A novel method of tunneling retroperitoneoscopic adrenalectomy: a prospective study.

BACKGROUND: To introduce the surgical technique and our team's extensive experience with tunnel method in laparoscopic adrenalectomy. METHODS: From July 2019 to June 2022, we independently designed and conducted 83 cases of " Tunnel Method Laparoscopic Adrenalectomy," a prospective study. There were 45 male and 38 female patients, ages ranged from 25 to 73 years(mean: 44.6 years).The cases included 59 adrenal cortical adenomas, 9 pheochromocytomas, 6 cysts, 4 myelolipomas, 1 ganglioneuroma, and 4 cases of adrenal cortical hyperplasia. In terms of anatomical location, there were 39 cases on the left side, 42 on the right side, and 2 bilateral cases. Tumor diameters ranged from 0.6 to 5.9 cm(mean: 2.9 cm). Utilizing ultrasound monitoring, percutaneous puncture was made either directly to the target organ or its vicinity, and the puncture path was manually marked. Then, under the direct view of a single-port single-channel laparoscope, the path to the target organ in the retroperitoneum or its vicinity was further delineated and separated. This approach allowed for the insertion of the laparoscope and surgical instruments through the affected adrenal gland, thereby separating the surface of the target organ to create sufficient operational space for the adrenalectomy. RESULTS: All 83 surgeries were successfully completed. A breakdown of the surgical approach reveals that 51 surgeries were done using one puncture hole, 25 with two puncture holes, and 7 with three puncture holes. The operation time ranged from 31 to 105 min (mean: 47 min), with a blood loss of 10 to 220mL (mean: 40 mL). Notably, there were no conversions to open surgery and no intraoperative complications. Postoperative follow-up ranged from 6 to 28 months, during which after re-examination using ultrasound, CT, and other imaging methods, there were no recurrences or other complications detected. CONCLUSIONS: The completion of the tunnel method laparoscopic adrenalectomy represents a breakthrough, transitioning from the traditional step-by-step separation of retroperitoneal tissues to reach the target organ in conventional retroperitoneoscopic surgery. This method directly accesses the target organ, substantially reducing the damage and complications associated with tissue separation in retroperitoneoscopic surgery, As a result, it provides a new option for minimally invasive surgery of retroperitoneal organs and introduces innovative concepts to retroperitoneoscopic surgery.

Comparative study of each surgical step in radical prostatectomy under 3D and 2D laparoscopy.

Objective: Comparing the specific advantages and surgical outcomes of each step in radical prostatectomy under 3D vs. 2D laparoscopy. Methods: From October 2019 to January 2023, our urology department treated 63 cases of prostate cancer, using an odd-even arrangement method to divide into two groups. This is a non-randomized prospective study, with 33 odd-numbered cases in the 3D group and 30 even-numbered cases in the 2D group. The surgery was divided into four steps: (1) establishing an extraperitoneal pneumoperitoneum (2) pelvic lymph node dissection (3)excising the prostate (4)bladder-urethral anastomosis, comparing the two groups in terms of surgical time, blood loss, and relevant postoperative indicators for each step. Results: All 63 surgeries were successfully completed without any conversions. Comparing 3D and 2D laparoscopy groups, there were statistically significant differences in total surgery time (123.5 ± 15.3 min vs. 145.6 ± 17.2 min, P < 0.05), total blood loss (198.3 ± 18.4 ml vs. 243.1 ± 20.1 ml, P < 0.05), prostate excision time (55.1 ± 8.4 min vs. 67.2 ± 9.3 min, P < 0.05) and blood loss (101.6 ± 12.2 ml vs. 123.8 ± 14.1 ml, P < 0.05), bladder-urethral anastomosis time (30.5 ± 4.3 min vs. 37.6 ± 5.1 min, P < 0.05) and blood loss (62.7 ± 9.7 ml vs. 82.5 ± 8.2 ml, P < 0.05). There were no statistical differences in the time and blood loss during the establishment of extraperitoneal pneumoperitoneum and the cleaning of pelvic lymph nodes (P > 0.05). In terms of urinary incontinence rates, the 3D laparoscopy group was lower than the 2D group, and in terms of preserving erectile function, the 3D group was higher than the 2D group, with significant statistical differences (P < 0.05). There were no statistically significant differences between the two groups in terms of postoperative drainage days, hospitalization days, hospitalization costs, time of catheter removaland positive margin rates (P > 0.05). Conclusion: Compared to traditional 2D laparoscopy, 3D laparoscopy can shorten the operation time and reduce bleeding in the steps of prostate excision and bladder-urethral anastomosis, but there was no significant difference in peri-operative outcomes.

