Factors influencing depressive symptoms in Chinese female breast cancer patients: a meta-analysis.

Objective: To systematically evaluate and explore the factors influencing depressive symptoms in female breast cancer patients in China through meta-analysis. Methods: Relevant data were retrieved from cross-sectional studies or cohort studies on depressive symptoms of Chinese breast cancer within the following databases: PubMed, Embase, Cohrane Library, Web of 105 Science, Database of Medical Literature (CBM), Wan Fang Data, CNKI, and VIP databases. The literature screening, data extraction and literature quality evaluation were performed by two researchers by carefully reading the title, abstract and full text, and meta-analysis was performed using Stata 1.5 software after extracting relevant data. Results: Fourteen papers were finally included, with a cumulative total of 3,071 people surveyed, and a total of 1,298 breast cancer patients were detected with depression, with a detection rate of depressive symptoms of 42.26%; meta analysis showed that age less than 40 years old, unmarried, less than undergraduate education, monthly income <5,000 yuan, advanced breast cancer, radical breast cancer surgery, family history, living in rural areas, underlying disease stage and chemotherapy were associated with an increased incidence of depression in breast cancer patients. Conclusion: The detection rate of depressive symptoms in female breast cancer patients is high, and there is a need to strengthen depression-related psychological screening of breast cancer patients and provide them with individualized interventions to reduce the incidence of depression in breast cancer patients and to lower the level of depression already present in the patients.

Predicting Severity in Hypertriglyceridemia-Induced Acute Pancreatitis: The Role of Neutrophils, Calcium, and Apolipoproteins.

BACKGROUND Hypertriglyceridemia-induced acute pancreatitis (HTG-AP), representing 10% of all acute pancreatitis cases, is characterized by younger onset age and more severe progression, often leading to higher ICU admission rates. This condition poses a significant challenge due to its rapid progression and the potential for severe complications, including multiple organ failure. HTG-AP is distinct from other forms of pancreatitis, such as those caused by cholelithiasis or alcohol, in terms of clinical presentation and outcomes. It's essential to identify early markers that can predict the severity of HTG-AP to improve patient management and outcomes. MATERIAL AND METHODS This study divided 127 HTG-AP patients into mild acute pancreatitis (MAP, n=71) and moderate-to-severe acute pancreatitis (MSAP/SAP, n=56) groups. Blood biological indicators within the first 24 hours of admission were analyzed. Risk factors for HTG-AP progression were determined using binary logistic regression and ROC curves. RESULTS Elevated levels of HCT, NLR, TBI, DBI, AST, Cre, and AMS were noted in the MSAP/SAP group, with lower levels of LYM, Na⁺, Ca²âº, ApoA, and ApoB compared to the MAP group (p<0.05). NEUT%, Ca²âº, ApoA, and ApoB were significantly linked with HTG-AP severity. Their combined ROC analysis yielded an area of 0.81, with a sensitivity of 61.8% and specificity of 90%. CONCLUSIONS NEUT%, Ca²âº, ApoA, and ApoB are significant risk factors for progressing to MSAP/SAP in HTG-AP. Their combined assessment provides a reliable predictive measure for early intervention in patients at risk of severe progression.

The Application of Artificial Intelligence in Thyroid Nodules: A Systematic Review Based on Bibliometric Analysis.

BACKGROUND: Thyroid nodules are common lesions in benign and malignant thyroid diseases. More and more studies have been conducted on the feasibility of artificial intelligence (AI) in the detection, diagnosis, and evaluation of thyroid nodules. The aim of this study was to use bibliometric methods to analyze and predict the hot spots and frontiers of AI in thyroid nodules. METHODS: Articles on the application of artificial intelligence in thyroid nodules were retrieved from the Web of Science core collection database. A website (https://bibliometric.com/), VOSviewer and CiteSpace software were used for bibliometric analyses. The collaboration maps of countries and institutions were analyzed. The cluster and timeline view based on cocitation references and keywords citation bursts visualization map were generated. RESULTS: The study included 601 papers about AI in thyroid nodules. China contributed to more than half (52.41%) of these publications. The cluster view and timeline view of co-citation references were assembled into 9 clusters, "AI", "deep learning", "papillary thyroid carcinoma", "radiomics", "ultrasound image", "biomarkers", "medical image segmentation", "central lymph node metastasis (CLNM)", and "self-organizing auto-encoder". The "AI", "radiomics", "medical image segmentation", "deep learning," and "CLNM", emerging in the last 10 years and continuing until recent years, were included. CONCLUSION: An increasing number of scholars were devoted to this field. The potential future research hotspots include risk factor assessment and CLNM prediction of thyroid carcinoma based on radiomics and deep learning, automatic segmentation based on medical images (especially ultrasound images).

