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Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder involved with genetic mutations. The individual's aberrant social communication and interaction and restricted repetitive behaviours are the manifestations. ASD can be diagnosed as young as age 2. ASD is classified as high functioning and low functioning disorders based on intelligence. Factors that influence ASD include "Theory of Mind" (ToM) and social Interaction, in which individuals with ASD have severe difficulty in understanding the thoughts of others, such as their emotions, feelings, beliefs, and opinions. This review is a retrospective study on social interaction impairment in ASD and the relevant interventions. This paper aims to evaluate social communication barriers and their impacts on school functioning, as well as the atypical social attention development during the early stage of ASD. The interventions are mainly divided into parent-child companionship, music therapy, video therapy, and active physical activity. There are still limitations in this review. Most of the methods quoted in the literature adopted cross-sectional designs, and the experimental techniques are relatively narrow. In addition, most intervention programs focused on the early developmental stage. More attention should be paid to the transition between developmental stages in the future. This review can provide some guidance to future intervention research and practice in the special education area for ASD.

Cancer‐associated fibroblasts (CAF) are the most abundant stromal cells in tumor and exert a pro‐tumoral effect in cancer progression. Numerous evidence shows long non‐coding RNA (lncRNA) abnormally regulates gene expression in various cancers. However, little is known about the role of lncRNA in the interaction between CAF and cancer cells. Here, we first identify an uncharacterized lncRNA, LOC100506114, which is significantly upregulated in CAF and is involved in the functional transformation of normal fibroblasts (NF) and CAF. Expression of LOC100506114 enhances the expression of fibroblast activation protein alpha and α‐smooth muscle actin in NF and promotes malignant characteristics of NF and CAF in vivo and in vitro. The profile of gene co‐expression analysis shows that growth differentiation factor 10 (GDF10) is positively correlated with the expression of LOC100506114. CAF promote stromal fibroblast activation and the proliferation and migration of tumor cells by secreting GDF10. Our data demonstrate that lncRNA plays a critical role in the interplay of stromal fibroblasts and tumor cells in oral squamous cell carcinoma., Abnormal expression of lncRNA LOC100506114 in oral squamous cell carcinoma (OSCC) induced normal fibroblasts (NF) to transform into CAF by upregulating growth differentiation factor 10 (GDF10) expression and secretion. The interaction of GDF10 with the transcription factor RUNX family transcription factor 2 further enhanced the growth and migration of OSCC tumor cells by activating the TGFβRI/Smad3/ERK pathway. Our results demonstrate that lncRNA play an important role in the functional transformation of human NF into CAF and promote OSCC tumorigenesis.

LS-007, an inhibitor of cyclin-dependent kinase 9 (CDK9), exhibits potential antitumor activity against chronic lymphocytic leukemia and ovarian cancer, but its effect on melanoma and tumor microenvironment (TME) has not been reported yet. This study aimed to investigate the role of LS-007 in B16F10 melanoma and relevant mechanisms. LS-007 significantly inhibited viability and induced apoptosis of B16F10 cells in a dose-dependent manner, which were accompanied with the increased ratio of Bax to Bcl-2 and decreased Mcl-1 mRNA level. Western blot analysis showed that LS-007 increased the expression of cleaved caspase-3 and poly ADP-ribose polymerase (PARP). Furthermore, flow cytometry analysis and qRT-PCR results showed that LS-007 treatment resulted in cell cycle arrest by changing cell cycle-related gene expression. Notably, in vivo evaluation showed that LS-007 significantly decreased the weight and volume of tumor and the expression of Ki67, promoted the expression of iNOS and inhibited the expression of CD206, suggesting that LS-007 might inhibit tumor growth by suppressing polarization of macrophages into tumor-associated macrophages (TAMs) in the TME. The increase in M1/M2 treated with LS-007 detected by flow cytometry hinted that macrophages were polarized towards an antitumor phenotype. In addition, LS-007 induced higher apoptotic rate of B16F10 cells when co-cultured B16F10 with BMDMs. LS-007 has inhibitory effects on B16F10 cells in vivo and in vitro via inducing apoptosis, cell cycle arrest, and changing macrophage function in the TME.