Ursolic acid-downregulated long noncoding RNA ASMTL-AS1 inhibits renal cell carcinoma growth via binding to HuR and reducing vascular endothelial growth factor expression.

It has been reported ursolic acid (UA), one of the naturally abundant pentacyclic triterpenes, possesses a wide range of biological activities including anti-inflammatory, anti-atherosclerotic, and anticancer properties. Renal cell carcinoma (RCC) is a severe malignancy due to its asymptomatically spreading ability. Our study aimed to investigate the role and molecular mechanism of UA in RCC. RCC cell proliferation, migration, invasion, and angiogenesis were assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, Transwell, and tube formation assays. Xenograft tumor models were established to confirm the role of UA and long noncoding RNA ASMTL antisense RNA 1 (ASMTL-AS1) in vivo. Expression levels of ASMTL-AS1 and vascular endothelial growth factor (VEGF) were measured using reverse transcriptase quantitative polymerase chain reaction and western blot analysis. The interaction probabilities of ASMTL-AS1 or VEGF with RNA-binding protein human antigen R (HuR) were verified by RNA immunoprecipitation experiment. The half-life period of messenger RNA (mRNA) was determined using actinomycin D. UA inhibited RCC cell growth in vivo and tumorigenesis in vitro. ASMTL-AS1 was highly expressed in RCC cell lines. Of note, UA downregulated ASMTL-AS1 expression, and overexpressed ASMTL-AS1 reversed the UA-induced suppression on RCC cell migration, invasion, and tube formation. Additionally, ASMTL-AS1 bound to HuR to maintain the stability of VEGF mRNA. Rescue experiments showed that the suppressed malignancy of RCC cells mediated by ASMTL-AS1 knockdown was counteracted by overexpression of VEGF. Moreover, silenced ASMTL-AS1 inhibited RCC tumor growth and metastasis in vivo. The obtained data suggest UA as a promising therapeutic agent to attenuate the development of RCC via regulation of the targeted molecules.

Silencing of FGF6 hampers aerobic glycolysis and angiogenesis in bladder cancer by regulating PI3K/Akt and MAPK signaling pathways.

Metabolic abnormalities and uncontrolled angiogenesis are two vital features of malignant tumors. Although fibroblast growth factor 6 (FGF6) is known to promote the proliferation and migration of bladder cancer (BC) cells, its influences on aerobic glycolysis and angiogenesis in BC remain unclear. Gene expression at messenger RNA and protein levels were examined by reverse transcription-quantitative polymerase chain reaction and Western blot analyses, respectively. Lactate production and glucose uptake in BC cells were evaluated by performing aerobic glycolysis assays. A vasculogenic mimicry assay was executed for assessing the angiogenesis of BC cells. The viability, migration, and angiogenesis of human umbilical vein endothelial cells (HUVECs) cocultured with supernatants of BC cells were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, wound healing assay, and tube formation assay. It was found that FGF6 displayed a high level in BC cell lines. Silencing of FGF6 reduced the levels of lactate production, glucose uptake, and the expression of angiogenic factors and glycolytic enzymes in BC cells, which also inhibited the viability and migration of HUVECs. In addition, FGF6 depletion or aerobic glycolysis inhibitor 2-deoxy-d-glucose treatment decreased the total branching length and intersection number of both BC cells and HUVECs. Moreover, glucose or lactate treatment reversed FGF6-induced suppression of cell viability, migration, tube formation, and vasculogenic mimicry. The activation of the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) and mitogen-activated protein kinase (MAPK) signaling pathways was blocked by silenced FGF6. Furthermore, PI3K/Akt inhibitor (LY2940002) and p38-MAPK inhibitor (SB203580) inhibited the levels of aerobic glycolysis-related proteins. In conclusion, FGF6 knockdown suppressed aerobic glycolysis, thereby inhibiting angiogenesis in BC via regulation of the PI3K/Akt and MAPK signaling pathways.

