Neuropilin-1 enhances temozolomide resistance in glioblastoma via the STAT1/p53/p21 axis.

Glioblastoma (GBM) is the most prevalent primary intracranial tumor. Temozolomide (TMZ) is the first-line chemotherapy for GBM. Nonetheless, the development of TMZ resistance has become a main cause of treatment failure in GBM patients. Evidence suggests that neuropilin-1 (NRP-1) silencing can attenuate GBM cell resistance to TMZ. This study aims to determine potential mechanisms by which NRP-1 affects TMZ resistance in GBM. The parental U251 and LN229 GBM cells were exposed to increasing concentrations of TMZ to construct TMZ-resistant GBM cells (U251/TMZ, LN229/TMZ). BALB/c nude mice were injected with U251/TMZ cells to establish the xenograft mouse model. Functional experiments were carried out to examine NRP-1 functions. Western blotting and real-time quantitative polymerase chain reaction were used to evaluate molecular protein and mRNA expression, respectively. Immunohistochemical staining showed NRP-1 and STAT1 expression in mouse tumors. The results showed that NRP-1 was highly expressed in TMZ-resistant cells. Moreover, knocking down NRP-1 attenuated the TMZ resistance of U251/TMZ cells, while upregulating NRP-1 enhanced TMZ resistance of the parental cells. NRP-1 silencing elevated GBM cell sensitivity to TMZ in tumor-bearing mice. Depleting NRP-1 reduced STAT1, p53, and p21 expression in U251/TMZ cells. STAT1 depletion offset NRP-1 silencing evoked attenuation of GBM cell resistance to TMZ. Collectively, our study reveals that NRP-1 enhances TMZ resistance in GBM possibly by regulating the STAT1/p53/p21 axis.

National Brain Tumour Registry of China (NBTRC) statistical report of primary brain tumours diagnosed in China in years 2019-2020.

Background: The lack of a well-designed brain tumour registry with standardized pathological diagnoses in underdeveloped countries hinders the ability to compare epidemiologic data across the globe. The National Brain Tumour Registry of China (NBTRC), created in January 2018, is the first multi-hospital-based brain tumour registry in China. Patient data reported to the NBTRC in years 2019-2020 were assessed. Methods: Tumour pathology was based on the 2016 World Health Organization (WHO) classification of tumours of the central nervous system and ICD-O-3. The anatomical site was coded per the Surveillance, Epidemiology, and End Results (SEER) solid tumour module (version of July 2019). The cases were tabulated by histology and anatomical site. Categorical variables were reported as numbers (percentages). The distribution of tumours by age (0-14, 15-19, 20-39, 40-64, and 65+ years) was analysed. Findings: There were a total of 25,537 brain tumours, foremost among them meningioma (23.63%), followed by tumours of the pituitary (23.42%), and nerve sheath tumours (9.09%). Glioblastoma, the most common and lethal form of primary brain cancer in adults, represented 8.56% of all cases. Of note, 6.48% of the malignant tumours were located in the brain stem. The percentage of malignant brain tumours decreased with increasing age, 24.08% in adults (40+ years), 30.25% in young adults (20-39 years), 35.27% in adolescents (15-19 years), and 49.83% in children (0-14 years). Among the 2107 paediatric patients, the most common sites were ventricle (17.19%), brainstem (14.03%), pituitary and craniopharyngeal duct (13.4%), and cerebellum (12.3%), a distribution that differed from that of the entire cohort. The histology distribution was also unique in children, with glioblastoma much less incident compared to the whole cohort (3% vs. 8.47%, p < 0.01). 58.80% of all patients chose higher-level neurosurgical hospitals outside of their province of residence. The median in-hospital length of stay (LOS) for the various pathologies ranged from 11 to 19 days. Interpretation: The histological and anatomical site distribution of brain tumours in the NBTRC was statistically different in the subgroup of children (0-14 years). Patient choice of pursuing trans-provincial treatment was common and the in-hospital LOS was longer compared to that reported in similar European and American patient populations, which merits further attention. Funding: The National Key Research and Development Program of China (2015BAI12B04, 2013BAI09B03, 2014BAI04B01, and 2021YFF1201104) and Chinese National Natural Science Foundation of China (81971668).

Molecular diagnosis and treatment of meningiomas: an expert consensus (2022).