Xinghan Liu,1 Yujun Xu,1 Lijie Yin,1 Yayi Hou,1,2 Shuli Zhao3 1The State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing, 210093, People’s Republic of China; 2Jiangsu Key Laboratory of Molecular Medicine, Nanjing University, Nanjing, 210093, People’s Republic of China; 3General Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, People’s Republic of ChinaCorrespondence: Yayi HouThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing, 210093, People’s Republic of China, Tel/Fax +86-25-8968-8441Email yayihou@nju.edu.cnShuli ZhaoGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, People’s Republic of China, Tel/Fax +86-25-8968-8441Email shulizhao79@163.comPurpose: Since immune cells in the tumor microenvironment (TME) can affect the development and progression of tumors, strategies modulating immune cells are considered to have an important therapeutic effect. As a TLR7/8 agonist, R848 effectively activates the innate immune cells to exert an anti-tumor effect. Mn2+ has been reported to strongly promote the maturation of antigen-presenting cells (APCs), thereby enhancing the cytotoxicity of CD8+ T cells. Thus, we tried to investigate whether chitosan-poly(acrylic acid) nanoparticles (CS-PAA NPs) loaded with R848 and MnCl2 (R-M@CS-PAA NPs) could exert an anti-tumor effect by regulating the function of immune cells.Methods: R-M@CS-PAA NPs were prepared, and their basic characteristics, anti-tumor effect, and potential mechanisms were explored both in vitro and in vivo.Results: R-M@CS-PAA NPs easily released MnCl2 and R848 at low pH. In B16F10 mouse melanoma model, R-M@CS-PAA NPs exerted the most significant anti-melanoma effect compared with the control group and CS-PAA NPs loaded with R848 or MnCl2 alone. FITC-labeled R-M@CS-PAA NPs were displayed to be accumulated at the tumor site. R-M@CS-PAA NPs significantly increased the infiltration of M1 macrophages and CD8+ T cells but reduced the number of suppressive immune cells in the TME. Moreover, in vitro experiments showed that R-M@CS-PAA NPs polarized macrophages into the M1 phenotype to inhibit the proliferation of B16F10 cells. R-M@CS-PAA NPs also enhanced the killing function of CD8+ T cells to B16F10 cells. Of note, R-M@CS-PAA NPs not only promoted the maturation of APCs such as dendritic cells and macrophages by STING and NF-кB pathways, but also enhanced the ability of dendritic cells to present ovalbumin to OT-I CD8+ T cells to enhance the cytotoxicity of OT-I CD8+ T cells to ovalbumin-expressing B16F10 cells.Conclusion: These data indicate that the administration of R-M@CS-PAA NPs is an effective therapeutic strategy against melanoma.Keywords: T cell, STING, NF-кB, antigen-presenting cell

Background: Regulating the polarization of macrophages to antitumor M1 macrophages is a promising strategy for overcoming the immunosuppression of the tumor microenvironment for cancer therapy. Ferumoxytol (FMT) can not only serve as a drug deliver agent but also exerts anti-tumor activity. β-glucan has immuno-modulating properties to prevent tumor growth. Thus, a nanocomposite of FMT surface-coated with β-glucan (FMT-β-glucan) was prepared to explore its effect on tumor suppression. Methods: Male B16F10 melanoma mouse model was established to explore the antitumor effect of FMT-β-glucan. The viability and apoptotic rates of B16F10 cells were detected by cell counting kit-8 and Annexin-V/PI experiments. The levels of M1 markers were quantified by quantitative reverse transcription-polymerase chain reaction and enzyme linked immunosorbent assay. Phagocytic activity and intracellular reactive oxygen species (ROS) in macrophages were evaluated by the neutral red uptake assay and flow cytometry, respectively. Small interfering RNA (siRNA) transfection was applied to knock down the Dectin-1 gene in RAW 264.7 cells. Results: FMT-β-glucan suppressed tumor growth to a greater extent and induced higher infiltration of M1 macrophages than the combination of FMT and β-glucan (FMT+β-glucan) in vivo. In vitro, supernatant from FMT-β-glucan-treated RAW 264.7 cells led to lower cell viability and induced more apoptosis of B16F10 cells than that from the FMT+β-glucan group. Moreover, FMT-β-glucan boosted the expression of M1 type markers, and increased phagocytic activity and ROS in RAW 264.7 cells. Further research indicated that FMT-β-glucan treatment promoted the level of Dectin-1 on the surface of RAW 264.7 cells and that knockdown of Dectin-1 abrogated the phosphorylation levels of several components in MAPK and NF-κB signaling. Conclusion: The nanocomposite FMT-β-glucan suppressed melanoma growth by inducing the M1 macrophage-activated tumor microenvironment.