LINC00265 promotes the viability, proliferation, and migration of bladder cancer cells via the miR-4677-3p/FGF6 axis.

BACKGROUND: Bladder cancer (BCa) is a common genitourinary malignancy with higher incidence in males. Long intergenic non-protein coding RNA 265 (LINC00265) is identified as an oncogene in many malignancies, while its role in BCa development remains unknown. PURPOSE: To explore the functions and mechanism of LINC00265 in BCa. RESEARCH DESIGN: Reverse transcription quantitative polymerase chain reaction was performed to examine LINC00265 expression in BCa cells. Cell counting kit-8 assays, colony formation assays, TdT-mediated dUTP Nick-End Labeling assays, and Transwell assays were conducted to examine BCa cell viability, proliferation, apoptosis, and migration. Luciferase reporter assays and RNA immunoprecipitation assays were carried out to explore the binding capacity between miR-4677-3p and messenger RNA fibroblast growth factor 6 (FGF6) (or LINC00265). Xenograft tumor model was established to explore the role of LINC00265 in vivo. RESULTS: LINC00265 was highly expressed in BCa cells. LINC00265 knockdown inhibited xenograft tumor growth and BCa cell viability, proliferation and migration while enhancing cell apoptosis. Moreover, LINC00265 interacted with miR-4677-3p to upregulate the expression of FGF6. FGF6 overexpression reversed the suppressive effect of LINC00265 knockdown on malignant phenotypes of BCa cells. CONCLUSIONS: LINC00265 promotes the viability, proliferation, and migration of BCa cells by binding with miR-4677-3p to upregulate FGF6 expression.

Long noncoding RNA KCNMB2-AS1 promotes the development of esophageal cancer by modulating the miR-3194-3p/PYGL axis.

Esophageal cancer (ESCA), as a common cancer worldwide, is a main cause of cancer-related mortality. Comprehensive studies on molecular mechanism of ESCA have been carried out. Though numerous long noncoding RNAs (lncRNAs) was reported to participate in the occurrence and development of ESCA, the potential role of lncRNA potassium calcium-activated channel subfamily M regulatory beta subunit 2 (KCNMB2) antisense RNA 1 (KCNMB2-AS1) in ESCA remains to be discovered. This study intends to investigate the detailed function and molecular mechanism of KCNMB2-AS1 in ESCA. Gene expression was evaluated by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Cell proliferation was examined by Cell Counting Kit-8 (CCK-8) assay and colony formation assay. Cell invasion and migration were measured by wound healing assay and Transwell assay. Luciferase reporter assay was adopted to validate the interaction between KCNMB2-AS1 and miR-3194-3p. Western blotting was performed to assess protein levels. We discovered that KCNMB2-AS1 was significantly upregulated in ESCA. KCNMB2-AS1 downregulation suppressed the growth, invasion, migration and stemness of ESCA cells. KCNMB2-AS1 bound with miR-3194-3p, and glycogen phosphorylase L (PYGL) was a direct target of miR-3194-3p. KCNMB2-AS1 upregulated PYGL expression by directly binding with miR-3194-3p. Additionally, PYGL overexpression abolished the inhibitory influence of KCNMB2-AS1 depletion on ESCA cell behaviors. Collectively, lncRNA KCNMB2-AS1 promotes ESCA development through targeting the miR-3194-3p/ PYGL axis, which might provide theoretical basis to explore novel biomarkers for ESCA treatment.

Association of Tumor Size with Risk of Lymph Node Metastasis in Clear Cell Renal Cell Carcinoma: A Population-Based Study.

