Baozhu Zhang

Background COLEC10 acts as a tumor suppressor in hepatocellular carcinoma (HCC) by inducing endoplasmic reticulum stress and inhibiting tumor stemness. However, we are curious whether it has other functions and protein interactions in HCC. Methods The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO)databases were used to determine COLEC10’s expression level and predictive power. Tumor, plate cloning, soft agar cloning, and nude mouse subcutaneous tumor formation experiments are conducted to detect the effect of COLEC10 on cancer proliferation. Furthermore, we performed KEGG functional enrichment, proteomics, immunoprecipitation, and immunofluorescence to search for proteins that interact with COLEC10. Results COLEC10 mRNA was significantly underexpressed in HCC. Overexpression of COLEC10 inhibited tumor growth of HCC cells. Mechanistically, COLEC10 inhibited the autophagy pathway via binding p32. High COLEC10 is positively correlated with the apoptosis pathway and negatively related to DNA replication, myc, and G2M checkpoint-related pathways. Conclusions COLEC10 inhibits HCC autophagy by reducing the protein level of p32, which serves as a valuable therapeutic target for HCC.

This review summarizes recent advances in extracellular vesicle-based carriers for glioblastoma diagnosis and therapy, and points out the current challenges and perspectives.

Background: Pyroptosis, a newly discovered type of programmed cell death, has both anti-tumor and tumor-promoting effects on carcinogenesis. In hepatocellular carcinoma (HCC), however, the associations between pyroptosis-regulated genes and prognosis, immune microenvironment, and immunotherapy response remain unclear.Samples and methods: Sequencing data were collected from The Cancer Genome Atlas database, The International Cancer Genome Consortium (ICGC), and The Integrative Molecular Database of Hepatocellular Carcinoma (HCCDB). First, we investigated the expression levels and copy number variations (CNVs) of 56 pyroptosis genes in HCC and pan-cancer. Next, we identified 614 genes related to 56 pyroptosis-associated genes at the expression, mutation, and CNVs levels. Pathway enrichment analysis of 614 genes in the Hallmark, KEGG, and Reactome databases yielded a total of 253 significant signaling pathways. The pyroptosis-regulated genes (PRGs) comprised 108 genes that were derived from the top 20 signaling pathways, of which 57 genes had prognostic value in HCC. The least absolute shrinkage and selection operator (LASSO) analysis was performed to screen for PRGs with prognostic values. Ultimately, we constructed a risk score model with seven PRGs to predict HCC prognosis and validated its predictive value in three independent HCC cohorts. Risk scores were used to illustrate receiver operating characteristic (ROC) curves predicting 1, 3, and 5-years overall survival (OS). Single-sample gene set enrichment analysis (ssGSEA), was performed to study 28 types of immune cells infiltrated in HCC. The relationship between the risk signature and six immune checkpoint genes and immunotherapy was analyzed.Results: A total of seven PRGs were obtained following multiple screening steps. The risk score model containing seven PRGs was found to correlate significantly with the HCC prognosis of the training group. In addition, we validated the risk score model in two additional HCC cohorts. The risk score significantly correlated with infiltrating immune cells (i. e. CD4⁺ T cells, etc.), ICB key molecules (i. e. HAVCR2, etc.), and ICB response.Conclusions: This study demonstrated a vital role of PRGs in predicting the prognosis and immunotherapy response of HCC patients. The risk model could pave the way for drugs targeting pyroptosis and immune checkpoints in HCC.

Few studies have examined the association of serum selenium with anemia‐related indicators and risk of anemia. We conducted a cross‐sectional analysis of 2,902 adults in 2003–2004 National Health and Nutrition Examination Survey database. Multivariable linear and logistic regression models were used to examine the association of serum selenium with anemia‐related indicators and risk of anemia. The nonlinear relationship was analyzed using a generalized additive model with the smoothing plot. A total of 1,472 males and 1,430 females with a mean age of 61.94 ± 13.73 years were included. Compared with the lowest quintile, the highest quintile of serum selenium was associated with increased level of serum iron (β = 12.44, 95% confidence interval [CI]: 7.14, 17.75, p < .001), mean corpuscular hemoglobin concentration (MCHC) (β = 0.14, 95%CI: 0.02, 0.26, p = .020), and hemoglobin (β = 0.40, 95%CI: 0.19, 0.61, p < .001), and decreased risk of anemia (odds ratio [OR] = 0.47, 95%CI: 0.28, 0.77, p = .002). Furthermore, smoothed plots suggested the nonlinear relationships between serum selenium and MCHC, hemoglobin level, and risk of anemia. Interestingly, on the left of inflection point, serum selenium was associated with decreased risk of anemia (OR = 0.972, 95%CI: 0.960, 0.985, p < .001), and then, the risk of anemia increased with increasing serum selenium concentration (OR = 1.011, 95%CI: 1.002, 1.021, p = .023). Future large‐scale, polycentric prospective studies should be conducted to verify our results.