Background Skin wounds in diabetic patients hardly recover. Accumulating evidence has shown that mammalian target of rapamycin (mTOR) pathway and myeloid-derived suppressor cells (MDSCs) are involved in inflammatory-related response. INK128 is a novel mTOR kinase inhibitor in clinical development. However, the exact roles of MDSCs and INK128 in healing wound of diabetic patients are unclear. Methods Mice models of normal, diabetic, and diabetic+INK128 were constructed. Bone marrow (BM)-derived macrophages and RAW264.7 cell line co-cultured with MDSCs, which were induced at different conditions. Flow cytometry, western blot, quantitative real-time PCR, and immunohistochemical analysis were performed. Results Diabetic mice (DM) had a slower recovery rate, thinner epidermis and dermis, and less blood vessels than those of normal mice. MDSCs were abnormally accumulated in DM, mTOR was activated in MDSCs of DM, and the cells were treated with high glucose. Moreover, mTOR signaling inhibitor INK128 could promote wound healing through reducing the MDSCs. MDSC function was disordered in DM and high-glucose environments, while INK128 could help retrieve their function. Furthermore, high glucose and other factors in DM could promote M-MDSC differentiation to M1 pro-inflammatory macrophage cells, thus inhibiting wound healing. The differentiation, which was dependent on mTOR signaling, could be reversed by INK128. Conclusion INK128 is potential to be developed as a clinical strategy to promote wound healing of diabetic patients.

Sepsis is a common serious clinical infectious disease accompanied by more severe injuries and higher mortality rates in men than women. The much higher level of 17β-estradiol (E2) in female is one of the significant reasons for better sepsis resistance ability. Trained immunity is a novel way to fight against infection by improving innate immunity. However, whether β-glucan-induced trained immunity can promote macrophage phagocytosis to clear infections in early sepsis has not been clarified. And whether E2 involved in this process needs further investigation. Symptoms among male, female and ovariectomized (OVX) C57BL/6 mice in early sepsis were detected. The effect of trained immunity on macrophage LC3B-associated phagocytosis (LAP) and the mechanism of E2 functioned in this process have also been explored. We demonstrated compared with male mice, female has significantly more mild symptoms and more reactive oxygen species (ROS) production and stronger NADPH oxidase 2 (NOX2) expression in the macrophage of major organs. In contrary, these characteristics are disappeared in OVX mice. Furthermore, in macrophage cell lines and primary bone marrow- derived macrophages (BMDMs), β-glucan-induced trained immunity can increase ROS production by activating NOX2 to promote macrophage LAP. E2 can up-regulate RUBICON through estrogen receptor α (ERα) to further facilitate macrophage LAP. These results indicated that trained immunity can improve sepsis resistance ability by stimulating macrophage LAP. E2 can boost ROS production and RUBICON expression to further promote macrophage LAP, which can provide a new perspective to recognize the mechanism of trained immunity in gender differences when responding to sepsis.

As absolute poverty in China, measured by the current standard, is being eliminated, the focus of future poverty reduction projects will necessarily shift to addressing relative poverty. Contiguous poverty areas have been identified in Hebei province around Beijing and Tianjin (HABT), and this is not conducive to the coordinated development of the Beijing-Tianjin-Hebei region. The dynamic identification of relative poverty at the county level within the region must be the basis for formulating scientific strategies for poverty reduction. Night light (NTL) data can reveal socio-economic information and reflect human activities, and has a wide range of other applications for evaluating and identifying poverty. For this reason, NPP/VIIRS (Visible Infrared Imaging Radiometer Suite equipped on the Suomi National Polar orbiting Partnership satellite) NTL data from 2012 to 2020 were corrected, and NTL data for HABT were obtained. A multidimensional relative poverty index (MRPI) that assesses being “free from worries over food and clothing and having access to compulsory education, basic medical services, and safe housing” using social statistical data was created with the analytic hierarchy process and entropy weight method. A panel regression model with fixed effects was established for MRPI and corrected NPP/VIIRS NTL data. The R2 of fitting was 0.6578 and confirmed a strong correlation between MRPI and corrected NPP/VIIRS NTL data. Based on this, the MRPI estimation model was constructed based on the MRPI and corrected NPP/VIIRS NTL data, and passed the accuracy test. Finally, using the national list of poverty counties, it was verified that, at the county scale, the corrected NPP/VIIRS NTL data could effectively identify areas of relative poverty. This study lays the foundation for the use of NPP/VIIRS NTL data in the identification of areas of relative poverty. It provides a feasible method and data reference for analyzing relative poverty at a smaller scale. The dynamic identification of areas of relative poverty can also provide a basis for formulating scientific poverty reduction strategies.

