T-box transcription factor 20 (TBX20) serves a crucial regulatory role in the process of tumor occurrence. In lung cancer, the upregulation of TBX20 expression is positively associated with a poor prognosis; however, the specific underlying mechanism remains unclear. Therefore, in the present study, the expression of TBX20 in normal lung epithelial BEAS-2B and cancer cells A549 was detected by quantitative PCR and western blot. Lung cancer cell lines with overexpression and interference of TBX20 were constructed. Cell proliferation was detected by Cell Counting Kit-8, cell migration and invasion were detected by Transwell, and cell spheroid formation was assessed. The expression of EMT markers (E-cadherin, N-cadherin, vimentin), stemness markers (CD44, Sox2, Nanog), and immune factors (PD-L1, IL-6, CCL2) was detected by qPCR and WB. A subcutaneous lung cancer model in nude mice was established. After 4 weeks, the tumor volume was observed. The expression of E-cadherin, N-cadherin, vimentin, CD44, and PD-L1 in tumor tissues was detected by IHC. The infiltration of immune cells (CD8+T, CD4+T, M1/M2 macrophages) was detected by flow cytometry. In vitro experiments revealed that the expression levels of TBX20 were increased in the A549 lung cancer cells compared with those in BEAS-2B normal lung epithelial cells. In addition, cell viability, migration, invasion and spheroid formation capacity were greater in the A549 group than in the BEAS-2B group. Compared with in the negative control (NC) group, the TBX20 overexpression plasmid (oe-TBX20) group exhibited enhanced cell viability, migration, invasion and spheroid formation capacity. Furthermore, E-cadherin expression was reduced, whereas N-cadherin, vimentin, Sox2, CD44, Nanog, PD-L1, IL-6 and CCL2 expression levels were elevated. Notably, these changes were reversed in the TBX20 knockdown group. In vivo experiments revealed that compared with in the NC group, the oe-TBX20 group had significantly increased tumor volume, decreased E-cadherin levels, and elevated expression levels of TBX20, N-cadherin, vimentin, CD44 and PD-L1. Compared with NC group, the oe-TBX20 group exhibited significantly lower infiltration of CD4+ T and CD8+ T cells and M1-type macrophage, whereas that of M2-type macrophages and regulatory T cells increased. Conversely, these indicators were reversed in the short hairpin RNA-TBX20 group. In conclusion, TBX20 may induce epithelial-mesenchymal transition and stem cell characteristics, enhance the malignant behavior of lung cancer cells, and upregulate PD-L1 expression to promote immune escape.

Fracture healing is a complex staged repair process in which the mechanical environment plays a key role. Bone tissue is very sensitive to mechanical stress stimuli, and the literature suggests that appropriate stress can promote fracture healing by altering cellular function. However, fracture healing is a coupled process involving multiple cell types that balance and limit each other to ensure proper fracture healing. The main cells that function during different stages of fracture healing are different, and the types and molecular mechanisms of stress required are also different. Most previous studies have used a single mechanical stimulus on individual mechanosensitive cells, and there is no relatively uniform standard for the size and frequency of the mechanical stress. Analyzing the mechanisms underlying the effects of mechanical stimulation on the metabolic regulation of signaling pathways in cells such as in bone marrow mesenchymal stem cells (BMSCs), osteoblasts, chondrocytes, and osteoclasts is currently a challenging research hotspot. Grasping how stress affects the function of different cells at the molecular biology level can contribute to the refined management of fracture healing. Therefore, in this review, we summarize the relevant literature and describe the effects of mechanical stress on cells associated with fracture healing, and their possible signaling pathways, for the treatment of fractures and the further development of regenerative medicine.