ABSTRACT: Meningiomas are the most common primary intracranial neoplasm with diverse pathological types and complicated clinical manifestations. The fifth edition of the WHO Classification of Tumors of the Central Nervous System (WHO CNS5), published in 2021, introduces major changes that advance the role of molecular diagnostics in meningiomas. To follow the revision of WHO CNS5, this expert consensus statement was formed jointly by the Group of Neuro-Oncology, Society of Neurosurgery, Chinese Medical Association together with neuropathologists and evidence-based experts. The consensus provides reference points to integrate key biomarkers into stratification and clinical decision making for meningioma patients. REGISTRATION: Practice guideline REgistration for transPAREncy (PREPARE), IPGRP-2022CN234.

Forkhead Box M1 promotes the growth and tube formation of human malignant meningioma cells via the aryl hydrocarbon receptor signaling pathway.

INTRODUCTION: Forkhead Box M1 (FOXM1) and aryl hydrocarbon receptor (AHR) signaling pathway participate in meningioma development, but their correlation was inadequately studied. The study is aimed to uncover their functions and correlation in malignant meningioma. MATERIAL AND METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect FOXM1 expression in malignant meningioma and adjacent tissues. The viability, proliferation, apoptosis and tube formation of meningioma IOMM-Lee and CH157-MN cells transfected with overexpressed FOXM1 were examined with MTT assay, clone formation assay, flow cytometry and tube formation assay, respectively. The expressions of AHR and cytochrome P450 family 1 subfamily A member 1 (CYP1A1) in meningioma and adjacent tissues were detected using qRT-PCR, and the correlation of AHR with FOXM1 was analyzed with Pearson's correlation analysis. Western blot was conducted for measuring the expressions of vascular endothelial growth factor A (VEGFA), AHR and CYP1A1. The cell viability, proliferation, apoptosis and tube formation capability were further determined after treatment with StemRegenin 1 (SR1) (an AHR signaling pathway inhibitor), and transfected with or without overexpressed FOXM1. RESULTS: FOXM1, AHR and CYP1A1 expressions were upregulated in malignant meningioma tissues. Overexpressed FOXM1 promoted meningioma cell viability, proliferation, tube formation, upregulated expressions of AHR, CYP1A1 and VEGFA, and inhibited the cell apoptosis. AHR was positively correlated with FOXM1. SR1 suppressed meningioma cell growth and the AHR signaling pathway, and also reversed the active effect of FOXM1 on meningioma cells. CONCLUSIONS: FOXM1 may promote malignant meningioma via the AHR signaling pathway, which improved the current understanding of the role of FOXM1 in meningioma.

BMP4 inhibits glioblastoma invasion by promoting E-cadherin and claudin expression.

Glioblastoma multiforme (GBM) is a brain tumor that deeply infiltrates adjacent tissues and causes significant mortality. Thus, understanding the mechanisms that derive the invasion of brain tissue by GBM might help the treatment of this cancer. To this end, we examined the impact of BMP4 on invasion of GBM. In this study, Human GBM samples, GBM cells and human orthotopic GBM-xenografted animal model, quantitative PCR, immunostaining, immunoblotting, Scratch wound and transwell assays were used to detect the effect and the mechanism of BMP4 in GBM cells. BMP4 expression was found to positively correlate with E-cadherin and claudin expression in human GBM samples. Elevation or suppression of BMP4 expression resulted in a respective increase or decrease in E-cadherin and claudin levels, both in vitro and in vivo. Suppression of BMP4 expression was associated with enhanced GBM cell migration and invasion, while BMP4 overexpression inhibited these processes. Smad1/5/8 protein phosphorylation positively correlated with BMP4 expression. Pharmacological blockade of Smad1/5/8 phosphorylation impaired BMP4-dependent inhibition of cell migration and invasion. Together, these findings suggest that BMP4 increases E-cadherin and claudin expression in GBM through activation of SMAD signaling, thereby suppressing tumor cell invasion.

A study on the correlation between STAT­1 and mutant p53 expression in glioma.