The interface/interphase is modeled by distributed springs, and the degree of interface damage is characterized by the flexibility coefficient of the springs. Considering different degrees of damage at different interfaces, a general dispersion equation by the transfer matrix method was obtained. For the purpose of application, the transmission coefficient of finite-period phononic crystals is also derived. Additionally, the band structures and the transmission coefficients are calculated for different degrees of damage to confirm the interface effect on band gaps. A numerical simulation of the transmission coefficient is performed using the commercial FEM software Comsol Multiphysics. The numerical results obtained agree well with the analytical solution. Finally, based on a monotonic decreasing relationship between the degree of interface damage and the central frequency of band gaps and a monotonic relationship between the degree of interface damage and the amplitude of transmission coefficients, a new method how to evaluate the degree of interface damage theoretically is proposed.

Background Sepsis is a life-threatening condition caused by dysregulated host responses to infection. Macrophages, which recognize microbial infections through identification of bacterial markers such as lipopolysaccharide (LPS), are crucial to the pathogenesis of sepsis-associated liver injury. However, the understanding of the SPIONs-mediated modulation of macrophage responses in LPS-induced sepsis and liver injury is limited. Materials and methods Superparamagnetic iron oxide nanoparticles (SPIONs) of γ-Fe2O3 nanoparticles were prepared, and their morphology and magnetic properties were characterized. Results Using a murine model of LPS-induced sepsis and liver injury, we found that SPIONs alleviated LPS-induced sepsis, preventing infiltration of inflammatory cells into the liver. SPIONs also increased the level of interleukin-10 (IL-10) in liver macrophages, while SPIONs's effect on LPS-induced sepsis was abrogated in IL-10-/- mice, indicating that the protective effect of SPIONs is dependent on IL-10+ macrophages. Moreover, SPIONs activated macrophage autophagy to increase IL-10 production, which was markedly attenuated by autophagy inhibition. Furthermore, SPIONs upregulated the expression of Caveolin-1 (Cav1) in macrophages, which plays a role in cellular uptake of metallic nanoparticles. Interestingly, activation of Cav1 and Notch1/HES1 signaling was involved in SPIONs-induced autophagy in both RAW 264.7 cells and bone marrow-derived macrophages (BMDMs). Our data reveal a novel mechanism for SPIONs -induced autophagy in macrophages, which occurs through activation of the Cav1-Notch1/HES1 signaling pathway, which promotes the production of IL-10 in macrophages, leading to inhibition of inflammation in LPS-induced sepsis and liver injury. Conclusion Our results suggest that SPIONs may represent a potential therapeutic agent for the treatment of sepsis and sepsis-induced liver injury.