Objectives: This study aims to investigate the impact of mesenchymal stem cell (MSC) -derived exosomes (Exo) on cerebral ischemia and reperfusion (I/R) injury, along with the underlying mechanism. Methods: An animal model of cerebral ischemia was induced using middle cerebral artery occlusion (MCAO), and a cell model utilizing Neuro-2a cells was established through oxygen -glucose deprivation/reoxygenation (OGD/ R). Exosomes isolated from mouse MSCs were administered to mice or used to stimulate Neuro-2a cells. Exosomes from MSCs transfected with miR-NC, miR-486-5p mimics, miR-486-5p inhibitor, or phosphatase and tensin homolog (PTEN) short hairpin RNAs (sh-PTEN) were employed to stimulate Neuro-2a cells. The regulatory axis of miR-486-5p and PTEN was confirmed through rescue experiments. Results: Exo-miR-486-5p mimics alleviated cerebral I/R injury, improving neurological deficits and reducing the infarct ratio. Furthermore, Exo-miR-486-5p mimics attenuated OGD/R-induced defects in cell viability and inhibited apoptosis in Neuro-2a cells. These mimics also reduced levels of lactate dehydrogenase (LDH) and malondialdehyde (MDA) while enhancing superoxide dismutase (SOD) activity, both in brain tissue homogenates of mice and cell supernatants. Mechanistically, PTEN was identified as a target of miR-486-5p, and the downregulation of PTEN notably elevated Exo-miR-486-inhibitor-induced reductions in cell viability while mitigating cell apoptosis. Conclusion: The results of this study demonstrate the potential of exosomes derived from MSCs to protect against cerebral I/R injury via the miR-486-5p and PTEN axis.

Objective Abnormal expression of CUT-like homeobox 2 gene (CUX2) has been highlighted as potential clinical biomarkers in human cancers. Notably, the function of CUX2 has been less elucidated in breast cancer (BC). We focused on the role of the CUX2 in tumorigenesis and progression of BC with the involvement of the lysine demethylase 5B (KDM5B)/sex determining region Y-box 17 (SOX17) axis. Methods CUX2, KDM5B, and SOX17 expression levels in BC tissues and cells were tested by reverse transcription quantitative PCR and Western blotting. Later, the effects of CUX2, KDM5B, and SOX17 on the malignant behaviors of MDA-MB-231 and MCF-7 cells were analyzed by CCK-8, colony formation, and Transwell assays in vitro. The interactions of CUX2, KDM5B, and SOX17 were validated by online website prediction, ChIP assay, and dual luciferase reporter gene assay. The subcutaneous tumorigenesis in nude mice was conducted to observe the roles of CUX2, KDM5B, and SOX17 in BC tumor growth in vivo. Results CUX2 and KDM5B were highly expressed while SOX17 had low expression in BC. Inhibition of CUX2 suppressed BC cell malignant phenotypes. CUX2 promoted KDM5B expression through transcriptional activation, enabling its high expression in BC. KDM5B inhibited SOX17 expression through histone demethylation. Overexpression of KDM5B or downregulation of SOX17 reversed the inhibitory effect of CUX2 downregulation on the malignant behaviors of BC cells. Inhibition of CUX2 impeded BC cell growth in vivo through the KDM5B/SOX17 axis. Conclusion This study highlights that suppression of CUX2 inhibits KDM5B to repress tumorigenesis and progression of BC through overexpressing SOX17.

Purpose Nectin-4 is specifically up-regulated in various tumors, exert crucial effects on tumor occurrence and development. Nevertheless, the role and molecular mechanism of Nectin-4 in osteosarcoma (OS) are rarely studied. Methods The expression of Nectin-4 and its relationship with clinical characteristics of OS were investigated using OS clinical tissues, tissue microarrays, TCGA, and GEO databases. Moreover, the effect of Nectin-4 on cell growth and mobility was detected by CCK-8, colony formation, transwell, and wound-healing assays. The RT-qPCR, Western blotting, and luciferase reporter assays were performed to explore molecular mechanisms through which Nectin-4 mediates the expression of miR-520c-3p, thus modulating PI3K/AKT/NF-κB signaling. In vivo mice models constructed by subcutaneous transplantation and tail vein injection were used to validate the functional roles of Nectin-4 and miR-520c-3p. Results Nectin-4 displayed a higher expression in OS tumor tissues compared with normal tissues, and its overexpression was positively associated with tumor stage and metastasis in OS patients. Functionally, Nectin-4 enhanced OS cells growth and mobility in vitro. Mechanistically, Nectin-4 down-regulated the levels of miR-520c-3p that directly targeted AKT-1 and P65, thus leading to the stimulation of PI3K/AKT/NF-κB signaling. In addition, the expression of miR-520c-3p was apparently lower in OS tissues than in normal tissues, and its low expression was significantly related to tumor metastasis. Furthermore, ectopic expression of miR-520c-3p markedly blocked the effect of Nectin-4 on OS cell growth and mobility. Knockdown of Nectin-4 could suppress the tumorigenesis and metastasis in vivo, which could be remarkably reversed by miR-520c-3p silencing. Conclusions Nectin-4 as an oncogene can promote OS progression and metastasis by activating PI3K/AKT/NF-κB signaling via down-regulation of miR-520c-3p, which could represent a novel avenue for identifying a potential therapeutic target for improving patient outcomes.

