An Essential Role of c-Fos in Notch1-mediated Promotion of Proliferation of KSHV-Infected SH-SY5Y Cells.

BACKGROUND: This study aimed to investigate the influence of Notch1 on c-Fos and the effect of c-Fos on the proliferation of Kaposi's sarcoma-associated herpesvirus (KSHV)-infected neuronal cells. METHODS: Real-time PCR and western blotting were used to determine c-Fos expression levels in KSHV-infected (SK-RG) and uninfected SH-SY5Y cells. C-Fos levels were measured again in SK-RG cells with or without Notch1 knockdown. Next, we measured c-Fos and p-c-Fos concentrations after treatment with the Notch1 γ-secretase inhibitor LY-411575 and the Notch1 activator Jagged-1. MTT and Ki-67 staining were used to evaluate the proliferation ability of cells after c-Fos levels downregulation. CyclinD1, CDK6, and CDK4 expression levels and cell cycle were analyzed by western blotting and flow cytometry, respectively. After the c-Fos intervention, the KSHV copy number and gene expression of RTA, LANA and K8.1 were analyzed by real-time TaqMan PCR. RESULTS: C-Fos was up-regulated in KSHV-infected SK-RG cells. However, the siRNA-mediated knockdown of Notch1 resulted in a significant decrease in the levels of c-Fos and p-c-Fos (P <0.01, P <0.001). Additionally, a decrease in Cyclin D1, CDK6, and CDK4 was also detected. The Notch1 inhibitor LY-411575 showed the potential to down-regulate the levels of c-Fos and p-c-Fos, which was consistent with Notch1 knockdown group (P <0.01), whereas the expression and phosphorylation of c-Fos were remarkably up-regulated by treatment of Notch1 activator Jagged-1 (P <0.05). In addition, our data obtained by MTT and Ki-67 staining revealed that the c-Fos down-regulation led to a significant reduction in cell viability and proliferation of the SK-RG cells (P <0.001). Moreover, FACS analysis showed that the cell cycle was arrested in the G0/G1 stage, and the expressions of Cyclin D1, CDK6, and CDK4 were down-regulated in the c-Fos-knockdown SK-RG cells (P <0.05). Reduction in total KSHV copy number and expressions of viral genes (RTA, LANA and K8.1) were also detected in c-Fos down-regulated SK-RG cells (P <0.05). CONCLUSION: Our findings strongly indicate that c-Fos plays a crucial role in the promotion of cell proliferation through Notch1 signaling in KSHV-infected cells. Furthermore, our results suggest that the inhibition of expression of key viral pathogenic proteins is likely involved in this process.

Comparison of the Laryngeal Mask Airway ProSeal and the Streamlined Liner of the Pharynx Airway During General Anesthesia: A Systematic Review and Meta-analysis.

PURPOSE: The purpose of this article is to compare the safety of the laryngeal mask airway ProSeal (PLMA) and the streamlined liner of the pharynx airway (SLIPA) during general anesthesia. DESIGN: This study is a systematic review and meta-analysis. METHODS: Two authors performed searches of Embase, Web of Science, and PubMed to identify clinical trials that compared PLMA and SLIPA in patients receiving general anesthesia. Relative risk (RR) with corresponding 95% confidence intervals (CI) were used to pool the dichotomous data. The mean difference (MD) and the associated 95% CI were applied to pool continuous data. RevMan 5.0 software was used for data analysis. FINDINGS: A total of 15 studies with 1263 patients were included. There was no significant difference between PLMA and SLIPA in the rate of insertion success on the first attempt (RR = 1.02, 95% CI [0.95, 1.09], P = .59), airway sealing pressure (MD = 0.75, 95% CI [-0.09, 1.58], P = .08) and the incidence of a sore throat (RR = 0.85, 95% CI [0.7, 1.04], P = .12). The insertion time of PLMA was shorter than SLIPA (MD = 5.24, 95% CI [0.51, 9.98], P = .03), and the incidence of bloodstaining on the device was lower (RR = 0.72, 95% CI [0.55, 0.94], P = .02). CONCLUSIONS: Both devices have a high rate of insertion success on the first attempt and airway sealing pressure. But PLMA has a shorter insertion time and less incidence of blood staining, which is more advantageous than SLIPA.