Glioma is the most common primary brain tumor in adults and the second most common malignant tumor in children. Aberrant expression of signal transducer and activator of transcription 1 (STAT­1) and p53 are known to affect the occurrence and progression of malignant tumors. The aim of the present study was to investigate the expression of STAT­1 and mutant p53 gene, as well as their correlation, in patients with glioma. The present study included 50 patients who underwent glioma resection at the First Affiliated Hospital of Inner Mongolia Medical University between December 2007 and December 2011, and 10 patients with acute cerebral contusion who underwent intracerebral hematoma removal at the same hospital between January 2013 and January 2014. The expression of STAT­1 and mutant p53 protein in patients with different grades of glioma was assessed by immunohistochemistry. Spearman's correlation coefficient was employed to examine the correlation between STAT­1 and the grade of glioma, and mutant p53 expression. The results demonstrated that the mean expression of STAT­1 in glioma was significantly lower compared with normal brain tissue (P<0.05). However, there was no significant difference in the STAT­1 positive expression rate between the two groups (χ2=1.38, P>0.05). The expression score (P<0.05) and positive expression rate (χ2=31.27, P<0.05) of mutant p53 in glioma was significantly higher compared with those in normal brain tissue. Statistical analysis revealed a negative correlation between STAT­1 expression and the grade of glioma (r=­0.767, P<0.05). In addition, mutant p53 expression was negatively correlated with STAT­1 expression in glioma (r=­0.876, P<0.05). The observed negative correlation between STAT­1 and the pathological grade of glioma suggested an association between STAT­1 and the occurrence and development of glioma, thus revealing the potential of STAT­1 as a diagnostic biomarker and therapeutic target for glioma.

Gamma Knife radiosurgery combined with stereotactic aspiration as an effective treatment method for large cystic brain metastases.

In the present study, the efficacy and clinical outcomes of stereotactic aspiration combined with the Gamma Knife radiosurgery (GKRS) method were evaluated retrospectively for patients with large cystic brain metastases. This combined method aims to decrease the tumor weight (volume) and increase the possible radiation dose. The present study involved 48 patients who were diagnosed with cystic metastatic brain tumors between January 2008 and December 2012 in the Department of Neurosurgery of Nanfang Hospital Southern Medical University (Guangzhou, China). Every patient underwent Leksell stereotactic frame, 1.5T magnetic resonance imaging (MRI)-guided stereotactic cyst aspiration and Leksell GKRS. Subsequent to the therapy, MRI was performed every 3 months. The results indicated that 48 cases were followed up for 24-72 months, with a mean follow-up duration of 36.2 months. Following treatment, 44 patients (91.7%) exhibited tumor control and 4 patients (8.3%) experienced progression of the local tumor. During this period, 35 patients (72.9%) succumbed, but only 2 (4.2%) of these succumbed to the brain metastases. The total local control rate was 91.7% and the median overall survival time of all patients was 19.5 months. The 1-year overall survival rate was 70.8% and the 2-year overall survival rate was 26.2%. In conclusion, these results indicated that the method of stereotactic cyst aspiration combined with GKRS was safe and effective for patients with large cystic brain metastases. This method is effective for patients whose condition is too weak for general anesthesia and in whom the tumors are positioned at eloquent areas. This method enables patients to avoid a craniotomy, and provides a good tumor control rate, survival time and quality of life.

Securin promotes migration and invasion via matrix metalloproteinases in glioma cells.

Human securin, encoded by pituitary tumor transforming gene 1, is implicated in several oncogenic processes in the pathogenesis of brain tumors, including glioma. The aim of the present study was to examine the effect of securin on the migration and invasion of glioma cells. The results revealed that the overexpression of securin in glioma LN-229 cells significantly increased the invasion and transmigration abilities. By contrast, these abilities were significantly reduced by the downregulation of securin in glioma U373 cells. Furthermore, the results demonstrated that securin overexpression and downregulation significantly increased and decreased the levels of matrix metalloproteinase 2 and 9, respectively. These findings indicate a promotive role for securin in glioma migration and invasion, which may involve the action of matrix metalloproteinases.

Preventive effect of dexamethasone gelatin sponge on the lumbosacral epidural adhesion.