The Nectin cell adhesion molecule (Nectin) family members are Ca2+‑independent immunoglobulin‑like cellular adhesion molecules (including Nectins 1‑4), involved in cell adhesion via homophilic/heterophilic interplay. In addition, the Nectin family plays a significant role in enhancing cellular viability and movement ability. In contrast to enrichment of Nectins 1‑3 in normal tissues, Nectin‑4 is particularly overexpressed in a number of tumor types, including breast, lung, urothelial, colorectal, pancreatic and ovarian cancer. Moreover, the upregulation of Nectin‑4 is an independent biomarker for overall survival in numerous cancer types. A large number of studies have revealed that high expression of Nectin‑4 is closely related to tumor occurrence and development in various cancer types, but the manner in which Nectin‑4 protein contributes to the onset and development of these malignancies is yet unknown. The present review summarizes the molecular mechanisms and functions of Nectin‑4 protein in the biological processes and current advances with regard to its expression and regulation in various cancer types.

Background: Bone marrow mesenchymal stem cells (BMSCs) are widely used in many fields such as wound repair, gene delivery, and microenvironment improvement. In some cases, BMSC transplantation requires long-term anesthesia. However, the effects of anesthetics on the characteristics of BMSCs are poorly understood. Methods: In this study, we examined the effect of sevoflurane, a gas anesthetic drug most commonly used in children, on the proliferation, differentiation, and homing potential of BMSCs. Results: Short-term (6 h) sevoflurane exposure had almost no effect on the proliferation, differentiation, and homing of BMSCs. However, long-term (24 h) sevoflurane exposure inhibited the proliferation of BMSCs, accelerated their differentiation into nerve cells, and inhibited their homing potential to damaged vascular endothelial cells and intact glioma cells. Conclusion: Short-term anesthesia with sevoflurane as the main inducer is safe and harmless to BMSCs, but long-term sevoflurane exposure may reduce their repair potential. Therefore, because of the high proportion of BMSCs in children, the application of long-term anesthesia with sevoflurane should be cautious, or more suitable anesthetic drugs are needed.

Background This retrospective study was conducted at a single center and aimed to evaluate operative and postoperative outcomes in patients with spinal metastases using vertebrectomy and combined vertebrectomy and radiofrequency ablation (RFA). Material/Methods Patients diagnosed with spinal metastases between April 2009 and March 2016 (n=49) included patients who underwent vertebrectomy (n=26) and patients who underwent combined vertebrectomy and RFA (n=23). The characteristics of the 2 groups were similar in primary tumor types, comorbidities, Tomita score, vertebral involvement, preoperative bone pain, and neurologic deficit. Results The results showed for the both groups that the visual analog scale (VAS) pain score was significantly decreased (P<0.05) and the neurological status was improved after treatment. Compared with the control group (vertebrectomy only), the combination group (combined vertebrectomy and RFA) had less intraoperative blood loss (P=0.002) and shorter operation time (P<0.001). The recurrence rate was lower (P=0.003) in the patients who received combined treatment, and the period of local recurrence was prolonged (P=0.030) in the combination group. Conclusions This retrospective study showed that the selective use of combined vertebrectomy and RFA significantly reduced surgical time and blood loss, improved recovery of neurologic deficit, and reduced the tumor recurrence rate in patients with spinal metastases.

