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Objective: The aim of this study was to assess the efficacy and safety of intrapleural perfusion with hyperthermic chemotherapy (IPHC) in treating malignant pleural effusion (MPE) compared to normothermic chemoperfusion of the pleural cavity (NCPC), and to investigate the better treatment to control MPE. Methods: Malignant pleural effusion patients were enrolled in the study and treated with NCPC or IPHC under video‐assisted thoracoscopic surgery (VATS). The chest drainage duration, clinical characteristics, and recurrence time of pleural effusion of patients were collected for statistical analysis. The chi‐squared test and the Fisher's exact test were applied to compare the distribution differences in categorical variables. Progression‐free survival (PFS) was estimated by the Kaplan–Meier method and was compared by the log‐rank test. The survival analysis was performed using the Cox proportional hazards method. Results: A total of 37 MPE patients were enrolled in this study. Twenty‐seven patients received NCPC and 10 patients received IPHC under VATS. Significant differences were found in pathological types (p = 0.011), chest drainage duration (p = 0.005), and remission rate (p = 0.009) between two different treatment groups. The chest drainage duration of IPHC under VATS was shorter than the NCPC group (t = 2.969, p = 0.005). The remission rate of MPE in IPHC group was better than the NCPC one (OR = 0.031, 95% CI: 0.002–0.507, p = 0.015). The result of the Kaplan–Meier method showed that IPHC group could significantly prolong the PFS of patients with MPE compared to NCPC group (log‐rank p = 0.002). Univariate cox regression analysis showed that patients with MPE in the IPHC group presented significant longer PFS than the NCPC group (HR = 0.264, 95% CI: 0.098–0.713, p = 0.009). Multivariate cox regression analysis further verified this conclusion (HR = 0.268, 95% CI: 0.096–0.753, p = 0.012). Conclusion: Compared to the NCPC, the IPHC under VATS presents a better control effect on MPE, shorter tube placement time, and longer complete remission time. For this reason, we recommend IPHC under VATS as the first‐line treatment for patients with MPE those who can tolerate minimally invasive surgery. [ABSTRACT FROM AUTHOR]

Objective: Neuroblastoma (NBL) is an extra‐cranial solid tumor in children. This study was attempted to investigate the regulatory mechanism of long noncoding RNA LINC01410 (LINC01410) on NBL. Methods: The expression of LINC01410, miR‐506‐3p, and WEE1 in NBL was evaluated by quantitative real time polymerase chain reaction. The proliferation and colony formation ability of NBL cells were analyzed by MTT and colony formation assay. Flow cytometry assay was executed to measure the apoptosis and cell cycle. Dual‐luciferase reporter assay was used to detect the targeted relationships among LINC01410, miR‐506‐3p, and WEE1. Additionally, the role of LINC01410 on NBL in vivo was evaluated according to a tumor xenograft model. Results: The expression of LINC01410 and WEE1 was enhanced and miR‐506‐3p was inhibited in NBL. LINC01410 knockdown attenuated the cell proliferation, colony formation ability, and inhibited tumor growth. Moreover, LINC01410 silencing facilitated the apoptosis and arrested the cell cycle. LINC01410 interacted with miR‐506‐3p to elevate the WEE1 expression in NBL. Additionally, miR‐506‐3p inhibition or WEE1 overexpression weakened the reduction effects of sh‐LINC01410 on cell proliferation, colony formation ability, apoptosis, and cell cycle. Conclusions: Knockdown of LINC01410 inhibited the development of NBL by miR‐506‐3p/WEE1 axis in vitro, which could serve as a potential therapeutic target for NBL therapy. [ABSTRACT FROM AUTHOR]

Homeobox A10 (HOXA10) has been implicated critical for the promotion of carcinogenesis, but the underlying mechanism between HOXA10 and malignant gastric cancer (GC) phenotype remains elusive. In the present study, we analyzed and validated that HOXA10 and BCL2 expressions were elevated both at the mRNA and protein levels in GC tissues. Upregulated HOXA10 promoted GC cell proliferation with reduced apoptosis in vitro and accelerated GC tumor growth in vivo. Bioinformatics analysis and quantitative real‐time polymerase chain reaction (qRT‐PCR) experiment inferred that HOXA10 might upregulate the expression of BCL2. By performing western blot, chromatin immunoprecipitation and quantitative PCR (ChIP‐qPCR), and rescue experiment, we found that HOXA10 might bind to BCL2 promoter region, induce its expression, and thus inhibit intrinsic apoptosis pathway. Moreover, higher expression of HOXA10 and BCL2 predicted poor overall survival (OS) in GC patients. In summary, our study indicated that HOXA10 was upregulated in GC, and that HOXA10 might promote cell proliferation by elevating BCL2 expression and inhibiting apoptosis. [ABSTRACT FROM AUTHOR]