to 1 mg mL-1) on hemolysis and the median lethal dose (50% mortality, LD50) values of the PTX formulations were significantly different (p < 0.01). Reductions in the number of white blood cells (WBCs) and monocytes (MNCs) and obvious pathological changes in the spleen, thymus, and mesenteric lymph nodes were observed and may have been related to the bone marrow inhibition effect of PTX. The tumor inhibition rate of NPs-PTX (60.8%) was higher than that of Taxol (31.2%) (p < 0.05) when the dose of NPs-PTX (equivalent PTX) was 2.5 times as that of Taxol (30 vs 12 mg kg-1). Taxol is highly toxic, whereas NPs-PTX is moderately toxic. Thus, NPs-PTX has advantages over the commercially available Taxol formulation in terms of low toxicity and increased dosage, indicating NPs-PTX is a better option for safe and effective PTX delivery.

AQP9 promotes astrocytoma cell invasion and motility via the AKT pathway.

The aquaporin (AQP) family, which includes 13 members identified in mammalian cells, is involved in cancer development and progression. AQP9 expression is upregulated in several tumor tissue types. However, the functions of AQP9 in astrocytoma remain elusive. The present study identified that AQP9 was expressed in astrocytoma cells. AQP9 expression was silenced by transfection with small interfering RNAs and increased by transfection with a plasmid containing the AQP9 gene. Using invasion and wound-healing assays, it was revealed that the knockdown of AQP9 suppressed astrocytoma cell invasion and motility, whereas overexpression of AQP9 promoted the invasion and motility of astrocytoma cells. It was further revealed that AQP9 could induce RAC serine/threonine-protein kinase (AKT) activation and decrease E-cadherin expression in astrocytoma cells. Inhibition of the AKT pathway attenuated AQP9-mediated invasion, motility and E-cadherin expression. Taken together, the results of the present study indicated that AQP9 promoted the invasion and motility of cells via the AKT pathway. Therefore, AQP9 may represent a potential target for therapeutic use of astrocytoma.

Effects of microRNA-26b on proliferation and invasion of glioma cells and related mechanisms.

Neuroglioma is the most common primary malignant tumor in neurosurgery. Due to its short survival period and high patient mortality rate, neuroglioma is a major challenge in clinics. Elucidating the pathogenic mechanisms and associated molecular targets of neuroglioma can therefore benefit diagnosis and treatment of glioma. Previous studies have established the role of microRNA (miR)­26b in various tumors, including breast cancer, lymphoma and glioma. Its function and mechanism in neuroglioma, however, remains to be elucidated. In the present study, in vitro cultured U87 glioma cells were randomly divided into miR­26b mimic, miR­26b inhibitor and respective control (NC) groups. MTT assay was performed to detect the effect of miR­26b on cell proliferation, while a cell invasion assay detected its effects on cell invasion. Caspase­3 activity was also quantified to test cell apoptosis, followed by reverse transcription-quantitative polymerase chain reaction and western blotting to detect the variation of Bcl­2 expression under the effect of miR­26b. miR­26b mimics transfection upregulated its expression in U87 cells, which had significantly reduced Bcl­2 mRNA and protein expression levels and higher casapse3 activity, and inhibited cell proliferation and invasion compared with the control group. The transfection of miR­26b inhibitor, in contrast, facilitated U87 cell proliferation and invasion, inhibited caspase­3 activity and elevated Bcl­2 mRNA/protein expression. In conclusion, miR­26 could facilitate apoptosis and inhibit proliferation/invasion of neuroglioma cells via downregulating Bcl­2 expression and potentiating caspase-3 activity.

Anxiety, depression and quality of life in patients with a treated or untreated unruptured intracranial aneurysm.