Background: Although it is well known that selective intra-arterial cooling (SI-AC) elicits cerebral protection against ischemia/reperfusion (I/R) injury, the underlying mechanism remains unclear. This study aimed to determine whether SI-AC can protect against cerebral I/R injury by inhibiting oxidative stress and mitochondrial dysfunction through regulation of Sirt3 deSUMOylation via SENP1. Methods: All mice were subjected to 2 h of cerebral ischemia followed by 24 h of reperfusion. SI-AC treatment was performed by infusion with cold saline (10 degrees C, 20 mL/kg) for 15 min through a microcatheter placed in the internal carotid artery immediately before reperfusion. The infarct volume, survival rate, neurological deficit scores, behavioral parameters, histopathology findings, and apoptosis were assessed. HT22 cells were subjected to 2 h of oxygen and sugar deprivation (OGD) and 22 h of reoxygenation. HA-SUMO1, Flag-Sirt3, a Sirt3 mutation plasmid (Flag-Sirt3 K288R), His-SENP1, and SENP1 small interfering RNA were transfected into HT22 cells 48 h before OGD. Apoptosis-related proteins were analyzed by western blotting. SUMOylation of Sirt3, acetylation of cyclooxygenase 1 (COX1), superoxide dismutase 2 (SOD2), and isocitrate dehydrogenase 2 (IDH2), the activities of COX1, 5OD2, and IDH2, oxidative stress, and mitochondrial dysfunction were evaluated. Results: Compared with the I/R group, SI-AC decreased cerebral infarct volume and neurological deficit scores and increased motor coordination, exploratory behavior, and memory. Hematoxylin and eosin and Nissl staining showed that SI-CA decreased karyopyknosis, nuclear fragmentation, and nucleolysis, increased neuron density, and decreased the cell apoptosis rate. In addition, Sirt3 was revealed as a target protein of SUMO1. SI-AC attenuated cerebral I/R injury through Sirt3 deSUMOylation via SENP1. Conclusions: SENP1-mediated deSUMOylation of Sirt3 plays an essential role in SI-AC-induced cerebral protection against I/R injury. Our findings provide a promising therapeutic approach for treatment of acute cerebral I/R injury.

Background Prognosis is poor for patients with malignant progression such as distant metastasis of oral squamous cell carcinoma (OSCC). Evidence indicates that miR-448 promotes the proliferation and inhibits apoptosis of OSCC cells. Therefore, we aimed to investigate the function of miR-448 to predict tumor progression and prognosis of OSCC. Methods Real-time quantitative reverse transcription PCR was used to measure miR-448 expression in 221 pairs of OSCC tissues and the corresponding noncancerous tissues. Patients were diagnosed with OSCC from 2009 through 2011 at the Tianjin Medical University Cancer Institute and Hospital. Chi-squared tests were performed to assess the associations between miR-448 expression and clinicopathological parameters. Kaplan–Meier analysis was employed to evaluate the association of overall survival (OS) and disease-free survival (DFS) with miR-448 levels. Univariate and multivariate analyses were performed using the Cox proportional hazards regression model. Results We show here that miR-448 expression was significantly up-regulated in OSCC tissues compared with noncancerous tissues ( P < 0.01). High miR-448 expression was significantly associated with advanced T stage ( P = 0.001), lymph node metastasis ( P = 0.007) and higher TNM stage ( P = 0.009). Moreover, Kaplan–Meier and univariate analyses revealed that patients with high expression of miR-448 experienced significantly shorter OS and DFS. Furthermore, multivariate analysis demonstrated that miR-448 expression was an independent prognostic factor for OS ( P = 0.004) and DFS ( P = 0.002). Conclusions Our present data suggests that miR-448 may play an important role in tumor progression and serves as a prognostic marker for OSCC. Further studies are required to assess the potential value of miR-448 to contribute to personalized treatment of OSCC.