Integrated Network Analysis to Determine CNN1, MYL9, TAGLN, and SORBS1 as Potential Key Genes Associated with Prostate Cancer.

BACKGROUND: Prostate cancer (PCa) is challenging to treat. It is necessary to screen for related biological markers to accurately predict the prognosis and recurrence of prostate cancer. METHODS: Three data sets, GSE28204, GSE30521, and GSE69223, from the Gene Expression Omnibus (GEO) database were integrated into this study. After the identification of differentially expressed genes (DEGs) between PCa and normal prostate tissues, network analyses including protein-protein interaction (PPI) network, and weighted gene co-expression network analysis (WGCNA) were used to select hub genes. Gene Ontology (GO) term analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to annotate the functions of DEGs and hub modules of the networks. Survival analysis was performed to validate the correlation between the key genes and PCa relapse. RESULTS: In total, 867 DEGs were identified, including 201 upregulated and 666 downregulated genes. Three hub modules of the PPI network and one hub module of the weighted gene co-expression network were determined. Moreover, four key genes (CNN1, MYL9, TAGLN, and SORBS1) were significantly associated with PCa relapse (p < 0.05). CONCLUSIONS: CNN1, MYL9, TAGLN, and SORBS1 may be potential biomarkers for PCa development.

Liquid metal integrated PU/CNT fibrous membrane for human health monitoring.

Wearable flexible sensors are widely used in several applications such as physiological monitoring, electronic skin, and telemedicine. Typically, flexible sensors that are made of elastomeric thin-films lack sufficient permeability, which leads to skin inflammation, and more importantly, affects signal detection and consequently, reduces the sensitivity of the sensor. In this study, we designed a flexible nanofibrous membrane with a high air permeability (6.10 mm/s), which could be effectively used to monitor human motion signals and physiological signals. More specifically, a flexible membrane with a point (liquid metal nanoparticles)-line (carbon nanotubes)-plane (liquid metal thin-film) multiscale conductive structure was fabricated by combining liquid metal (LM) and carbon nanotubes (CNTs) with a polyurethane (PU) nanofibrous membrane. Interestingly, the excellent conductivity and fluidity of the liquid metal enhanced the sensitivity and stability of the membrane. More precisely, the gauge factor (GF) values of the membrane is 3.0 at 50% strain and 14.0 at 400% strain, which corresponds to a high strain sensitivity within the whole range of deformation. Additionally, the proposed membrane has good mechanical properties with an elongation at a break of 490% and a tensile strength of 12 MPa. Furthermore, the flexible membrane exhibits good biocompatibility and can efficiently monitor human health signals, thereby indicating potential for application in the field of wearable electronic devices.

M2 tumor-associated macrophage mediates the maintenance of stemness to promote cisplatin resistance by secreting TGF-ß1 in esophageal squamous cell carcinoma.

BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is a deadly gastrointestinal malignancy, and chemotherapy resistance is a key factor leading to its poor prognosis. M2 tumor-associated macrophages (M2-TAMs) may be an important cause of chemoresistance in ESCC, but its exact mechanism is still unclear. METHODS: In order to study the role of M2-TAMs in ESCC chemoresistance, CCK-8, clone formation assay, flow cytometric apoptosis assay, qRT-PCR, western blotting, and serum-free sphere formation assays were used. In vivo animal experiments and human ESCC tissues were used to confirm the findings. RESULTS: In vitro and in vivo animal experiments, M2-TAMs reduced the sensitivity of ESCC cells to cisplatin. Mechanistically, M2-TAMs highly secreted TGF-ß1 which activated the TGFßR1-smad2/3 pathway to promote and maintain the stemness characteristic of ESCC cells, which could inhibit the sensitivity to cisplatin. Using TGFß signaling inhibitor SB431542 or knockdown of TGFßR1 could reverse the cisplatin resistance of ESCC cells. In 92 cases of human ESCC tissues, individuals with a high density of M2-TAMs had considerably higher levels of TGF-ß1. These patients also had worse prognoses and richer stemness markers. CONCLUSION: TGF-ß1 secreted from M2-TAMs promoted and maintained the stemness characteristic to induce cisplatin resistance in ESCC by activating the TGFß1-Smad2/3 pathway.

Arthrostoma leucurus sp. n. (Nematoda: Ancylostomatidae), A New Hookworm Species Isolated from Asian Badger in China.

PURPOSE: To date, ten validated Arthrostoma species were reported. Here, a new hookworm species was found from Asian badger (Meles leucurus). METHODS: Nineteen hookworms (9 males and 10 females) were collected from the small intestine of two Asian badgers in Xinjiang Uygur Autonomous Region, northwestern China. The hookworms were morphologically examined according to key taxonomic characters, such as anterior extremity direction, structures of oral opening (cutting plates or teeth), vulva location, buccal capsule anatomy (integrated or formed by articulating plates), the length of spicule and gubernaculum, number of plates of buccal capsule, and presence or absence of vulvar papillae. RESULTS: The hookworm species from Asian badger, here named as Arthrostoma leucurus sp. n., was different from the previously described ten Arthrostoma species. The phylogenetic tree based on the cox1 gene showed that Arthrostoma leucurus sp. n. formed a separate clade, as a sister group to Ancylostoma and Uncinaria species. CONCLUSION: Arthrostoma leucurus sp. n., the eleven validated Arthrostoma species, was identified from Asian badger in China.

Defective expression of C20orf54 in esophageal dysplasia: a possible biomarker of esophageal carcinoma for early detection.

BACKGROUND: C20orf54 has been identified as an esophageal squamous cell carcinoma (ESCC) susceptibility gene in previous genome-wide association studies. Here, we attempted to clarify the expression level of C20orf54 in ESCC, non-tumoral esophageal tissues, and esophageal squamous intraepithelial neoplasia (ESIN). METHODS: We assessed C20orf54 expression in 146 ESCC, 108 non-tumoral esophageal tissues, and 148 ESIN using immunohistochemistry on tissue microarrays. We also evaluated the possible correlations of C20orf54 expression with clinicopathological characteristics. The survival rates were analyzed using the Kaplan-Meier method and log-rank test. RESULTS: C20orf54 expression was significantly lower in ESCC, high-grade ESIN, and low-grade ESIN than in the non-tumoral esophageal tissues. The level observed for ESCC was also significantly lower than that in low-grade ESIN and high-grade ESIN, whereas no difference was observed between high-grade ESIN and low-grade ESIN. Furthermore, the C20orf54 defective expression correlated significantly with differentiation, lymph node metastasis, and invasion depth. The overall survival time was inversely associated with lymph node metastasis, an advanced TNM stage (III + IV), and deeper invasion. CONCLUSIONS: This study provides the first evidence of C20orf54 defective expression in ESCC and precancerous lesions, demonstrating a potential role in tumor progression and metastasis. C20orf54 could be used as a potential biomarker for the early detection of ESCC.

Effects of the Separator MOF-Al2O3 Coating on Battery Rate Performance and Solid-Electrolyte Interphase Formation.

