Résumé
Abstract Objectives Accurate prognosis assessment across the heterogeneous population of brain metastases is very important, which may facilitate clinical decision-making and appropriate stratification of future clinical trials. Previous studies have shown the L1 Cell Adhesion Molecule (L1CAM) is potentially involved in human malignancies of multiple different samples and unfavorable survival. However, no data of L1CAM are available for the brain metastases from lung adenocarcinoma, especially for the one with neurosurgical resection. Method The authors investigated the L1CAM expression in cranial metastatic lesions for patients with brain metastases from lung adenocarcinoma after neurosurgical resection using tissue microarrays that were obtained from the Department of Neurosurgery at the Cancer Hospital of the Chinese Academy of Medical Sciences. Furthermore, the relationship between L1CAM expression and clinic-pathological parameters, including overall survival time, was analyzed to assess the prognostic value of L1CAM. Results L1CAM high expression was found in 62.30% of brain metastases from lung adenocarcinoma and significantly correlated with brain metastasis number (p = 0.028) and Lung-molGPA score (p = 0.042). Moreover, L1CAM expression was an independent predictor of survival for brain metastases after neurosurgical resection in a multivariate analysis. Patients with L1CAM high expression had unfavorable overall survival time (p = 0.016). In addition, the multivariate analysis also showed age and extracranial transfer were also the independent prognostic factors for this type of patient with brain metastases. Conclusions A subset of brain metastases from lung adenocarcinoma aberrantly expresses L1CAM. L1CAM is a novel independent prognostic factor for brain metastasis from lung adenocarcinoma after neurosurgical resection.
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Objective To study the mechanism of brain development delay in rats with intrauterine growth retardation(IUGR) through establishing IUGR animal model by low protein diet during pregnancy and examining the expressions of cannabinoid receptorl (CB1) and L1 cell adhesion molecule (NCAM-L1) in IUGR and normal rats.Methods Thirty-two pregnant rats were randomly fed with normal diet or lower protein diet during pregnancy (16 rats in each group).The offspring rats were divided into IUGR group and control group by birth weight,and sacrificed on day 0,7,14,21 after birth,brain weight was recorded.The expressions of CB1 and NCAM-L1 in the brain were examined by immunohistochemistry staining.Image-Pro Plus 5.1 image processing software was used for semi-quantitative analysis.The integrated optical density of the CB1 and NCAM-L1 of the positive cells was calculated.Results The expressions of CB1 and NCAM-L1 in offspring rats brain were basically in the same area,the changes in both was in accord with the brain weight change.The expression of CB1 in the brain of the pup rats in the IUGR group was significantly lower than that in the control group 0,7,14,21 days after birth,by contrast,the expression of NCAM-L1 was significantly higher (all P ＜ 0.05),and the expressions of CB1 and NCAM-L1 were negatively correlated between both groups(P =0.032,0.010).Conclusions CB1 and NCAM-L1 were involved in the process of rat brain development.The effect of CB1 on rat brain development may be achieved by NCAM-L1.
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Objective To evaluate the effect of L1 cell adhesion molecule (L1CAM) gene expression silencing by short hairpin RNA (shRNA) on perineural invasion of pancreatic cancer Capan-2 cells in vitrr. Methods We transfected Capan-2 cellswith lentivirus-mediated shRNA targeting L1CAM (L1CAM-shRNA) and negative control shRNA (L1 CAM-NC), and then the transfected Capan-2 cells were co-culturedwith mouse dorsal root ganglia (DRG) in matrigel matrix. The procession of neurite outgrowth and cell colony growth were observed by inverted microscope. Areas of cell colonies and neurites were quantitated using Image pro plus software. Results The cancer cells migrated to DRG and grew around the neurites in the L1CAM-NC/DRG group, which was not observed in the L1CAM-shRNA/DRG group. On day 3 and 5 of co-culture, the area of cell colonies in the L1CAM-shRNA/DRG group was significantly less than that in L1CAM-NC/DRG group (P<0. 01); however, there was no difference in neurite outgrowth between the two groups. Conclusion It is demonstrated that down-regulation of L1CAM can suppress the perineural invasion of Capan-2 cells in vitrr by inhibiting cell proliferation and migration.
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Objective To evaluate the effect of L1 cell adhesion molecule (L1CAM) gene expression silencing by short hairpin RNA (shRNA) on perineural invasion of pancreatic cancer Capan-2 cells in vitrr. Methods We transfected Capan-2 cellswith lentivirus-mediated shRNA targeting L1CAM (L1CAM-shRNA) and negative control shRNA (L1 CAM-NC), and then the transfected Capan-2 cells were co-culturedwith mouse dorsal root ganglia (DRG) in matrigel matrix. The procession of neurite outgrowth and cell colony growth were observed by inverted microscope. Areas of cell colonies and neurites were quantitated using Image pro plus software. Results The cancer cells migrated to DRG and grew around the neurites in the L1CAM-NC/DRG group, which was not observed in the L1CAM-shRNA/DRG group. On day 3 and 5 of co-culture, the area of cell colonies in the L1CAM-shRNA/DRG group was significantly less than that in L1CAM-NC/DRG group (P<0. 01); however, there was no difference in neurite outgrowth between the two groups. Conclusion It is demonstrated that down-regulation of L1CAM can suppress the perineural invasion of Capan-2 cells in vitrr by inhibiting cell proliferation and migration.