OBJECTIVE: This study aims to explore the preventive effect of dexamethasone gelatin sponge on the lumbosacral epidural adhesion in the laminectomy. METHODS: A total of 36 Wista rats were divided into A, B, C and D groups randomly. Dexamethasone was not used in group A, Dexamethasone was used in group B, Dexamethasone was not used in group C but covered with gelatin sponge, dexamethasone gelatin sponge was used in group D. 3 rats in each group were sacrificed at 4, 8 and 12 weeks after operation respectively and the wound was opened to observe the dural scar formation and the dura adhesion. Immunohistochemical technique was used for histology observation. The expressions of VEGF and VEGFR2 in the epidural scar and surrounding tissues were detected with western blotting and immunohistochemical methods. RESULTS: According to the Rydell score standard, there were different degree of adhesion formation in A, B and C groups while there was no obvious adhesion formation in D group. It was confirmed that the expressions of VEGF and VEGFR2 in group D were lower than that of the other groups. CONCLUSIONS: Dexamethasone gelatin sponge could significantly reduce the occurrence of epidural scar tissue hyperplasia and adhesion after laminectomy in rats, and its mechanism may be related to the decreased expression of VEGF and VEGFR2.

Association of LIG4 and XRCC4 gene polymorphisms with the risk of human glioma in a Chinese population.

We conducted a case-control study to assess the LIG4 and XRCC4 genes polymorphisms and development of glioma. A case-control study including 162 glioma cases and 324 controls was conducted in a Chinese population. Genotypes of rs10131 and rs1805388 in LIG4 and rs2075685 and rs1805377 in XRCC4 were conducted by polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) assay. Conditional logistic regression analysis showed that subjects carrying AA genotype of LIG4 rs10131 was associated with increased risk of glioma when compared with GG genotype, and the OR (95% CI) was 3.26 (1.50-7.23). We found that GA+AA of LIG4 rs10131 was associated with increased risk of glioma in those without family history of cancer, and the OR (95% CI) was 1.78 (1.12-2.83). However, no association was found between variants of LIG4 rs1805388, XRCC4 rs2075685 and XRCC4 rs1805377 and development of glioma. In conclusion, our results suggest that LIG4 rs10131 polymorphism in the DNA repair pathways plays an important role in the risk of glioma in a Chinese population.

Relationships of LDLR genetic polymorphisms with cerebral infarction: a meta-analysis.

This meta-analysis was undertaken to identify the relationships between genetic polymorphisms in the LDLR gene and the risk of cerebral infarction. The Web of Science (1945-2013), the Cochrane Library Database (Issue 12, 2013), PubMed (1966-2013), EMBASE (1980-2013), CINAHL (1982-2013) and the Chinese Biomedical Database (CBM) (1982-2013) were searched for relevant articles without language restrictions. Meta-analysis was conducted using the STATA 12.0 software. Crude odds ratios (OR) with their corresponding 95% confidence interval (CI) were calculated. Eight case-control studies with a total of 4,655 patients with cerebral infarction and 15,920 healthy control subjects were included in our meta-analysis. Five common polymorphisms in the LDLR gene were evaluated, including rs11669576 A > T, rs1433099 C > T, rs5925 C > T, rs688 C > T, rs1122608 T > G in the LDLR gene. The results of this meta-analysis revealed that cerebral infarction patients had a higher frequency of LDLR genetic polymorphisms than that of healthy controls (allele model: OR 1.17, 95% CI 1.05-1.30, P = 0.004; dominant model: OR 1.18, 95% CI 1.05-1.33, P = 0.007; homozygous model: OR 1.50, 95% CI 1.03-2.16, P = 0.032; respectively), especially for the rs11669576 A > T, rs1433099 C > T and rs5925 C > T polymorphisms. Among different ethnic subgroups, the results demonstrated positive correlations between LDLR genetic polymorphisms and an increased risk of cerebral infarction among both Asians and Caucasians under the allele and dominant models (all P < 0.05). Our findings indicate that LDLR genetic polymorphisms may be strongly involved in the pathogenesis of cerebral infarction, especially the rs11669576 A > T, rs1433099 C > T, rs5925 C > T polymorphisms.

[Expression and role of Caveolin-1 in the angiogenesis of cerebral arteriovenous malformation].