Metal organic frameworks (MOFs) have unique advantages in optimizing the ionic conductivity of battery separators because of their rich cavity structure and highly ordered and connected pores. In this study, we used a hydrothermal method to synthesize a functional material, Ag-MOF crystal, as a separator coating content, and then studied the properties and application effect of the MOF-Al2O3-blended coating applying to a polyethylene (PE) separator (MOFxAl1-x/PE). Results show that MOF0.08Al0.92/PE (MOF/Al2O3 = 0.08:0.92) used in NCM811||Li cells significantly not only improves the fast charge-discharge performance of the cells but also inhibits the growth of lithium dendrites during long-term charge-discharge cycling; the Li+ transference number (tLi+) of the MOF0.08Al0.92/PE composite separator is 0.61; the Li||separator||Li half-cell circulates stably for 1000 h at varying current density from 0.5 to 10 mA cm-2 and only produces low overpotentials, indicating that MOF0.08Al0.92 stabilizes lithium. The initial capacity of the NCM811||Li cell using the MOF0.08Al0.92/PE separator is 165.0 mA h g-1, its capacity retention is 70.67% after 300 cycles at 5 C, and the interface resistance of the cells only increases from 13.8 to 31.5 Ω, whereas the capacity retention of Al2O3/PE separator batteries is only 40.41% (62.2 mA h g-1) under the same conditions. During the charge-discharge cycling, the MOF-Al2O3 coating induces the lithium anode to quickly form a stable and dense solid-electrolyte interphase layer, promotes the uniform deposition of Li+, and inhibits the growth of lithium dendrites as well.

ETV5-mediated upregulation of lncRNA CTBP1-DT as a ceRNA facilitates HGSOC progression by regulating miR-188-5p/MAP3K3 axis.

High-grade serous ovarian cancer (HGSOC) is a common and lethal cancer of the female reproductive system. Long non-coding RNAs (lncRNAs) are aberrantly expressed in various cancers and play crucial roles in tumour progression. However, their function and molecular mechanism in HGSOC remain largely unknown. Based on public databases and bioinformatics analyses, the overexpression of lncRNA CTBP1-DT in HGSOC tissues was detected and validated in a cohort of HGSOC tissues. High expression of lncRNA CTBP1-DT was associated with poor prognosis and was an independent risk factor for survival. Overexpression of lncRNA CTBP1-DT promoted malignant biological behaviour of HGSOC cells, whereas its depletion induced growth arrest of HGSOC cells by vitro and in vivo assays. Mechanistically, lncRNA CTBP1-DT could competitively bind to miR-188-5p to protect MAP3K3 from degradation. Moreover, our results revealed that ETV5 could specifically interact with the promoter of lncRNA CTBP1-DT and activate its transcription. Collectively, these results reveal a novel ETV5/lncRNA CTBP1-DT/miR-188-5p/MAP3K3 pathway for HGSOC progression and suggest that lncRNA CTBP1-DT might be a potential biomarker and therapeutic target for HGSOC.

Multi-physics coupling simulation of electrode induction melting gas atomization for advanced titanium alloys powder preparation.

A numerical modeling method is proposed for the melting process of Titanium metals of Titanium alloys powder preparation used for 3D printing. The melting process simulation, which involves the tight coupling between electromagnetic field, thermal field and fluid flow as well as deformation associated during the melting process, is conducted by adopting the finite element method. A two-way coupling strategy is used to include the interactions between these fields by incorporating the material properties dependent on temperature and the coupling terms. In addition, heat radiation and phase change are also considered in this paper. The arbitrary Lagrangian-Eulerian formulation is exploited to model the deformation of Titanium metal during the melting process. The distribution of electromagnetic flux density, eddy current density, temperature, and fluid flow velocity at different time can be determined by utilizing this numerical method. In a word, the method proposed in this paper provides a general way to predict the melting process of electrode induction melting gas atomization (EIGA) dynamically, and it also could be used as a reference for the design and optimization of EIGA.

Epigenetically associated CCL20 upregulation correlates with esophageal cancer progression and immune disorder.