Background: Skin wounds in diabetic patients are hardly to recover. Accumulating evidence has shown that mammalian target of rapamycin (mTOR) pathway and myeloid-derived suppressor cells (MDSCs) are involved in inflammation-related response. INK128 is a novel mTOR kinase inhibitor in clinical development. However, the exact roles of MDSCs and INK128 in healing wound of diabetic patients are unclear.Methods: Mice models of normal, diabetic, and diabetic+INK128 were constructed. Bone marrow (BM)-derived macrophages and RAW264.7 cell line co-cultured with MDSCs, which were induced at different conditions. Flow cytometry, western blot, quantitative real-time PCR, and immunohistochemical analysis were performed.Results: Diabetic mice (DM) had a slower recovery rate, thinner epidermal and dermal, and less blood vessels than those of normal mice. MDSCs were abnormally accumulated in DM and mTOR was activated in MDSCs from DM or treated with high glucose. Moreover, mTOR signaling inhibitor INK128 could promoted wound healing through reducing the MDSCs. MDSCs function was disordered in DM and high glucose environments, while INK128 could help retrieve their function. Furthermore, high glucose and other factors in DM could promote M-MDSCs differentiation to M1 pro-inflammatory macrophage cells, thus inhibiting wound healing. The differentiation, which was dependent on mTOR signaling, could be reversed by INK128.Conclusion: INK128 is potential to be developed as a clinical strategy to promote wound healing of diabetic patients.

Purpose: Single nucleotide variations in the liver fatty acid binding protein (L-FABP, FABP1) gene lead to changes in cellular signaling pathways and lipid metabolism. FABP1 polymorphisms were associated with some liver diseases, like steatotic hepatocellular carcinoma. However, the association between FABP1 rs1545224 and rs2241883 polymorphisms and hepatitis B virus-related liver cirrhosis (LC) and hepatocellular carcinoma (HCC) has not been reported. We performed this study to explore their relationship. Methods: One thousand individuals (250 healthy controls, 250 chronic HBV (CHB), 250 LC, and 250 HCC patients) were recruited. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were applied to assess the difference in allele and genotype frequencies. Cochran-Armitage trend test was used to evaluate the cumulative effect. Significant difference would be defined when the P value was less than 0.05. Results: The distribution of rs1545224 GG, AG and AA genotypes in healthy controls or CHB carriers was not significant when compared to LC or HCC patients (P>0.05). LC patients carrying at least one A allele are more likely to develop HCC in contrast with those with G allele (P0.05). Conclusions: Taken together, FABP1 rs1545224 polymorphism might increase HCC risk in LC patients, indicating that FABP1 rs1545224 polymorphism may be related to the process of developing HCC in Chinese patients with LC.

Cong Dai,1,* Meng Wang,1,* Jun Lu,2,* Zhiming Dai,3 Shuai Lin,1 Pengtao Yang,1 Tian Tian,1 Xinghan Liu,1 Weili Min,1 Zhijun Dai1 1Department of Oncology, The Second Affiliated Hospital of Xi’an Jiaotong University, 2Clinical Research Center, The First Affiliated Hospital of Xi’an Jiaotong University, 3Department of Anesthesia, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, People’s Republic of China *These authors contributed equally to this workBackground: PD-L1 has been reported to be expressed in diverse human malignancies. However, the prognostic value of PD-L1 in digestive system cancers remains inconclusive. Therefore, we conducted this meta-analysis to evaluate the prognostic impact of PD-L1 expression in digestive system cancers.Materials and methods: We searched the PubMed, Embase, and the Chinese National Knowledge Infrastructure for publications concerning PD-L1 expression in digestive system cancers. Correlations of PD-L1 expression level with overall survival (OS), disease-free survival (DFS), and recurrence-free survival (RFS) were analyzed.Results: Finally, 32 studies with 7,308 patients were included. Our results show that PD-L1 expression was significantly associated with poorer OS (hazard ratio [HR] =1.44, 95% confidence interval [CI] =1.18–1.76, P