Living with an untreated unruptured intracranial aneurysm(UIA) is stressful, this study was aimed to assess the influence of UIA treatment (surgery clipping and endovascular coiling) on behavior such as anxiety and depression, as well as QoL. A series of 296 UIA patients (including 162 treated and 134 untreated) were analyzed. Postal questionnaires were sent to these patients, included Self-Rating Anxiety Scale (SAS), Self-Rating Depression Scale(SDS) and Short Form-36(SF-36). In total, 198 (66.9%) patients responded to our questionnaires. Patients with surgical clipping or endovascular coiling had a significant improvement in the physical function, body pain and mental health domains. No significant difference in the SAS, SDS and SF-36 was observed between the clipping and coiling group, while SF-36 in body pain domain was significant higher in the coiling group. Moreover, patients diagnosed 5years ago with or without treatment got lower score of SAS and SDS, higher SF-36 score than those diagnosed one year ago. Neurological complications may be an important factor causing lower quality of life. The QoL of patients with endovascular coiling appear to be better than those of surgical clipping, with no difference in anxiety or depression.

Relighting Photosensitizers by Synergistic Integration of Albumin and Perfluorocarbon for Enhanced Photodynamic Therapy.

Photodynamic therapy (PDT) is hampered by poor water solubility and skin phototoxicity of photosensitizers (PSs). Incorporation of PSs into nanocarrier (Nano-PDT) has been designed to overcome these problems. However, self-quenching of PSs highly condensed in Nano-PDT significantly reduced singlet oxygen (1O2) generation, resulting in unsatisfactory PDT efficacy. Here, we developed a novel tripleffect Nano-PDT, which has a special core-shell nanostructure by synergistic integration of perfluorotributylamine (PFTBA) and human serum albumin (HSA) to improve PDT. It has three mechanisms to relight quenched PSs, thereby generating more 1O2. First, PSs uniformly dispersed in the shell, preventing self-quenching caused by π-π stacking. Second, HSA as nanocarrier extends the triplet-state lifetimes of PSs, increasing the amount of 1O2. Third, PFTBA as core dissolves and protects1 O2 to extend the duration time of action of 1O2. Compared with PS-encapsulated Nano-PDT, the self-quenching of PSs in tripleffect Nano-PDT can be effectively overcome. The fluorescence and 1O2 generation of PS are increased by approximately 100-fold and 15-fold, respectively. After intravenous injection into tumor-bearing mice, the tumor growth is significantly inhibited, while the PS-encapsulated Nano-PDT has almost no effect. The novel tripleffect Nano-PDT may guide improvement of existing clinical PDT and future PDT design.

Switchable PDT for reducing skin photosensitization by a NIR dye inducing self-assembled and photo-disassembled nanoparticles.

Photodynamic therapy (PDT) is the combination of light and photosensitizer (PS) to kill tumor cells, which has the potential to meet many currently unmet medical needs. However, the whole body distribution and activatability by sunlight of photosensitizers to induce skin photosensitivity have limited the extensive clinic application of PDT. Herein, a novel strategy is presented to overcome these limitations by using a hydrophobic Near-infared (NIR) dye IR-780 iodide (IR780) to induce the self-assembly of albumin-PS conjugates, as a switchable PDT (Switch-PDT) agent. The PDT effect of PS is effectively inhibited by IR780 and recovered by NIR light irradiation in vitro. This quench/recovery strategy dose not sacrifice the anti-tumor ability in vivo, and the combined PDT and PTT (photothermal) effect contributes a very effective tumor inhibition rate of 100%. More importantly, the PDT effect is significantly suppressed after intravenous administration in mice or subcutaneous administration in rabbits as exhibited by the negligible skin response, while traditional PDT agent arouses severe skin erythema and edema. To the best of our knowledge, the switchable PDT is the first time to be used to eradicate the skin photosensitization of PS in vivo.

Application of human bone marrow-derived mesenchymal stem cells in the treatment of radiation-induced Gastrointestinal syndrome.