Chemokines have distinct effects on tumor progression by affecting cancer immunity and tumorigenesis. However, the characteristic chemokine profiles and their roles in immune cell recruitment and cancer cell biology are not entirely understood in esophageal cancer. Here, we scrutinized chemokine's expression profiles in independent esophageal cancer cohorts and identified the elevated CCL20 as a risk factor to predict patients' prognosis regardless of histology subtypes. Enhanced CCL20 expression was also associated with the acquisition of metastatic potential. Mechanistically, the upregulation of CCL20 in tumor cells was associated with promoter hypomethylation. Furthermore, by analyzing single-cell RNA sequencing data of a mouse model mimicking human ESCC development, we observed an imbalance among CD4+ T subtypes in the tumor microenvironment, namely Ccr6+ Th17 and Treg cells infiltration alongside the elevated Ccl20 expression in abnormal epithelial cells during the tumorigenic process. Together, these results reveal that hypomethylation-induced CCL20 promotes esophageal cancer progression and immune disorder. Targeting CCL20 might be a promising therapeutic approach in esophageal cancer.

Biological and prognostic value of ETV5 in high-grade serous ovarian cancer.

BACKGROUND: ETS transcription factors are known to act as either positive or negative regulators of the expression of genes involved in various biological processes. It was reported that ETS variant transcription factor 5 (ETV5), a key member of the ETS family, mainly plays a role as an potential oncogene in various malignant tumors. However, the role and mechanism of ETV5 in high-grade serous ovarian cancer (HGSOC) have not been elucidated. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) assay was used to detect ETV5 messenger ribonucleic acid (mRNA) expression in 87 HGSOC tissues and 35 normal fallopian tube tissues. Western blotting and qRT-PCR were used to detect the protein and mRNA expression of ETV5 in six ovarian cancer (OC) and human embryonic cell lines. Knockdown or overexpression of ETV5 in HGSOC cell lines, Cell Counting Kit-8, colony formation, and transwell assays were used to detect HGSOC cell proliferation, invasion, and migration capabilities. The chi-square test was used to analyze the clinicopathological characteristics of HGSOC patients. Survival analysis was performed using the Kaplan-Meier method, and the log-rank test was used to analyze the correlation between ETV5 expression and HGSOC patient prognosis. Univariate and multivariate analyses using the Cox regression model were conducted to determine the independent significance of relevant clinical covariates. RESULTS: Bioinformatic analysis demonstrated that ETV5 expression was significantly upregulated in OC (p < 0.05). qRT-PCR showed that ETV5 was significantly overexpressed in HGSOC tissues than in fallopian tube tissues (p < 0.05). qRT-PCR and western blotting assays demonstrated that ETV5 was relatively highly expressed in OC cell lines. ETV5 overexpression was positively associated with poor survival in HGSOC patients, therefore making it a high-risk factor for HGSOC progression. Furthermore, ETV5 promoted the proliferation, migration, and invasion capabilities of HGSOC cells. CONCLUSION: ETV5 has a carcinogenic effect in HGSOC and can be used as a clinically effective biomarker to determine the prognosis of HGSOC patients.

A biomimetic orthogonal-bilayer tubular scaffold for the co-culture of endothelial cells and smooth muscle cells.

In blood vessels, endothelial cells (ECs) grow along the direction of blood flow, while smooth muscle cells (SMCs) grow circumferentially along the vessel wall. To mimic this structure, a polycaprolactone (PCL) tubular scaffold with orthogonally oriented bilayer nanofibers was prepared via electrospinning and winding. ECs were cultured on the inner layer of the scaffold with axial nanofibers and SMCs were cultured on the outer layer of the scaffold with circumferential nanofibers. Fluorescence images of the F-actin distribution of ECs and SMCs indicated that cells adhered, stretched, and proliferated in an oriented manner on the scaffold. Moreover, layers of ECs and SMCs formed on the scaffold after one month of incubation. The expression levels of platelet-endothelial cell adhesion molecule 1 (PECAM-1) and a contractile SMC phenotype marker in the EC/SMC co-culture system were much higher than those in individual culture systems, thus demonstrating that the proposed biomimetic scaffold promoted the intercellular junction of ECs and preserved the contractile phenotype of SMCs.