Cannabinoid type 2 receptors play a crucial role in social defeat-induced depression.

BACKGROUND: The endocannabinoid system plays a crucial role in regulating mood, but the specific involvement of cannabinoid receptor type 2 (CB2R) in depression remains poorly understood. Similarly, the mechanisms by which electroacupuncture (EA) provides therapeutic benefits for depression are not clearly defined. This research aims to explore the function of CB2R in depression and examine if the therapeutic effects of EA are associated with the hippocampal CB2R system. METHODS: Mice experiencing social defeat stress (SDS) were used to model depression and anxiety behaviors. We quantified hippocampal CB2R and N-arachidonoylethanolamide (AEA) levels. The efficacy of a CB2R agonist, JWH133, in mitigating SDS-induced behaviors was evaluated. Additionally, EA's impact on CB2R and AEA was assessed, along with the influence of CB2R antagonist AM630 on EA's antidepressant effects. RESULTS: SDS led to depressive and anxiety-like behaviors, with corresponding decreases in hippocampal CB2R and AEA. Treatment with JWH133 ameliorated these behaviors. EA treatment resulted in increased CB2R and AEA levels, while AM630 blocked these antidepressant effects. LIMITATIONS: The study mainly focused on the SDS model, which may not entirely reflect other depression models. Besides, further investigation is needed to understand the precise mechanisms by which CB2R and AEA contribute to EA's effects. CONCLUSIONS: The study suggests hippocampal downregulation of CB2R and AEA contributes to depression. Upregulation of CB2R and AEA in response to EA suggests their involvement in EA's antidepressant effects. These findings provide insights into the role of the hippocampal CB2R system in depression and the potential mechanisms underlying EA's therapeutic effects.

Integrating fractional amplitude of low-frequency fluctuation and functional connectivity to investigate the mechanism and prognosis of severe traumatic brain injury.

Objective: Functional magnetic resonance imaging (fMRI) has been used for evaluating residual brain function and predicting the prognosis of patients with severe traumatic brain injury (sTBI). This study aimed to integrate the fractional amplitude of low-frequency fluctuation (fALFF) and functional connectivity (FC) to investigate the mechanism and prognosis of patients with sTBI. Methods: Sixty-five patients with sTBI were included and underwent fMRI scanning within 14 days after brain injury. The patient's outcome was assessed using the Glasgow Outcome Scale-Extended (GOSE) at 6 months post-injury. Of the 63 patients who met fMRI data analysis standards, the prognosis of 18 patients was good (GOSE scores ≥ 5), and the prognosis of 45 patients was poor (GOSE scores ≤ 4). First, we apply fALFF to identify residual brain functional differences in patients who present different prognoses and conjoined it in regions of interest (ROI)-based FC analysis to investigate the residual brain function of sTBI at the acute phase of sTBI. Then, the area under the curve (AUC) was used to evaluate the predictive ability of the brain regions with the difference of fALFF and FC values. Results: Patients who present good outcomes at 6 months post-injury have increased fALFF values in the Brodmann area (7, 18, 31, 13, 39 40, 42, 19, 23) and decreased FC values in the Brodmann area (28, 34, 35, 36, 20, 28, 34, 35, 36, 38, 1, 2, 3, 4, 6, 13, 40, 41, 43, 44, 20, 28 35, 36, 38) at the acute phase of sTBI. The parameters of these alterations can be used for predicting the long-term outcomes of patients with sTBI, of which the fALFF increase in the temporal lobe, occipital lobe, precuneus, and middle temporal gyrus showed the highest predictive ability (AUC = 0.883). Conclusion: We provide a compensatory mechanism that several regions of the brain can be spontaneously activated at the acute phase of sTBI in those who present with a good prognosis in the 6-month follow-up, that is, a destructive mode that increases its fALFF in the local regions and weakens its FC to the whole brain. These findings provide a theoretical basis for developing early intervention targets for sTBI patients.

The role of the immune response and inflammatory pathways in TNF-related apoptosis-inducing ligand (TRAIL) resistance in triple-negative breast cancer cells.

