Human cancers, including hepatocellular carcinoma (HCC), are characterized by a high degree of drug resistance in chemotherapy. However, the underlying molecular mechanism remains unknown. To the role of interleukin-6 (IL-6)/signal transducer and activator of transcription 3 (STAT3) signaling pathway in the regulation of macrophage polarization, M1-type and M2-type macrophages were separately induced using lipopolysaccharide and interleukin-4 (IL-4), and we found that the IL-6/STAT3 signaling pathway was inhibited in M1-type macrophages but activated in M2-type macrophages. After anti-IL-6-treated macrophages were separately induced by lipopolysaccharide and IL-4, we found that the inhibition of IL-6/STAT3 signaling pathway turned macrophages into M1-type. Co-culture with M1-type macrophages reduced HCC cell viability, proliferation, invasion, migration, drug resistance, but increased apoptosis. Co-culture with M2-type macrophages yielded reciprocal results. The inhibition of IL-6/STAT3 signaling pathway mediated by anti-IL6 was shown to significantly enhance the effects of M1-type macrophages on HCC cells and rescue HCC cells from co-culture with M2-type macrophages. Tumor xenografts of co-cultured HCC cells were established in nude mice and the results showed that the inhibition of IL-6/STAT3 signaling pathway mediated by anti-IL6 was found to reduce tumor formation of HCC cells co-cultured with M1- or M2-type macrophages and lung metastases. The current study reveals a novel mechanism of IL-6/STAT3 signaling pathway in the regulation of macrophage polarization, thus contributing to HCC metastasis and drug resistance in chemotherapy.

Periodontitis (PD) is a common chronic infectious disease. The local inflammatory response in the host may cause the destruction of supporting periodontal tissue. Macrophages play a variety of roles in PD, including regulatory and phagocytosis. Moreover, under the induction of different factors, macrophages polarize and form different functional phenotypes. Among them, M1-type macrophages with proinflammatory functions and M2-type macrophages with anti-inflammatory functions are the most representative, and both of them can regulate the tendency of the immune system to exert proinflammatory or anti-inflammatory functions. M1 and M2 macrophages are involved in the destructive and reparative stages of PD. Due to the complex microenvironment of PD, the dynamic development of PD, and various local mediators, increasing attention has been given to the study of macrophage polarization in PD. This review summarizes the role of macrophage polarization in the development of PD and its research progress.

Nowadays, developing indoor positioning systems (IPSs) has become an attractive research topic due to the increasing demands on location-based service (LBS) in indoor environments. WiFi technology has been studied and explored to provide indoor positioning service for years in view of the wide deployment and availability of existing WiFi infrastructures in indoor environments. A large body of WiFi-based IPSs adopt fingerprinting approaches for localization. However, these IPSs suffer from two major problems: the intensive costs of manpower and time for offline site survey and the inflexibility to environmental dynamics. In this paper, we propose an indoor localization algorithm based on an online sequential extreme learning machine (OS-ELM) to address the above problems accordingly. The fast learning speed of OS-ELM can reduce the time and manpower costs for the offline site survey. Meanwhile, its online sequential learning ability enables the proposed localization algorithm to adapt in a timely manner to environmental dynamics. Experiments under specific environmental changes, such as variations of occupancy distribution and events of opening or closing of doors, are conducted to evaluate the performance of OS-ELM. The simulation and experimental results show that the proposed localization algorithm can provide higher localization accuracy than traditional approaches, due to its fast adaptation to various environmental dynamics.

Long noncoding RNAs (lncRNAs) have been proven to play critical roles in cancer progression. Recently, lncRNA MAGI2‐AS3 has been revealed to be a tumor suppressor and inhibit cell growth by targeting the Fas/FasL signalling pathway in breast cancer. However, the role and underlying mechanism of MAGI2‐AS3 in hepatocellular carcinoma (HCC) remain largely unknown. In the current study, we found that MAGI2‐AS3 expression is downregulated in HCC tissues and closely associated with some clinical characteristics (tumor size, lymph node metastasis, and TNM stage) and poor overall survival. Overexpression of MAGI2‐AS3 inhibits HCC cell proliferation and migration in vitro, while impedes tumor growth in vivo accordantly. In addition, our data suggest that MAGI2‐AS3 could function as an endogenous sponge of miR‐374b‐5p by directly binding to it and suppressing its expression. Furthermore, miR‐374b‐5p upregulation could restore the inhibitory effect of MAGI2‐AS3 on HCC cells processes. Moreover, suppressor with morphogenetic effect on genitalia family member 1 (SMG1) is positively regulated by MAGI2‐AS3 via absorbing miR‐374b‐5p in HCC cells. More important, SMG1 knockdown reverses the suppressive function of MAGI2‐AS3 in HCC cell processes. Taken together, we reveal a functional MAGI2‐AS3/miR‐374b‐5p/SMG1 axis that suppresses HCC progression, potently suggesting a new road for HCC treatment.