OBJECTIVE: To explore the expression and role of Caveolin-1 in the angiogenesis of cerebral arteriovenous malformation (AVM). METHODS: A total of 55 fresh AVM samples at Affiliated Hospital, Inner Mongolia Medical University and Beijing Tiantan Hospital from August 2013 to May 2014 were collected to test the expressions of Caveolin-1, vascular endothelial growth factor (VEGF), vascular endothelial growth factor-receptor 2 (VEGF-R2) and endothelial nitric oxide synthase (eNOS) by immunohistochemistry and Western blot. And the relationship between the expressions of Caveolin-1 and VEGF, VEGF-R2 and eNOS was analysed. RESULTS: The expression rates of Caveolin-1, VEGF, VEGF-R2 and eNOS in human AVM were 100%, 87.27%, 76.36% and 85.45%. And the values were significantly higher than those in normal superficial temporal artery. Western blot showed that the expressions of Caveolin-1, VEGF, VEGF-R2 and eNOS in hemorrahge AVM were higher than those in non-hemorrahge counterpart (P < 0.05). The expressions of Caveolin-1, VEGF, VEGF-R2 and eNOS were consistent. CONCLUSION: Caveolin-1 plays a positive regulatory role in the angiogenesis of AVM through the PI3K/Akt signaling pathway. In cerebral AVM, Caveolin-1 plays an important role in occurrence, progression, hemorrahge and degradation of brain AVM.

Dendritic cell-glioma fusion activates T lymphocytes by elevating cytotoxic efficiency as an antitumor vaccine.

BACKGROUND: Hybrid cells produced by fusions of tumor and dendritic cells (DC) have demonstrated remarkable efficacy for priming the anti-tumor immune response. In the current study, we examined the antitumor activity of cytotoxic T lymphocytes (CTLs) primed in response to a tumor vaccine comprising a glioma-DC fusion as part of a therapeutic against glioma. MATERIAL AND METHODS: Primary cultured glioma cells were fused with peripheral blood DC under conditions of polyethylene glycol (PEG) incubation. Glioma cell suspensions were designated as three groups to include (1) CTL-effective cell group activated by fused cells; (2) CTL-effective cell group stimulated by co-cultured glioma cells and DC cells; and (3) lymphocyte-only group as a control, which was not stimulated by the DC. Cytotoxicity of CTLs on glioma cells was accessed by MTT assay in vitro. RESULTS: Glioma cells with peripheral blood DC were cultured and fused. The killing effect of CTLs pre-activated by fused cells was significantly higher than that of the co-culture CTL group with unsensitized lymphocytes (p < 0.01). The killing activity, as measured by an enhanced efficiency ratio, was increased significantly in the co-cultures of fused cells with CTL groups (p < 0.01). CONCLUSIONS: The glioma-dendritic cell fusion vaccine possessed a more effective anticancer activity by stimulating the effector activity of CTLs.

Mediation of multiple pathways regulating cell proliferation, migration, and apoptosis in the human malignant glioma cell line U87MG via unphosphorylated STAT1: laboratory investigation.

OBJECT: Signal transducer and activator of transcription 1 (STAT1) is thought to be a tumor suppressor protein. The authors investigated the expression and role of STAT1 in glioblastoma. METHODS: Immunohistochemistry was used to detect the expression of STAT1 in glioblastoma and normal brain tissues. Reverse transcription-polymerase chain reaction and Western blot analysis were used to detect mRNA and protein expression levels of STAT1. Cell growth, proliferation, migration, apoptosis, and the expression of related genes and proteins (Bcl-2, Bax, cleaved caspase-3, caspase-9, p21, and proliferating cell nuclear antigen) were examined in vitro via cell counting kit-8, wound-healing, flow cytometry, Rhodamine B, TUNEL, and Western blot assays. RESULTS: Human glioblastoma had decreased expression of STAT1 proteins. Transfection of the U87MG cells with STAT1 plasmid in vitro demonstrated significant inhibition of cell growth and an increase in apoptotic cell death compared with cells transfected with vector or mock plasmids. These effects were associated with the upregulation of cleaved caspase-3, Bax, and p21 and the downregulation of Bcl-2 expression. CONCLUSIONS: The results of this study suggest that increased expression of STAT1 by transfection with STAT1 plasmid synergistically inhibits human U87MG glioblastoma cell growth in vitro.

Human leptin triggers proliferation of A549 cells via blocking endoplasmic reticulum stress-related apoptosis.