Triple-negative breast cancer (TNBC) is an aggressive form of breast cancer, and the majority of TNBC lacks targeted therapies. Previous studies have shown that TNBC cells are highly sensitive to TNF-related apoptosis-inducing ligand (TRAIL), making it a potentially viable treatment option for TNBC. However, the development of TRAIL resistance limits its potential for clinical use, and the underlying mechanisms are not fully understood. To better understand the mechanism of resistance to TRAIL, we performed RNA sequencing to identify the candidates that are responsible for resistance to TRAIL in two previously established TRAIL-resistant MDA231 and SUM159 cells. This approach led us to identify differentially expressed genes (DEGs) and pathways in TRAIL-resistant MDA231 and SUM159 cells compared to their TRAIL-sensitive counterparts. We showed that several DEGs and pathways were associated with inflammation in TRAIL-resistant cells, including IL-1α and IL6. By downregulating IL-1α and IL6 expression, we showed that TRAIL sensitivity can be significantly restored in TRAIL-resistant cells. Therefore, this study identifies a mechanism by which the inflammation pathway promotes TRAIL resistance, which could be targeted for enhancing TRAIL-based therapies in TNBC cells.

Multi-omics analysis of the oncogenic role of optic atrophy 1 in human cancer.

OBJECTIVE: To investigate the prognostic significance of optic atrophy 1 (OPA1) in pan-cancer and analyze the relationship between OPA1 and immune infiltration in cancer. RESULTS: OPA1 exhibited high expression levels or mutations in various types of tumor cells, and its expression levels were significantly correlated with the survival rate of tumor patients. In different tumor tissues, there was a notable positive correlation between OPA1 expression levels and the infiltration of cancer-associated fibroblasts in the immune microenvironment. Additionally, OPA1 and its related genes were found to be involved in several crucial biological processes, including protein phosphorylation, protein import into the nucleus, and protein binding. CONCLUSION: OPA1 is highly expressed or mutated in numerous tumors and is strongly associated with protein phosphorylation, patient prognosis, and immune cell infiltration. OPA1 holds promise as a novel prognostic marker with potential clinical utility across various tumor types. METHODS: We examined OPA1 expression in pan-cancer at both the gene and protein levels using various databases, including Tumor Immune Estimation Resource 2.0 (TIMER 2.0), Gene Expression Profiling Interactive Analysis (GEPIA2), UALCAN, and The Human Protein Atlas (HPA). We utilized the Kaplan-Meier plotter and GEPIA datasets to analyze the relationship between OPA1 expression levels and patient prognosis. Through the cBioPortal database, we detected OPA1 mutations in tumors and examined their relationship with patient prognosis. We employed the TIMER 2.0 database to explore the correlation between OPA1 expression levels in tumor tissue and the infiltration of cancer-associated fibroblasts in the immune microenvironment. Furthermore, we conducted a gene search associated with OPA1 and performed enrichment analysis to identify the main signaling pathways and biological processes linked to them.

The value of radiomics-based CT combined with machine learning in the diagnosis of occult vertebral fractures.

PURPOSE: To develop and evaluate the performance of radiomics-based computed tomography (CT) combined with machine learning algorithms in detecting occult vertebral fractures (OVFs). MATERIALS AND METHODS: 128 vertebrae including 64 with OVF confirmed by magnetic resonance imaging and 64 corresponding control vertebrae from 57 patients who underwent chest/abdominal CT scans, were included. The CT radiomics features on mid-axial and mid-sagittal plane of each vertebra were extracted. The fractured and normal vertebrae were randomly divided into training set and validation set at a ratio of 8:2. Pearson correlation analyses and least absolute shrinkage and selection operator were used for selecting sagittal and axial features, respectively. Three machine-learning algorithms were used to construct the radiomics models based on the residual features. Receiver operating characteristic (ROC) analysis was used to verify the performance of model. RESULTS: For mid-axial CT imaging, 6 radiomics parameters were obtained and used for building the models. The logistic regression (LR) algorithm showed the best performance with area under the ROC curves (AUC) of training and validation sets of 0.682 and 0.775. For mid-sagittal CT imaging, 5 parameters were selected, and LR algorithms showed the best performance with AUC of training and validation sets of 0.832 and 0.882. The LR model based on sagittal CT yielded the best performance, with an accuracy of 0.846, sensitivity of 0.846, and specificity of 0.846. CONCLUSION: Machine learning based on CT radiomics features allows for the detection of OVFs, especially the LR model based on the radiomics of sagittal imaging, which indicates it is promising to further combine with deep learning to achieve automatic recognition of OVFs to reduce the associated secondary injury.

The Role of TRAIL in Apoptosis and Immunosurveillance in Cancer.