Nuclear accidents and terrorism present a serious threat for mass casualty. Accidental or intended radiation exposure leads to radiation-induced gastrointestinal (GI) syndrome. However, currently there are no approved medical countermeasures for GI syndrome. Thus, developing novel treatments for GI syndrome is urgent. Mesenchymal stem cells (MSCs) derived from bone marrow are a subset of multipotent adult somatic stem cells that have the ability to undergo self-renewal, proliferation and pluripotent differentiation. MSCs have advantages over other stem cells; they can be easily isolated from patients or donors, readily expanded ex vivo, and they possess reparative and immunomodulatory properties. Moreover, MSCs have been shown to be powerful tools in gene therapy and can be effectively transduced with vectors containing therapeutic genes. Therefore, the therapeutic potential of MSCs has been brought into the spotlight for the clinical treatment of GI syndrome. In this review, we discuss the possible role of MSCs in radiation-induced GI syndrome.

Ertapenem prophylaxis of surgical site infections in elective colorectal surgery in China: a multicentre, randomized, double-blind, active-controlled study.

OBJECTIVES: Our purpose was to evaluate ertapenem versus ceftriaxone/metronidazole for prophylaxis of surgical site infections (SSIs) following elective colorectal surgery in Chinese adult patients. METHODS: Eligible Chinese adults aged 18-80 years scheduled to undergo elective colorectal surgery by laparotomy were randomized to receive a 30 min infusion of 1 g of ertapenem/metronidazole placebo or 2 g of ceftriaxone/500 mg of metronidazole within 2 h before initial incision. The study endpoint was the proportion of patients with successful prophylaxis at 4 weeks after treatment. The primary analysis was based on the evaluable population (PP population) and the pre-specified non-inferiority margin was set at -15%. ClinicalTrials.gov: NCT01254344. RESULTS: Of 599 patients randomized, 499 (251 ertapenem and 248 ceftriaxone) were eligible for inclusion in the PP population. The proportions of patients with successful prophylaxis in the ertapenem and ceftriaxone groups were 90.4% (227/251) and 90.3% (224/248), respectively. The difference in the proportion of successful outcomes was 0.1% (95% CI -5.2%, 5.5%). Unexplained antibiotic use was the most frequent reason for prophylaxis failure in both groups [ertapenem 4.8% (12/251), ceftriaxone 4.4% (11/248); difference 0.3%; 95% CI -3.6, 4.3]. Pathogen species isolated from SSI sources were consistent with previously conducted studies and the product package insert. The incidence of adverse events (AEs) was similar between the groups, with the most common AE being pyrexia [ertapenem 7.6% (22/290), ceftriaxone 5.7% (17/297)]. CONCLUSIONS: Ertapenem is as effective as ceftriaxone/metronidazole for SSI prophylaxis in patients undergoing elective colorectal surgery, and is well tolerated.

Downregulation of LKB1 suppresses Stat3 activity to promote the proliferation of esophageal carcinoma cells.

The tumor suppressor liver kinase B1 (LKB1) encodes a serine/threonine kinase. The defect in LKB1 is the primary cause of Peutz-Jeghers syndrome (PJS). Inactivation of LKB1 by mutations or loss of LKB1 expression is associated with ovarian, lung and pancreatic cancer; however, the correlation between LKB1 and esophageal carcinoma remains unknown. Thus, quantitative PCR was performed to determine the clinical significance of LKB1 expression in 60 cases of esophageal cancer and its adjacent normal epithelium. LKB1 expression was observed to significantly downregulate the accompanying cancer progression, which was verified at the protein level by western blot analysis. Furthermore, the phosphorylated signal transducer and activator of transcription 3 (Stat3) level is reversibly associated with LKB1 expression. To determine the function of LKB1 in esophageal cancer, LKB1 expression is induced in TE1 esophageal cancer cells. The results show that LKB1 overexpression suppresses the proliferation of TE1 cells, downregulates the expression of cyclin D1 and Myc and represses Stat3 phosphorylation. Suppression of cell proliferation and cyclin D1 expression by LKB1 is fully inhibited by constitutively active Stat3C coexpression, suggesting that LKB1 inhibits esophageal cancer cell proliferation through suppression of Stat3 transaction. In conclusion, downregulation of LKB1 expression suppresses Stat3 activity that may promote tumor growth during esophageal cancer progression.