The purpose of this article was to explore the association of tumor size with lymph node metastases (LNM) risk in patients with clear cell renal cell carcinoma (ccRCC). Based on the Surveillance, Epidemiology, and End Result (SEER) database, patients diagnosed with ccRCC from 1988 to 2015 were included in this study. For each patient, personal characteristics, clinicopathological data, and survival outcomes were, respectively, collected. Subsequently, the odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to investigate the potential risk factors for LNM in ccRCC. Finally, Kaplan-Meier (KM) survival plots of overall survival (OS) and ccRCC-specific survival (CSS) were evaluated on the basis of different tumor sizes. A total of 8,292 patients were finally enrolled in the study, 1,170 of whom (14.11%) had LNM. According to the heatmap, we could intuitively interpret that larger tumor size was related to an increased risk of LNM obviously. The risk of LNM was evidently greater for larger tumor size (4-7 cm: OR = 2.415, 95% CI = 1.708-3.415; 7-10 cm: OR = 3.746, 95% CI = 2.677-5.242; and >10 cm: OR = 4.617, 95% CI = 3.302-6.457) compared with smaller tumor size (≤4 cm). According to the KM survival plots of OS and CSS, we observed a gradual decline in survival with increasing tumor size, while the smallest tumor size had the best survival outcomes. These results indicated the positive relationship of tumor size with risk of LNM in ccRCC. And we also noticed continual decrease survival rates of OS and CSS with increasing tumor size.

Circ_0062020 Knockdown Strengthens the Radiosensitivity of Prostate Cancer Cells.

BACKGROUND: Prostate cancer (PCa) is a major contributor to reduce the life quality of males. Circular RNAs were frequently reported to be associated with cancers. In the case of radiotherapy to PCa, the role of circ_0062020 was still inconclusive, which was further explored in this study. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expression of circ_0062020, miR-615-5p and thyroid hormone receptor interactor 13 (TRIP13) in PCa tissues and cells, as well as in normal tissues and cell. Meanwhile, the proliferation of PCa cells was evaluated by clone formation assay and cell counting kit 8 (CCK8) assay. Moreover, the metastasis of PCa cells was assessed by transwell and wound healing assays. Furthermore, the apoptosis of PCa cells was determined by flow cytometry assay. Besides, dual-luciferase reporter system was applied to verify the correlation between miR-615-5p and circ_0062020 or TRIP13, which was predicted by online tool CircRNA interactome or TargetScan. In addition, the protein expression of TRIP13 was measured by Western blot in PCa tissues and cells and normal tissues and cells. Finally, xenograft tumor assay was performed to further confirming the function of circ_0062020 in PCa in vivo. RESULTS: Circ_0062020 and TRIP13 were upregulated, while miR-615-5p was downregulated in PCa tissues and cells. Circ_0062020 knockdown or miR-615-5p overexpression inhibited the proliferation and metastasis, and promoted apoptosis, which could be reversed by miR-615-5p inhibitor or pc-TRIP13 in ionizing radiation (IR)-treated PCa cells. As expected, circ_0062020 sponged miR-615-5p to regulate TRIP13 expression in PCa cells. Circ_0062020 knockdown also suppressed PCa tumor growth in vivo. CONCLUSION: Circ_0062020 suppressed the radiosensitivity by miR-615-5p/TRIP13 axis in PCa cells, which might provide insights into the radiotherapy for PCa.

Toxoplasma gondii infection in children with lymphoma in Eastern China: seroprevalence, risk factors and case-control studies.

Epidemiological data for Toxoplasma gondii regarding malignancy have gained increasing attention; however, the information about T. gondii infection among children with malignant lymphoma (ML) in China is unclear. Therefore, 314 children with lymphoma and 314 healthy children, age- and gender-matched, were recruited to estimate the seroprevalence of T. gondii in the participants and identify the risk factors of infection. Blood samples from all participants were collected and examined for T. gondii IgG and IgM antibodies using ELISA. The results showed that the overall seroprevalence of T. gondii antibodies (including IgG and/or IgM) in ML patients and healthy controls was 19.8% and 9.9%, respectively. Contact with the cats, consumption of oysters and history of chemotherapy were estimated to be the risk factors for T. gondii infection in children with lymphoma by multivariable logistic regression analysis, whereas in healthy children, contact with cats and consumption of oysters were the risk factors. Moreover, among various histological types of lymphoma, individuals with NK/T-cell lymphoma, B-small lymphocytic lymphoma, marginal zone B-lymphoma and Hodgkin's lymphoma had a higher seroprevalence than healthy controls (P < 0.05). These findings indicated the high prevalence of T. gondii infection in children with lymphoma, and hence, efforts should be performed to evaluate the effect of the infection further in lymphoma patients.

CircHIPK3 overexpression accelerates the proliferation and invasion of prostate cancer cells through regulating miRNA-338-3p.