Giant Cell-Rich Solitary Fibrous Tumor in the Nasopharynx: Case Report and Literature Review.

Solitary fibrous tumors (SFTs) can occur in several locations outside the pleura, but rarely in the sinonasal tract, and particularly not in the nasopharynx. Herein, we describe an unusual case of giant cell-rich SFT (GCRSFT) occurring in the nasopharynx. A 64-year-old man experienced dizziness and headache for more than 10 years with no obvious cause. Computed tomography (CT) scan showed a 3.9 cm × 2 cm tumor on the posterior lateral wall of the left nasopharynx, and angiography revealed a hypervascular tumor fed by branches of the left carotid artery. Hence, preoperative embolization was performed, and then the tumor was endoscopically resected. The symptoms were relieved after the resection, and postoperative head CT and video laryngoscopy showed that the tumor was completely resected. We next characterized the specific pathological characteristics of the resected tumor. Histologically, the tumor was characterized by varying cellular proliferation of cytologically bland spindle cells within a collagenous stroma, with prominent interspersed branching vessels. Mitotic activity was low (2/50HPF), and there was no evidence of pleomorphism or tumor necrosis. Moreover, multinucleated giant cells with deep nuclear staining and distributed in pseudovascular spaces were found within the tumor. We ruled out the possibility that our case was giant cell fibroblastoma (GCF) by immunohistochemical analysis, showing that the tumor cells were positive for CD34, CD99, STAT6, and BCL-2, and that the Ki-67 labeling index was 3%, indicating that our case was SFT and not GCF. The patient's condition is generally good after a 14-month follow-up. This report serves to broaden the morphologic spectrum of GCRSFT and will help clinicians and pathologists better understand this entity to prevent misdiagnosis.

MiR-212-3p suppresses high-grade serous ovarian cancer progression by directly targeting MAP3K3.

MicroRNAs (miRNAs) are small regulatory non-coding RNAs that have been reported to play an important role in the tumorigenesis of many cancers. In addition, miRNAs might serve as new promising biomarkers for diagnosis and prognosis and as effective therapeutic targets for patients with such malignancies. Accordingly, the dysregulation of miR-212-3p has been reported in a variety of human cancers. However, its biological functions and molecular mechanisms high-grade serous ovarian cancer (HGSOG) remain unknown. In this study, we demonstrated that miR-212-3p interacts with MAP3K3 based on bioinformatics-based predictions. Further, MAP3K3 was identified as a direct target gene of miR-212-3p in HGSOC. In addition, overexpression of miR-212-3p in HGSOC inhibited cell proliferation, colony formation, invasion, and migration. In contrast MAP3K3 mitigated the suppressive effects of miR-212-3p on HGSOC cell proliferation, invasion, and migration. Furthermore, miR-212-3p was significantly downregulated in HGSOC tissues compared to expression in normal fallopian tube tissues and was inversely associated with MAP3K3 levels. Accordingly, low miR-212-3p expression was also correlated with poor prognosis for HGSOC patients. In conclusion, miR-212-3p might act as a suppressor of HGSOC carcinogenesis by directly targeting MAP3K3. Therefore, this miRNA could be a novel and effective target for the treatment of patients with HGSOC.

Construction and Investigation of an LINC00284-Associated Regulatory Network in Serous Ovarian Carcinoma.