[Effects and reasons of conversion during video-assisted thoracic surgery lobectomy].

OBJECTIVE: To explore the impact and reasons of conversion during video-assisted thoracic surgery (VATS) lobectomy. METHODS: A total of 374 patients undergoing VATS lobectomy during May 2007 and May 2012 were divided into 2 groups according to whether conversion was necessary. And their clinical data were retrospectively analyzed. RESULTS: Among them, 36 cases (9.6%) converted into thoractomy during VATS lobectomy. Their clinical profiles of age, gender and surgical type were similar. The conversion group had longer operative duration, more blood loss and more benign proportion than VATS group.No inter-group difference existed in postoperative complication, mortality; tube removal time or hospitalization length. The reasons of conversion included hemorrhage (n = 12), vascular adhesion (n = 6), instrumentation complication (n = 5), incomplete fissure (n = 5), uncertain anatomy (n = 3), abnormal blood vessels (n = 3) and insufficient margin (n = 2). CONCLUSION: Conversion during VATS lobectomy may prolong operative duration and increase blood loss.However there is no effect upon patient recovery.

Metformin inhibits lung cancer cells proliferation through repressing microRNA-222.

Metformin, which is commonly used as an oral anti-hyperglycemic agent of the biguanide family, may reduce cancer risk and improve prognosis. However, the mechanism by which metformin affects various cancers, including lung cancer, remains unknown. MiR-222 induces cell growth and cell cycle progression via direct targeting of p27, p57 and PTEN in cancer cells. In the present study, we used A549 and NCI-H358 human lung cancer cell lines to study the effects and mechanisms of metformin. Metformin treatment reduced expression of miR-222 in these cells (p < 0.05). As a result, protein abundance of p27, p57 and PTEN were increased in cells exposed to metformin. Therefore, these data provide novel evidence for a mechanism that may contribute to the anti-neoplastic effects of metformin suggested by recent population studies and justifying further work to explore potential roles for it in lung cancer treatment.

Association between folate intake, serum folate levels and the risk of lung cancer: a systematic review and meta-analysis.

BACKGROUND: Folate plays a critical role in nucleotide synthesis and DNA methylation, and was considered to be associated with anti-carcinogenesis. RESULTS: from studies that concern the relationship between the folate intake or serum folate levels and lung cancer risk showed no consistency, which requires our further comprehensive meta-analysis. METHODS: Systematic literature search was conducted to identify the relevant studies (published prior to February 2013) according to standard protocol. Estimated effects were calculated under both random-effects and fixed-effects models. Heterogeneity between studies and publication bias were also evaluated. RESULTS: A total of 4390 cases and 6138 controls from 6 case-control studies revealed a significant overall inverse association between folate intake and lung cancer risk (OR = 0.74, 95%CI = 0.65 - 0.84, P < 0.001). Summary of 1438 cases and 2582 controls from 4 case-control studies and 44 cases out of a cohort of 1988 participants suggested a marginal association without significance (OR = 0.78, 95%CI = 0.60 - 1.02, P = 0.075) between high serum folate levels and less lung cancer susceptibility; however, subgroup analysis about population-based case-control studies showed that high serum folate levels significantly associated with the reduced lung cancer risk (OR = 0.76, 95%CI = 0.58 - 1.00, P = 0.048). CONCLUSION: Higher folate intake can be a protective factor against lung cancer risk, and higher serum folate level is probably associated with reduced lung cancer risk in marginal manner, though more studies are warranted to confirm these associations.

Congenital bronchial atresia: diagnosis and treatment.