Objective: Circular RNA is a type of endogenous RNA molecule with a stable closed-loop structure which is ubiquitous in mammals. Circular RNA HIPK3 (circHIPK3) is highly expressed in hepatocellular carcinoma and promotes the growth of hepatoma cells. However, its role in prostate cancer (PCa) has not been reported. This study aims to explore whether circHIPK3 could affect the proliferative and invasive potentials of PCa cells by regulating miRNA-338-3p. Methods: Expression levels of circHIPK3 and miRNA-338-3p in PCa tissues and cells were determined by RT-qPCR. The regulatory effects of circHIPK3 and miRNA-338-3p on proliferative and invasive potentials of PCa cells were evaluated by CCK-8 and transwell assay, respectively. We verified the binding between miRNA-338-3p and ADAM17, as well as miRNA-338-3p and circHIPK3 through dual-luciferase reporter gene assay. Rescue experiments were conducted to clarify whether circHIPK3 affected the proliferative and invasive potentials of PCa cells by regulating miRNA-338-3p. Results: Expression level of circHIPK3 in PCa tissues was remarkably higher than that of paracancerous tissues. Knockdown of circHIPK3 inhibited the proliferative and invasive rates of PC-3 and DU145 cells. Dual-luciferase reporter gene assay indicated that circHIPK3 could bind to miRNA-338-3p. Moreover, miRNA-338-3p expression was downregulated in PCa tissues. miRNA-338-3p expression was negatively correlated with lymph node metastasis and distant metastasis. miRNA-338-3p overexpression markedly reduced proliferative and invasive abilities of PC-3 and DU145 cells. Furthermore, ADAM17 was confirmed to be the target gene of miRNA-338-3p. Overexpression of ADAM17 enhanced proliferative and invasive abilities of PC-3 and DU145 cells. Finally, rescue experiments indicated that miRNA-338-3p knockdown in PC-3 and DU145 cells partially reversed the regulatory effects of circHIPK3 on proliferative and invasive potentials. Conclusion: Overexpression of circHIPK3 promotes the proliferative and invasive potentials of PCa cells through sponging miRNA-338-3p to regulate ADAM17 expression, thus accelerating the malignant progression of PCa.

Ultraviolet light-emitting diode irradiation-induced cell death in HL-60 human leukemia cells in vitro.

Ultraviolet (UV) radiation is considered to be a potent cell-damaging agent in various cell lineages; however, the effect of UV light­emitting diode (LED) irradiation on human cells remains unclear. The aim of the present study was to examine the effect of UV LED irradiation emitting at 280 nm on cultured HL­60 human leukemia cells, and to explore the underlying mechanisms. HL­60 cells were irradiated with UV LED (8, 15, 30 and 60 J/m2) and incubated for 2 h after irradiation. The rates of cell proliferation and apoptosis, the cell cycle profiles and the mRNA expression of B­cell lymphoma 2 (Bcl­2) were detected using cell counting kit­8, multicaspase assays, propidium iodide staining and reverse transcription­quantitative polymerase chain reaction, respectively. The results showed that UV LED irradiation (8­60 J/m2) inhibited the proliferation of HL­60 cells in a dose­dependent manner. UV LED at 8­30 J/m2 induced dose­dependent apoptosis and G0/G1 cell cycle arrest, and inhibited the expression of Bcl­2 mRNA, while UV LED at 60 J/m2 induced necrosis. In conclusion, 280 nm UV LED irradiation inhibits proliferation and induces apoptosis and necrosis in cultured HL­60 cells. In addition, the cell cycle arrest at the G0/G1 phase and the downregulation of Bcl­2 mRNA expression were shown to be involved in UV LED-induced apoptosis.

Solitary juvenile xanthogranuloma with tibial involvement: a case report.

Juvenile xanthogranuloma (JXG) is a rare disease that is part of a spectrum of histiocytic dendritic cell disorders. Most patients present with a solitary cutaneous lesion; however, others present with extracutaneous manifestations or even with systemic involvement. We present the first report of an 11-month-old girl in whom was diagnosed a unifocal extracutaneous JXG involving the tibia. Histological and immunohistochemical staining results are presented. A review of the literature on these unusual lesions is conducted, along with discussion of their differential diagnosis and key aspects of the patient's evaluation, management, and pathological diagnosis.

Involvement of the nuclear factor-κB signaling pathway in the regulation of CXC chemokine receptor-4 expression in neuroblastoma cells induced by tumor necrosis factor-α.