The low survival rate associated with serous ovarian carcinoma (SOC) is largely due to the lack of relevant molecular markers for early detection and therapy. Increasing experimental evidence has demonstrated that long noncoding RNAs (lncRNAs) are involved in cancer initiation and development, and a competitive endogenous RNA (ceRNA) hypothesis has been formulated. Therefore, the characterization of new lncRNA and lncRNA-related networks is crucial for early diagnosis and targeted therapy of SOC. Data on lncRNAs, mRNAs, and miRNAs with differential expression in SOC, compared to normal ovarian tissue, were obtained from the Gene Expression Omnibus (GEO) database. Data on lncRNA expression and clinical data in SOC were obtained from The Cancer Genome Atlas (TCGA). lncRNA-miRNA interactions were predicted by the miRBase database. Different online tools, i.e., TargetScan, RNA22, miRmap, microT, miRanda, StarBase, and PicTar, were cooperatively utilized to predict the mRNAs targeted by miRNAs. The plugin of BiNGO in Cytoscape and KOBAS 3.0 were used to conduct the functional and pathway enrichment analyses. The lncRNA, miRNAs, and mRNAs identified to be expressed at statistically significant and different levels between SOC and healthy fallopian tube tissues were further validated using qRT-PCR. A total of 4 lncRNAs (LINC00284, HAGLR, HCAT158, and BLACAT1) and 111 mRNAs were found to be upregulated in SOC tissues compared to normal tissues, based on the GEO database. LINC00284 was found to be highly expressed in SOC, in association with the upregulation of the transcription factor SOX9. The high LINC00284 expression was associated with poor prognosis and proved to be an independent risk factor in patients with SOC, based on TCGA database. The qRT-PCR validation results closely recapitulated the expression profiles and prognostic scores of the aforementioned bioinformatic analyses. The LINC00284-related ceRNA network was found to be associated with SOC carcinogenesis by biofunctional analysis. In conclusion, the LINC00284-related ceRNA network may provide valuable information on the mechanisms of SOC initiation and progression. Importantly, LINC00284 proved to be a new potential prognostic biomarker for SOC.

Low-Grade Chondrosarcoma In The Sellar Area: Case Report And Literature Review.

Low-grade chondrosarcoma (LGC) is a very rare intracranial tumor, particularly in the sellar area. Herein, we describe an unusual case of LGC occurring in the sellar area. A 52-year-old man presented with diminution of vision for more than 3 months, but did not exhibit headaches reported in previous cases. MRI showed that the maximum size of the tumor was 7 cm on the left side of the saddle. We characterized the specific pathological characteristics. Histologically, the tumor had polypoid areas and a lobulated growth pattern under low-power examination. At high magnification, the tumor consisted of small cells with hyperchromatic nuclei in the cartilage matrix, with an alternating loose hypocellular zone and rich myxoid area. In our case, LGC needed to be distinguished from chordoma. Immunohistochemically, the tumor cells showed diffuse positivity for S-100 and vimentin, IDH1 was weakly cytoplasm positive. The Ki-67 labeling index was less than 5%. Additionally, AE1/3, EMA, and CK19 were negative, which could be used to exclude chordoma. This case report expands the literature on LGC and will help clinicians and pathologists better understand this entity.

Galectin-3 may serve as a marker for poor prognosis in colorectal cancer: A meta-analysis.

Galectin-3 has an important function in the development of tumors. The purpose of this meta-analysis was to explore the relationships between the expression of galectin-3 on clinicopathological features and prognosis of colorectal cancer (CRC). A comprehensive literature search was used to identify eligible studies, and Stata software was conducted using in this meta-analysis. A total of 15 studies, including 1661 cases, were matched in the inclusion criteria. The pooled analysis indicated that galectin-3 expression was related to the poor overall survival (OS) in CRC patients (HR: 1.77, 95% CI: 1.36-2.31, P < 0.0001). Our meta-analysis also showed that cancerous tissues have higher levels of galectin-3 expression than normal tissues. Besides, positive galectin-3 expression was also related to advanced TNM stages(III/IV vs. I/II: OR 5.30, 95% CI: 2.42-11.61, P < 0.0001), higher Duke's stages (C/D vs. A/B: OR 4.00, 95% CI: 2.22-7.22, P < 0.0001), venous invasion (venous invasion vs. not: OR 3.02, 95%CI: 1.75-5.22, P < 0.0001) and higher CEA level (CEA≥5 ng/ml vs. ≤ 5 ng/ml: OR 2.09, 95% CI: 1.09-4.03, P = 0.03). In summary, our results indicated that overexpression of galectin-3 is significantly related to the tumor progression and could be a efficient in predicting the prognosis of patients with CRC.