The modification of proteins by small ubiquitin-like modifier (SUMO), known as SUMOylation, regulates biological function by changing protein transcription and translation. During the estrous cycle the endometrium undergoes continual change to processes including cell proliferation, secretion and exfoliation and these changes are regulated by the levels of ovarian hormones. Increasing the expression of SUMO family members has previously been shown to promote proliferation and invasion of endometrial cancer cells. However, limited research has been carried out into the expression and function of SUMO in the mammalian endometrium. In the present study, the level and localization of SUMO-associated proteins throughout the natural estrous cycle in the mouse uterus was determined using immunohistochemical staining and western blot analysis. The association between the spatiotemporal expression of these SUMO modified proteins and SENPs in endometrium and the concentration of ovarian hormones during estrous cycle was revealed. The present study clarified the role of SUMOylation in maintenance of normal estrous cycling and may have important significance in the study of hormone-dependent endometrial diseases.

Dexamethasone can alleviate the severity of bronchial and alveolar edema and therefore is widely applied in the treatment of various exudative diseases including pulmonary edema. However, the effectiveness of dexamethasone is still being questioned and its mechanism is not fully understood. Aquaporins (AQPs) are mainly responsible for the transmembrane transport of water, which is tightly associated with pulmonary edema. Small ubiquitin-like modifiers (SUMOs) are considered to play a protective role in some pathological conditions. In this study, we demonstrated that dexamethasone can upregulate the expression of AQPs in A549 cells by inducing SUMOylation. We found that a low dose of dexamethasone significantly upregulated the levels of SUMOylation and AQP expression in A549 cells, accompanied by a translocation of SUMOs from the cytoplasm to the nucleus. We also explored the possible relation between SUMOylation and AQPs. Knockdown of SUMO2/3 by RNA interference decreased the level of AQP4 in A549 cells after dexamethasone stimulation. Together, our findings demonstrated that AQP4 expression was upregulated in A549 cells exposed to dexamethasone, and SUMOylation may participate in the regulation of AQP4.

Moderate hypothermia plays a major role in myocardial cell death as a result of hypoxia/reoxygenation (H/R) injury. However, few studies have investigated the molecular mechanisms of hypothermic cardioprotection. Several responses to stress and other cell functions are regulated by post‑translational protein modifications controlled by small ubiquitin‑like modifier (SUMO). Previous studies have established that high SUMOylation of proteins potentiates the ability of cells to withstand hypoxic‑ischemic stress. The level to which moderate hypothermia affects SUMOylation is not fully understood, as the functions of SUMOylation in the heart have not been studied in depth. The aim of the present study was to investigate the effect of moderate hypothermia (33˚C) on the protective functions of SUMOylation on myocardial cells. HL‑1 and H9c2 cells were treated with the hypoxia‑mimetic chemical CoCl2 and complete medium to simulate H/R injury. Hypothermia intervention was then administered. A Cell Counting kit‑8 assay was used to analyze cell viability. Mitochondrial membrane potential and the generation of reactive oxygen species (ROS) were used as functional indexes of mitochondria dysfunction. Bcl‑2 and caspase‑3 expression levels were analyzed by western blotting. The present results suggested that moderate hypothermia significantly increased SUMO1 and Bcl‑2 expression levels, as well as the mitochondrial membrane potential, but significantly decreased the expression levels of caspase‑3 and mitochondrial ROS. Thus, moderate hypothermia may enhance SUMOylation and attenuate myocardial H/R injury. Moreover, a combination of SUMOylation and moderate hypothermia may be a potential cardiovascular intervention.