Background: The nuclear division cycle 80 (NDC80) complex assures proper chromosome segregation during the cell cycle progression. SPC25 is a crucial component of NDC80, and its role in hepatocellular carcinoma (HCC) has been explored recently. This study characterized the differential expression of SPC25 in HCC patients of different races and HBV infection status. Methods: Expression patterns of SPC25 were evaluated in TCGA and Chinese HCC patients. Kaplan-Meier analysis was applied to examine the predictive value of SPC25. In vitro and in vivo functional assays were conducted to explore the role of SPC25 in HCC. Bioinformatics methods were applied to investigate the regulatory mechanisms of SPC25. Findings: The mRNA levels of SPC25 were up-regulated in HCC. SPC25 has a significantly higher transcriptional level in Asian patients than Caucasian patients. SPC25 promoted HCC cell proliferation in vitro and tumor growth in vivo by accelerating the cell cycle. We identified transcription factors, miRNAs, and immune cells that may interact with SPC25. Interpretation: The findings suggest that increased expression of SPC25 is associated with poor prognosis of HCC and enhances the proliferative capacity of HCC cells. SPC25 could serve as a valuable prognostic marker and a novel treatment target for HCC.

There are many disputes about the definition, diagnosis, therapy, and prognosis of collision tumors. We describe a rare patient with a collision tumor consisting of neuroendocrine carcinoma (NEC) and squamous cell carcinoma (SCC) in the nasal cavity and paranasal sinus. She received operation, concurrent chemoradiotherapy, and then two cycles of palliative chemotherapy. Follow-up at 12 mo after diagnosis showed that this patient experienced a complete response with no signs of recurrence or metastasis. A literature review of previous 26 cases diagnosed with collision tumor of NEC and SCC in the head and neck was also undertaken. It is challenging to manage collision tumors because there are two morphologically and etiologically distinct tumors. Well-designed multimodality therapy including surgery and chemoradiotherapy might lead to a long survival in these patients.

The optimal therapy for advanced thymic carcinoma has long been controversial. Despite that complete (R0) resection is recommend as the first-line treatment, multidisciplinary approach including chemotherapy and radiotherapy should be considered for patients who lost the operation chance or received incomplete resection. Here, we present a case who received concurrent chemoradiotherapy (CCRT) after cytoreductive surgery. A complete response was observed and the patient has remained disease free for over 4 years. To our knowledge, this is the first report to demonstrate the efficacy of CCRT with cisplatin plus etoposide after incomplete surgery for advanced thymic carcinoma.

Background and Aims: Cancer cells prefer aerobic glycolysis to maintain growth advantages, but the role of long non-coding RNAs (lncRNAs) in glycometabolism still remains unclear. Here we identified one cytoplasmic lncRNA LINC01554 as a significantly downregulated lncRNA in hepatocellular carcinoma (HCC) and aimed to investigate its role in cellular glucose metabolism in the development and progression of HCC.

Purpose: Collectin subfamily member 10 (COLEC10) encodes for collectin liver 1 (CL-L1), which is highly expressed in normal liver. Nevertheless, the association between COLEC10 and the prognosis of patients with hepatocellular carcinoma (HCC) remains unclear. To address this question, the prognostic value of COLEC10 expression in HCC was explored in this study. Patients and methods: Data from The Cancer Genome Atlas were used to compared transcriptional levels of COLEC10 in HCC samples and samples from healthy controls. In addition, COLEC10 mRNA and protein expression levels were analyzed in HCC tissue samples from Chinese patients and matched adjacent nontumorous tissue samples, by quantitative reverse-transcription polymerase chain reaction and immunohistochemistry, respectively. The prognostic value of COLEC10 was further examined using the Gene Expression Profiling Interactive Analysis online tool. Results: Both the mRNA and protein levels of COLEC10 were found to be downregulated in HCC tissues compared with normal controls. Survival analysis indicated that decreased mRNA and protein levels of COLEC10 were related with shorter overall survival in patients with HCC. In addition, univariate and multivariate analysis demonstrated that COLEC10 is an independent prognostic factor for overall survival of HCC patients. Conclusion: Together, the results suggest that decreased expression of COLEC10 may predict poor overall survival in patients with HCC.

Beta-transducin repeat containing E3 ubiquitin protein ligase (BTRC) is crucial for the degradation of IκBα. Our previous transcriptome sequencing analysis revealed that tetraspanin 15 (TSPAN15) was significantly upregulated in clinical oesophageal squamous cell carcinoma (OSCC) tissues. Here, we show that high TSPAN15 expression in OSCC tissues is significantly associated with lymph node and distant metastasis, advanced clinical stage, and poor prognosis. Elevated TSPAN15 expression is, in part, caused by the reduction of miR-339-5p. Functional studies demonstrate that TSPAN15 promotes metastatic capabilities of OSCC cells. We further show that TSPAN15 specifically interacts with BTRC to promote the ubiquitination and proteasomal degradation of p-IκBα, and thereby triggers NF-κB nuclear translocation and subsequent activation of transcription of several metastasis-related genes, including ICAM1, VCAM1, uPA, MMP9, TNFα, and CCL2. Collectively, our findings indicate that TSPAN15 may serve as a new biomarker and/or provide a novel therapeutic target to OSCC patients.