Balanced influence maximization in social networks based on deep reinforcement learning.

Balanced influence maximization aims to balance the influence maximization of multiple different entities in social networks and avoid the emergence of filter bubbles and echo chambers. Recently, an increasing number of studies have drawn attention to the study of balanced influence maximization in social networks and achieves success to some extent. However, most of them still have two major shortcomings. First, the previous works mainly focus on spreading the influence of multiple target entities to more users, ignoring the potential influence of the correlation between the target entities and other entities on information propagation in real social networks. Second, the existing methods require a large amount of diffusion sampling for influence estimation, making it difficult to apply to large social networks. To this end, we propose a Balanced Influence Maximization framework based on Deep Reinforcement Learning named BIM-DRL, which consists of two core components: an entity correlation evaluation module and a balanced seed node selection module. Specifically, in the entity correlation evaluation module, an entity correlation evaluation model based on the users' historical behavior sequences is proposed, which can accurately evaluate the impact of entity correlation on information propagation. In the balanced seed node selection module, a balanced influence maximization model based on deep reinforcement learning is designed to train the parameters in the objective function, and then a set of seed nodes that maximize the balanced influence is found. Extensive experiments on six real-life network datasets demonstrate the superiority of the BIM-DRL over state-of-the-art methods on the metrics of balanced influence spread and balanced propagation accuracy.

HOPX Is an Epigenetically Inactivated Tumor Suppressor and Overexpression of HOPX Induce Apoptosis and Cell Cycle Arrest in Breast Cancer.

BACKGROUND: Evidence has been shown that abnormal DNA methylation plays a vital role in the progression of breast cancer via silencing of gene expression. The results of bisulfite sequencing showed that the methylation status of HOPX in breast cancer tissues was higher than that in normal breast cancer tissues, but little known about the biological functions of HOPX in breast cancer. METHODS: A total of 13 paired breast cancer and adjacent noncancerous tissues were subjected to bisulfite sequencing. Meanwhile, the methylation levels of cg218995965 and cg24862548 in breast cancer cells were detected by methylation-specific PCR (MSP). Flow cytometry, wound healing and transwell invasion assays were used to detect the apoptosis, migration and invasion in breast cancer cells. In addition, the expressions of HOPX, p21, cyclin D1 and CDK4 in cells were detected with Western blot assay. RESULTS: Bisulfite sequencing indicated that the CpG sites (cg218995965 and cg24862548) in the HOPX promoter region showed significantly higher methylation in breast cancer tissues. In addition, methylation-specific PCR revealed that HOPX was significantly hypermethylated in breast cancer cell lines MDA-MB-468 and MCF-7. Furthermore, overexpression of HOPX significantly inhibited the proliferation of MDA-MB-468 and MCF-7 cells via inducing the apoptosis. Moreover, upregulation of HOPX markedly inhibited the migration and invasion abilities of MDA-MB-468 cells. Meanwhile, overexpression of HOPX obviously induced cell cycle arrest in MDA-MB-468 cells via upregulation of p21, and downregulation of cyclin D1 and CDK4. Additionally, overexpression of HOPX suppressed tumor growth of breast cancer in vivo. CONCLUSION: Our data showed that HOPX, a tumor suppressor, is epigenetically silenced in breast cancer. Overexpression of HOPX could suppress the progression of breast cancer, and thus indicating that it might serve as a potential target for the treatment of patients with breast cancer.

Hodgkin's lymphoma with marked granulomatous reaction: a diagnostic pitfall.

Hodgkin's lymphoma (HL) is a lymphoid malignant tumor characterized by the presence of Hodgkin and Reed-Sternberg (HRS) cells, the variants of which are reported to be involved in the inflammatory reaction. Epithelioid histiocytes, representing granuloma formation, often occur in the environment as single cells or clustered in nodules. This study was performed to report a case of HL in a cervical lymph node, accompanied by a notable granulomatous reaction. A granulomatous reaction might mask the presence of lymphomas, which is easily misdiagnosed as lymph node tuberculosis and other granulomatous lesions. This present case report may provide new insight for avoiding misdiagnosis of such lesions.

MiR-25-3p attenuates the proliferation of tongue squamous cell carcinoma cell line Tca8113.

OBJECTIVE: To investigate the effects of miR-25-3p on the occurrence, development and proliferation of tongue squamous cell carcinoma cells. METHODS: To establish tongue squamous cell carcinoma cell line Tca8113 that stably and highly express miR-25-3p using recombinant retroviral vector-mediated gene transfer method. The proliferation of transfected Tca8113 was detected by thiazolyl blue tetrazolium bromide (MTT) and cell colony formation assays. cyclinD1, p21(cip1) and p27(kip1) mRNA expressions in the transfected Tca-8113 were detected by quantitative PCR. cyclinD1, p21, p27(kip1), AKT, p-AKT, FOXO1 and p-FOXO1 expressions in the transfected Tca8113 were detected by western blot analysis. In addition, miR-25-3p expression in the tongue squamous cell carcinoma cell line and tissue specimen was also detected by quantitative PCR. RESULTS: Quantitative PCR showed that miR-25-3p expression in the tongue squamous cell carcinoma cell lines and tissue specimen was significantly lower than that in the adjacent tissue. MTT and cell colony formation assays showed that after miR-25-3p overexpression, the proliferation of transfected Tca8113 was obviously attenuated. Western blot analysis and quantitative PCR showed that after miR-25-3p overexpression, p21(cip1) and p27(kip1) expressions were upregulated, while cyclinD1, AKT, FOXO1 expressions were downregulated, and AKT and FOXO1 phosphorylation was inactivated in the transfected Tca8113 cells. CONCLUSIONS: MiR-25-3p inhibited the proliferation of tongue squamous cell carcinoma cells and regulated cell cycle-related protein expression, playing an important role in the occurrence and development of squamous cell carcinoma of the tongue.