BACKGROUND:Spinal metastases can cause metastatic epidural spinal cord compression (MESCC), which can result in neurological dysfunction and impaired quality of life. This study investigated the safety and effectiveness of posterior decompression surgery and radiofrequency ablation followed by vertebroplasty in spinal metastasis from lung cancer. MATERIAL AND METHODS:From June 2008 to September 2015, a retrospective analysis was conducted in 15 patients with spinal metastasis from lung cancer. All cases suffered MESCC and underwent posterior decompression surgery to relieve the compression of spinal cord, and had radiofrequency ablation followed by vertebroplasty. All patients received postoperative multidisciplinary therapy. The operative time, blood loss, complications, pain, neurologic deficit, quality of life, and survival were assessed preoperatively and postoperatively. RESULTS:Patients were followed from 6 to 56 months. The mean time of operation was 154±50 minutes and the mean blood loss was 210±90 mL. In the pre-operation analysis found the mean visual analogue scale (VAS) was 7.86±0.86. In the post-operation analysis at 3 months, the mean VAS score was 3.51±1.32. The VAS improved significantly (t=7.95, P<0.01). The Frankel grade was improved 1 grade or 2 grades in 14 patients when pre-operation was compared to post-operation. Only 1 patient kept Frankel grade D after surgery. Eight patients with sphincteric dysfunction preoperatively were improved after surgery. The EORTC QLQ-C30 score was 86.13±8.51 preoperatively and 52.21±13.28 postoperatively. The quality of life was improved significantly (t=11.8, P<0.01). The median survival time was 11 months. CONCLUSIONS:Through posterior decompression surgery and radiofrequency ablation followed by vertebroplasty, the quality of life was improved significantly. This palliative treatment was effective and safe in spinal metastasis from lung cancer.

The purpose of the present study was to characterize the prevalence, associated factors, and to construct a nomogram for predicting bone metastasis (BM) with different histological types of lung cancer. This study was a descriptive study that basing on the invasive lung cancer patients diagnosed between 2010 and 2014 in Surveillance, Epidemiology, and End Results program. A total of 125,652 adult patients were retrieved. Logistic regression analysis was conducted to investigate homogeneous and heterogeneous factors for BM occurrence. Nomogram was constructed to predict the risk for developing BM and the performance was evaluated by the receiver operating characteristics curve (ROC) and the calibration curve. The overall survival of the patients with BM was analyzed using the Kaplan–Meier method and the survival differences were tested by the log-rank test. A total of 25,645 (20.9%) were reported to have BM, and the prevalence in adenocarcinoma, squamous cell carcinoma, small cell lung cancer (SCLC), large cell lung cancer (LCLC), and non-small cell lung cancer/not otherwise specified lung cancer (NSCLC/NOS) were 24.4, 12.5, 24.7, 19.5 and 19.4%, respectively, with significant difference (P < 0.001). Male gender, more metastatic sites and lymphatic metastasis were positively associated with BM in all lung cancer subtypes. Larger tumor size was positively associated with BM in all the lung cancer subtypes except for NSCLC/NOS. Poorly differentiated histology was positively associated with adenocarcinoma, squamous cell carcinoma and NSCLC/NOS. The calibration curve and ROC curve exhibited good performance for predicting BM. The median survival of the bone metastatic lung cancer patients was 4.00 (95%CI: 3.89–4.11) months. With the increased number of the other metastatic sites (brain, lung and liver metastasis), the survival significantly decreased (p < 0.001). Different lung cancer histological subtypes exhibited distinct prevalence and homogeneity and heterogeneity associated factors for BM. The nomogram has good calibration and discrimination for predicting BM of lung cancer.

Objectives: Identify the efficacy of multidisciplinary treatment including palliative spinal surgery on patients with Tomita type 7 spinal metastases. Patients and methods: A retrospective analysis of surgery treated spinal metastatic patients from January 2013 to December 2016 in Tianjin Medical University Cancer Institute and Hospital were performed. Surgical procedures and intraoperative parameters and postoperative adjuvent treatments were studied. Patients' demographic characteristics and medical conditions including paralysis statues, quality of life and pain levels and postoperative survival time were identified. Results: 50 patients were identified with mean age at the time of surgery of 57.68 years old (range 27-78 years). The mean Tokuhashi score was 8.48 and the spinal instability neoplastic score (SINS) averaged at 10.52 points. 48 patients (96%) encountered epidural spinal cord compression. Kaplan-Meier method determined median postoperative survival time was 12.00 months (95% CI: 7.05-16.95 months). The mean score of visual analogue scale (VAS) decreased from 7.66 preoperatively to 1.96 postoperatively. The Frankel scale was improved by at least one grade in 47 patients. Patient's quality of life showed significant improvements. Conclusion: Multidisciplinary treatment including palliative spinal surgery was associated with alleviating pain, improving neurologic function and quality of life in patients with Tomita type 7 spinal metastases.