This study aimed to retrospectively summarize the clinical signs, diagnosis, and treatment of congenital bronchial atresia (CBA) in 12 patients. Chest radiographs and computed tomographic (CT) images of 12 patients with CBA treated in the Chinese People's Liberation Army General Hospital were reviewed. Analysis of chest radiographs revealed ten patients had hilar mass-like shadows and two had pneumonia-like shadows; most patients (n = 8) showed hyperlucency of the peripheral lung fields. CT revealed a mucocele in all the patients (n = 12); the mucoceles were round in four patients and club-like in eight. In 80% of the cases (n = 10), associated anomalies, including occlusions of the bronchus central to the mucocele, emphysematous changes of the peripheral lung fields, bronchogenic cyst, and anomalous branching of the bronchial tree and vascular structure were observed. CBA was detected in the right lobe in eight patients and the left lobe in the remaining four. No surgical intervention was performed in 5 CBA patients and the remaining 7 patients underwent surgery, including lobectomy in 5 patients and local resection in 2 patients. Among these 7 patients, 3 had a preoperative diagnosis of malignant disease, and the remaining 4 had severe clinical symptoms that could not be effectively treated by medicines. All patients were followed up, and none experienced obvious discomfort. CBA is a relatively rare and benign malformation disease. Chest CT is the procedure of choice for diagnosis. The presence of a bronchocele and surrounding emphysematous changes are typical radiologic findings in CBA. Surgery should be reserved only for patients with serious complications secondary to the atretic bronchus.

[Preliminary application study of Ligasure in video-assisted thoracic pulmonary surgery].

OBJECTIVE: To investigate the application and techniques of Ligasure in video-assisted thoracic pulmonary surgery. METHODS: Use Ligasure to dissect lung parenchyma, small pulmonary vessel and stop bleeding in 15 cases spontaneous pneumothorax and 20 cases peripheral single lung node who undertaken video-assisted thoracic surgery during October 2008 to June 2010. RESULT: All the procedures were successful, no severe complications, as active bleeding, continuous air leak occurred. A period of 9.3 months (2 - 18 months) follow-up of all patients shows no delayed bleeding or recurrence pneumothorax. CONCLUSION: Ligasure is safe, easy to use. It can optimize operation and reduce the operation time.

Formation of α-helix-based twisted ribbon-like fibrils from ionic-complementary peptides.

Ionic-complementary peptides (ICPs) are well known for their strong propensity to form amyloid-like ß-sheet fibrils. Here, we present the first example that α-helical based ICPs can self-assemble into a highly ordered fibrillar structure. Intriguingly, the individual α-helices in such fibrils are arranged shoulder-to-shoulder, making them distinct from conventional coiled-coil-based fibrils.

Survival benefit of neoadjuvant chemotherapy in non-small cell lung cancer: an updated meta-analysis of 13 randomized control trials.

INTRODUCTION: The survival effectiveness of neoadjuvant chemotherapy in non-small cell lung cancer (NSCLC) is still unclear based on the study of most up-to-date literatures. This article contributes to this problem by conducting an updated meta-analysis. METHODS: Based on Burdett et al's (J Thorac Oncol 2006;1:611-621) systematic review, this meta-analysis was conducted. Articles were searched electrically. The possible survival benefit of neoadjuvant chemotherapy was assessed by hazard ratio (HR) in terms of overall survival. A subgroup meta-analysis with only stage III NSCLC was also conducted. The software of Review Manager was used for data management. RESULTS: Thirteen randomized control trials, 6 of which were new ones, were included into this meta-analysis. The overall survival of NSCLC patients in neoadjuvant chemotherapy arm were improved significantly, comparing with those in surgery-alone arm (combined HR = 0.84; 95% confidence interval, 0.77-0.92; p = 0.0001). When only patients with stage III NSCLC were considered, the result was similar (combined HR = 0.84; 95% confidence interval, 0.75-0.95; p = 0.005). CONCLUSION: Neoadjuvant chemotherapy, as an addition of surgery, would significantly improve the overall survival of operable NSCLC patients, including patients with stage III NSCLC.