Metastasis is a hallmark of malignant neuroblastoma and is the main reason for therapeutic failure and recurrence of the tumor. The CXC chemokine receptor-4 (CXCR4), a Gi protein-coupled receptor for the ligand CXCL12/stromal cell-derived factor-1α (SDF-1α), is expressed in various types of tumor. This receptor mediates the homing of tumor cells to specific organs that express the ligand, CXCL12, for this receptor and plays an important role in tumor growth, invasion, metastasis and angiogenesis. In the present study, the inflammatory cytokine, tumor necrosis factor­α (TNF­α) upregulated CXCR4 expression in neuroblastoma cells and increased migration to the CXCR4 ligand SDF­1α. In addition, this effect was dependent upon NF-κB transcriptional activity, as blocking the NF-κB pathway with pyrrolidinedithiocarbamic acid ammonium salt suppressed TNF-α­induced upregulation of CXCR4 expression and reduced the migration towards the CXCR4 ligand, SDF-1α. Treating neuroblastoma cells with TNF-α resulted in the activation of nuclear factor-kappa B (NF-κB) and subsequently, the translocation of NF-κB from the cytoplasm to the nucleus. Using immunohistochemistry, NF­κB and CXCR4 were significantly correlated with each other (P=0.0052, Fisher's exact test) in a cohort of neuroblastoma samples (n=80). The present study indicates that the inflammatory cytokine, TNF-α, partially functions through the NF­κB signaling pathway to upregulate CXCR4 expression to foster neuroblastoma cell metastasis. These findings indicate that effective inhibition of neuroblastoma metastasis should be directed against the inflammatory cytokine-induced NF­κB/CXCR4/SDF­1α signaling pathway.

Lentivirus-mediated Persephin over-expression in Parkinson's disease rats.

Persephin, together with glial cell line-derived neurotrophic factor and neurturin, has a neurotrophic effect and promotes the survival of motor neurons cultured in vitro. In this study, dopaminergic neurons in the substantia nigra of rats were transfected with the Persephin gene. One week later 6-hydroxydopamine was injected into the anterior medial bundle to establish a Parkinson's disease model in the rats. Results found that the number of dopaminergic neurons in the substantia nigra increased, tyrosine hydroxylase expression was upregulated and concentrations of dopamine and its metabolites in corpus striatum were increased after pretreatment with Persephin gene. In addition, the rotating effect of the induced Parkinson's disease rats was much less in the group pretreated with the Persephin gene. Persephin has a neuroprotective effect on the 6-hydroxydopamine-induced Parkinson's disease through protecting dopaminergic neurons.

NF-κB signaling pathway confers neuroblastoma cells migration and invasion ability via the regulation of CXCR4.

BACKGROUND: Accumulating evidence implicates the transcription factor NF-κB as a positive mediator of tumor metastasis, but the molecular mechanism(s) involved in this process remains largely unknown. In this study, we investigated the role of NF-κB signaling pathway in the regulation of CXC chemokine receptor-4 (CXCR4) in neuroblastoma metastasis. MATERIAL AND METHODS: NF-κB, CXCR4 mRNA and protein expression were measured by RT-PCR, and Western blot. Tumor necrosis factor-α (TNF-α) was used to induce the upregulation of NF-κB and CXCR4. The knockdown of NF-κB and CXCR4 was achieved by PDTC. Transwell assay was used to investigate the role of NF-κB (P65) in neuroblastoma cell migration and invasion. An in vitro co-culture system was established to investigate the role of tumor microenvironment in regulation of the NF-κB signaling pathway. RESULTS: Over-expression of NF-κB (p65) promoted tumor migration and invasion through the upregulation of CXCR4; however, knockdown of NF-κB(P65) inhibited tumor migration and invasion through blocking the expression of CXCR4. Consistently, in the co-culture system, the expression of CXCR4 was partly dependent on the expression of NF-κB (p65). CONCLUSIONS: Our studies reveal critical roles for the NF-κB signaling pathway in neuroblastoma migration and invasion. The mechanism may be through up-regulation of CXCR4, mediated by the NF-κB signaling pathways. Targeting NF-κB signalling pathways and ultimately CXCR4 could be a strategy in neuroblastoma therapy.