Objective To investigate prognostic factors and the efficacy of surgery-based comprehensive treatment for patients with synovial sarcoma. Methods We retrospectively analyzed the medical records of 95 synovial sarcoma patients. Factors associated with survival were identified with univariate analysis by log-rank test and multivariate analysis by Cox proportional hazard regression model. Kaplan-Meier method was applied to do the survival analysis. Results Patients were followed up for 8-296 months and the median follow-up time was 62 months. The median overall survival time of all patients was 76 months (95%CI: 67.9-84.1 months). The 5-year OS and PFS of this cohort were 70.7% and 22.5%, respectively. Multivariable analysis indicated that AJCC staging at diagnosis (P < 0.001), primary tumor site (P=0.027), tumor size (P=0.015), time of adjuvant therapy (P=0.004), therapeutic regimen (P=0.005) and recurrence and metastasis (P=0.016) were independent prognostic factors of OS. Kaplan-Meier method showed that the median overall survival time of patients with more than 4 courses chemotherapy was 84 months, significantly better than 66 months of those patients with less than 4 courses(P=0.007). Conclusion Several clinical features could affect the prognosis of synovial sarcoma. Adjuvant chemotherapy, adjuvant radiotherapy and combining radiotherapy and chemotherapy are all effective for prolonging patients' survival time. After surgery, a sooner adjuvant therapy before disease progression could achieve better treatment effect. For patients accepting chemotherapy, 4 and above chemotherapy courses are favorable to obtain better therapeutic results.

After the publication of the article, the authors retrospectively noticed that the first author affiliation was incorrectly split across three affiliations for the various parts of the same address. The correct author list (and affiliations) should therefore have been published as follows: Fengting Liu1, Lili Li1, Yanxia Li2, Xiaofang Ma3, Xiyun Bian2, Xiaozhi Liu2, Guowen Wang1* and Dianying Zhang3* 1Department of Bone and Soft Tissue Tumors, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060; 2Central Laboratory, The Fifth Central Hospital of Tianjin, Tianjin 300450; 3Department of Trauma and Orthopedics, Peking University People's Hospital, Beijing 100044, P.R. China The authors regret that this error was allowed to remain in the published paper, and apologize for any inconvenience caused. [the original article was published in International Journal of Oncology 53: 2010‑2020, 2018; DOI: 10.3892/ijo.2018.4537].

滑膜肉瘤(synovial sarcoma,SS)是一种罕见的高度恶性软组织肉瘤(soft tissue sarcoma,STS),该疾病的重要特征是18号染色体上的SS18基因[亦称为滑膜肉瘤易位基因(synovial sarcoma translocation,SYT)]与滑膜肉瘤X染色体断点基因(synovial sarcomaX chromosome breakpoint,SSX)(包括SSX1、SSX2、SSX4)发生了特异性染色体易位,并形成融合基因.当前SS的治疗以综合治疗为主,但个体治疗方案尚存差异.与其他STS相比,SS对化疗药物更为敏感.局灶性SS的标准治疗方案是广泛的手术切除联合适当的放疗和/或(新)辅助化疗,晚期患者常以细胞毒药物为一线治疗,姑息性药物治疗方案尚不统一,已发生转移的晚期患者,应用葸环类药物与异环磷酰胺联合或序贯疗法作为一线治疗;二线治疗方案药物包括曲贝替定和帕唑帕尼等.本文总结近年来SS的治疗研究进展,重点明确药物治疗的现状,并简要阐述与SS分子和免疫学特性相关的新疗法.