Overexpression of ICAM-1 Predicts Poor Survival in High-Grade Serous Ovarian Carcinoma: A Study Based on TCGA and GEO Databases and Tissue Microarray.

Intercellular cell adhesion molecule-1 (ICAM-1), an important adhesion molecule in the immunoglobulin superfamily, is expressed on many cell types. Recent studies have identified ICAM-1 as a potential oncogene that promotes the development of epithelial ovarian cancer (EOC); it was also found to be associated with poor survival. However, the clinical significance of its expression in high-grade serous ovarian carcinoma (HGSOC) is unclear. Thus, this study aimed to investigate the significance of ICAM-1 expression in HGSOC. Data on ICAM1 expression and mutations in serous ovarian carcinoma (SOC) were obtained from the Cancer Genome Atlas (TCGA), and ICAM1 mRNA expression data in HGSOC were obtained from the Gene Expression Omnibus (GEO) database. ICAM-1 expression was evaluated by immunohistochemistry in HGSOC and normal fallopian tube tissues microarray. In TCGA data, amplification/mutation of ICAM1 was identified in 12% of serous ovarian carcinoma samples, and overexpression of ICAM1 mRNA predicted reduced overall survival in SOC. From TCGA and GEO data, SOC patients with ICAM1 mRNA overexpression treated with chemotherapeutic drugs that contained taxol or taxol and platin together had significantly reduced progression-free survival. According to GEO data, ICAM1 mRNA expression was found significantly higher in HGSOC than in control samples. In our study, ICAM-1 overexpression was observed in 63.1% (65/103) of HGSOCs. As a prognostic biomarker, overexpression of ICAM-1 predicted reduced recurrence-free and overall survival and is an independent risk factor for poor prognosis. These findings suggest that overexpression of ICAM-I is an independent indicator of poor prognosis for HGSOC and that it can serve as an effective clinical prognostic biomarker for this disease.

Overexpression of MAP3K3 promotes tumour growth through activation of the NF-κB signalling pathway in ovarian carcinoma.

Mitogen-activated protein kinase kinase kinase 3 (MAP3K3), a member of the serine/threonine protein kinase family, is ubiquitously expressed and acts as an oncogene. However, the expression and exact molecular mechanism of MAP3K3 in ovarian carcinoma (OC) remain unclear. Here, we found that MAP3K3 protein was highly expressed in 70.5% of high-grade serous ovarian carcinoma (HGSOC) samples. MAP3K3 overexpression was significantly associated with the FIGO stage and chemotherapy response. Additionally, MAP3K3 overexpression was associated with reduced disease-free survival and overall survival. In vitro experiments showed that MAP3K3 overexpression promoted cell proliferation, inhibited apoptosis, and enhanced the migration and invasion of OC cells. Moreover, in vivo tumourigenesis experiments confirmed that silencing MAP3K3 significantly reduced the growth rate and volume of transplanted tumours in nude mice. Drug sensitivity experiments demonstrated that differential expression of MAP3K3 in OC cell lines correlates with chemotherapy resistance. Functionally, the MAP3K3 gene regulated the malignant biological behaviour of OC cells by mediating NF-κB signalling pathways, affecting the downstream epithelial-mesenchymal transition and cytoskeletal protein expression. Our results unveiled the role of MAP3K3 in mediating NF-κB signalling to promote the proliferation, invasion, migration, and chemotherapeutic resistance of OC cells, highlighting a potential new therapeutic and prognostic target.