Lung cancer is a disease characterized by uncontrolled cell growth in tissues of the lung. Leptin is a pleiotropic hormone with antiapoptotic and proliferative roles involved in several systems. However, there is no known antiapoptotic mechanism of leptin in non-small cell lung cancer (NSCLC). So, we investigated the antiapoptotic mechanism of leptin in NSCLC. Proliferation, apoptosis, and the specific mechanism of leptin-transfected cells were analyzed in this study. Leptin, p-Perk, IRE1, cleaved ATF6, spliced XBP1, eIF2-α, TRAF2, CHOP, and caspase 12 proteins were detected by Western blot, and endoplasmic reticulum (ER) stress-related mRNA was detected by semi-quantitative reverse transcription PCR (RT-PCR). Leptin in A549 and transfected cells inhibited cisplatin-activated ER stress-associated mRNA transcription and activation of proteins. ER stress unfolded protein response (UPR) proteins, PERK and ATF6, were involved in leptin-triggered apoptosis. XBP1 and TRAF2 were increased significantly when treated with cisplatin in A549-siLPT and non-transfected cells. CHOP expression was blocked in A549 and transfected cells (LPT-PeP and LPT-EX cells). In conclusion, leptin can promote the proliferation of A549 cells through blocking ER stress-mediated apoptosis. This blocking is mediated by the p-Perk and ATF6 pathway through blocking activation of CHOP.

Comprehensive study on associations between nine SNPs and glioma risk.

AIM: Glioma cancer is the most common type of adult brain tumor. Recent genome-wide association studies (GWAS) have identified various new susceptibility regions and here we conducted an extensive analysis of associations between 12 single nucleotide polymorphisms (SNPs) and glioma risk. METHODS: A total of 197 glioma cases and 197 health controls were selected, and 9 SNPs in 8 genes were analyzed using the Sequenom MassARRAY platform and Sequenom Assay Design 3.1 software. RESULTS: We found the MAF among selected controls were consistent with the MAF from the NCBI SNP database. Among 9 SNPs in 8 genes, we identified four significant SNP genotypes associated with the risk of glioma, C/C genotype at rs730437 and T/T genotype at rs1468727 in ERGF were protective against glioma, whereas the T/T genotype at rs1799782 in XRCC1 and C/C genotype at rs861539 in XRCC3 conferred elevated risk. CONCLUSION: Our comprehensive analysis of nine SNPs in eight genes suggests that the rs730437 and rs1468727 in ERGF, rs1799782 in XRCC1 gene, and rs861539 in XRCC3 gene are associated with glioma risk. These findings indicate that genetic variants of various genes play a complex role in the development of glioma.

[Correlations of angio-architectural factors with cerebral arteriovenous malformation hemorrhage].

OBJECTIVE: To explore the relationship between angio-architectures of cerebral arteriovenous malformations (AVM) and hemorrhage. METHODS: A total of 55 consecutive surgical cases of AVM were collected in August 2010 to May 2011 at Beijing Tiantan Hospital. There were 34 males and 21 females with an average age of 32.5 years (range: 3 - 59). The initial symptoms included bleeding (n = 20), epilepsy (n = 21), headache (n = 7), neurological dysfunctions (n = 6) and others (n = 1). The relationship between size, location, type of feeding artery, type of draining vein, complicated venous aneurysm and hemorrhage was analyzed by single factor test. RESULTS: The cases of AVM fed by perforators, located in basal ganglia and post-cranial fossa, with small size, exclusively deep drainage and complicated venous aneurysm were more likely to present with hemorrhage. CONCLUSION: The hemorrhage of AVM is significantly correlated with many factors, such as the type of feeding artery, size and location of AVM, the type of draining vein and complicated venous aneurysm. But the number of draining vein is irrelevant.

[Effects of Newcastle disease virus on the expression of survivin and cell cycle in human tongue squamous carcinoma TSCCa cells].

OBJECTIVE: To investigate the effects of Newcastle disease virus (NDV) infection on the expression of survivin and cell cycle in human tongue squamous carcinoma TSCCa cells. METHODS: The proliferation of TSCCa cells infected with NDV in vitro was evaluated by means of MTT assay, and survivin expression in the infected cells was detected using RT-PCR and Western blotting. Flow cytometry was performed to assess the changes in the cell apoptosis, cell cycle and cell proliferation index (PI) of the cells. RESULTS: NDV infection resulted in decreased survivin expression and increased apoptosis of TSCCa cells, with reduced cell percentage in G2/M and S phases and lowered PI of the cells, showing significant differences from those of the negative control cells (P<0.05). CONCLUSION: NDV infection can inhibit survivin expression, affect the cell cycle of TSCCa cells and induce their apoptosis.