// Zhi-Jun Dai 1, * , Xing-Han Liu 1, * , Meng Wang 1, * , Yan Guo 2 , Wenge Zhu 3 , Xiao Li 4 , Shuai Lin 1 , Tian Tian 1 , Kang Liu 1 , Yi Zheng 1 , Peng Xu 1 , Tianbo Jin 5 and Xiaopeng Li 6 1 Department of Oncology, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, China 2 School of Life Science and Technology, Xi’an Jiaotong University, Xi’an, China 3 Department of Biochemistry and Molecular Medicine, The George Washington University Medical School, Washington, DC, USA 4 Department of Hepatobiliary Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, China 5 National Engineering Research Center for Miniaturized Detection Systems, School of Life Sciences, Northwest University, Xi’an, China 6 Department of Ultrasound, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, China * These authors contributed equally to this work Correspondence to: Xiaopeng Li, email: xiaopengli8@126.com Zhi-Jun Dai, email: dzj0911@126.com Keywords: IL-18, HBV, susceptibility Received: February 24, 2017 Accepted: June 04, 2017 Published: June 17, 2017 ABSTRACT IL-18 polymorphisms influence the transcriptional activity of the IL-18 gene and associated with various diseases. However, their relationships with hepatitis B virus-related liver diseases had not reached a consensus. So we conducted this case-control study with a view to clarifying the association. We included four groups: healthy controls, chronic hepatitis B virus (CHB) carriers, liver cirrhosis (LC) and hepatocellular carcinoma (HCC) groups with each group of 250 persons. Odd ratios (ORs) and 95% confidence intervals (95%CIs) with or without adjustment were calculated. Haplotype analysis was also performed. The results showed people carrying rs187238 CG genotype had a lower risk of LC (CG vs. CC: OR = 0.59, 95%CI = 0.38–0.91, P = 0.02), while GG genotype carriers had a higher risk of HCC (GG vs. CC+CG: OR = 4.73, 95%CI = 1.01–22.1, P = 0.03) than those with CC and CG genotypes in healthy group. Rs187238 GG genotype increased the risk from CHB to LC status (GG vs. CC: OR = 4.81, 95%CI = 1.03–22.6; GG vs. CC+CG: OR = 4.73, 95%CI = 1.01–22.1), meanwhile the trend also existed by controlling confounding factors (GG vs. CC: OR = 6.25, 95%CI = 1.09–35.8; GG vs. CC+CG: OR = 5.91, 95%CI = 1.04–33.7). Haplotype Crs187238Trs1946518 moderately decreased the risk of CHB carriers developing into HCC (OR = 0.69, 95%CI = 0.50–0.96, P = 0.03) after adjustment. In conclusion, IL-18 rs187238 GG genotype may increase the risk of HCC in healthy population and the risk of LC in CHB carriers.

// Zhe Dou 1, * , Shuai Lin 1, * , Cong Dai 1, * , Ye Lu 2 , Tian Tian 1 , Meng Wang 1 , Xinghan Liu 1 , Yi Zheng 1 , Peng Xu 1 , Shanli Li 1 , Qianwen Sheng 1 , Yujiao Deng 1 and Zhijun Dai 1 1 Department of Oncology, Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710004, China 2 Department of Student Affairs, Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710004, China * ZD, SL and CD have contributed equally to this work Correspondence to: Zhijun Dai, email: dzj0911@126.com , dzj0911@ xjtu.edu.cn Keywords: miRNA-100, diagnosis, prognosis, meta-analysis Received: December 14, 2016 Accepted: May 15, 2017 Published: June 27, 2017 ABSTRACT Many studies manifested miRNA-100 was deregulated in various cancers, which indicated that miRNA-100 might be a potential biomarker of cancer diagnosis and prognosis. However, the role of miRNA-100 was still uncertain. We searched for qualified studies using PubMed, EMBASE, Web of Science, Cochrane library and CNKI databases. The diagnostic effect was evaluated by the pooled sensitivity, specificity, and other indexes. Pooled hazard ratios (HRs) with 95% confidence intervals (CIs) for overall survival (OS) were calculated to assess the prognostic value. This meta-analysis included 7 and 19 studies about diagnosis and prognosis, respectively. The results of pooled sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR) and diagnostic odds ratio (DOR) were 0.75 (95%CI: 0.71-0.78), 0.74 (95%CI: 0.69-0.78), 2.61 (95%CI: 1.81-3.76), 0.33 (95%CI: 0.24-0.45), 8.46 (95%CI: 4.85-14.77), respectively. And, the area under SROC curve (AUC) was 0.8141. We also found that lower expression of miRNA-100 in cancer tissues could significantly predict poorer prognosis in overall cancer (HR = 0.59, 95%CI: 0.39-0.90), especially in genital system tumors (HR = 0.42, 95%CI: 0.27-0.66, P = 0.431), bladder cancer (HR = 0.21, 95%CI: 0.06-0.73, P = 0.143) and esophageal squamous cell carcinoma (HR = 0.26, 95%CI: 0.13-0.52, P = 0.164). Our studies concluded that miRNA-100 has a certain value in diagnosis and it may indicate a poor prognosis of cancers.