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF superfamily that selectively induces apoptosis in tumor cells without harming normal cells, making it an attractive agent for cancer therapy. TRAIL induces apoptosis by binding to and activating its death receptors DR4 and DR5. Several TRAIL-based treatments have been developed, including recombinant forms of TRAIL and its death receptor agonist antibodies, but the efficacy of TRAIL-based therapies in clinical trials is modest. In addition to inducing cancer cell apoptosis, TRAIL is expressed in immune cells and plays a critical role in tumor surveillance. Emerging evidence indicates that the TRAIL pathway may interact with immune checkpoint proteins, including programmed death-ligand 1 (PD-L1), to modulate PD-L1-based tumor immunotherapies. Therefore, understanding the interaction between TRAIL and the immune checkpoint PD-L1 will lead to the development of new strategies to improve TRAIL- and PD-L1-based therapies. This review discusses recent findings on TRAIL-based therapy, resistance, and its involvement in tumor immunosurveillance.

Association of NCAP family genes with prognosis and immune infiltration of human sarcoma.

OBJECTIVE: This study was conducted to explore the correlation of NCAP family genes with expression, prognosis, and immune infiltration in human sarcoma. RESULTS: Compared with normal human tissues, six NCAP family genes were highly expressed in sarcoma tissues, and high expression of the six genes were significantly associated with the poor prognosis of sarcoma patients. The expression of NCAPs in sarcoma was significantly related to the low infiltration level of macrophages and CD4+ T cells. GO and KEGG enrichment analysis showed that NCAPs and their interacting genes were mainly enriched in organelle fission for biological processes (BP), spindle for cellular component (CC), tubulin binding for molecular function (MF), and 'Cell cycle' pathway. METHODS: We explored the expression of NCAP family members by ONCOMINE, and GEPIA databases. Additionally, the prognostic value of NCAP family genes in sarcoma was detected by Kaplan-Meier Plotter and GEPIA databases. Moreover, we explored the relationship between NCAP family gene expression level and immune infiltration using the TIMER database. Finally, we performed GO and KEGG analysis for NCAPs-related genes by DAVID database. CONCLUSION: The six members of NCAP gene family can be used as biomarkers to predict the prognosis of sarcoma. They were also correlated with the low immune infiltration in sarcoma.

Neuroprotective Effects of an N-Salicyloyl Tryptamine Derivative against Cerebral Ischemia/Reperfusion Injury.

Cerebral ischemia/reperfusion (I/R) injury is a key reason for the poor prognosis of ischemic stroke. As only a few neuroprotective medications for cerebral I/R injury have been applied in the clinic, it is necessary to design a new therapeutic strategy to treat cerebral I/R injury. The N-salicyloyl tryptamine derivative LZWL02003, synthesized from melatonin and salicylic acid, exhibits a wide range of biological properties. In this study, we assessed the neuroprotective capabilities of LZWL02003 in vivo and in vitro and investigated its possible mechanisms. Oxygen-glucose deprivation/reoxygenation was utilized to create an in vitro model of cerebral I/R damage. Middle cerebral artery occlusion/reperfusion was employed to imitate cerebral I/R injury in vivo. Neuronal apoptosis, oxidative stress, mitochondrial dysfunction, and neuroinflammation are associated with the pathogenesis of cerebral I/R injury. Our findings demonstrated that LZWL02003 upregulated the expression of Bcl-2 and downregulated the expression of Bax, thus maintaining the homeostasis of Bcl-2/Bax proteins and preventing apoptosis. LZWL02003 also reduced oxidative stress by reducing malondialdehyde and reactive oxygen species levels, increasing the superoxide dismutase activity, and resolving mitochondrial malfunction. LZWL02003 can lower interleukin (IL)-1ß, tumor necrosis factor (TNF)-α, and IL-6 levels, which in turn suppress neuroinflammation. Activation of the nuclear factor-kappa B (NF-κB) pathway is involved in various pathophysiologies, including cerebral I/R injury. We discovered that LZWL02003 suppressed the phosphorylation activation of NF-κB pathway-related proteins and decreased the nuclear translocation of NF-κB p65 subunits. Taken together, our results suggest that LZWL02003 is a neuroprotective drug with pleiotropic effects and may be a candidate for treating cerebral I/R injury.

Association of SMC4 with prognosis and immune infiltration of sarcoma.

OBJECTIVE: This study was performed to explore the prognostic relevance of structural maintenance of chromosomes 4 (SMC4) in pan-cancer and explore the association between SMC4 and immune infiltration of sarcoma. RESULTS: Elevated expression of SMC4 was detected in cancer tissues compared to normal tissue, which was confirmed in synovial sarcoma tissues with immunohistochemistry (IHC). Additionally, higher expression of SMC4 was connected to worse outcomes of sarcoma, gastric cancer, breast cancer, liver cancer or ovarian cancer. Moreover, SMC4 was positively connected to immune cell infiltrates in sarcoma. In addition, infiltrating immune cell markers including monocyte, TAM, M1 and M2 presented different SMC4-associated immune infiltration patterns. CONCLUSION: The results from our study showed that SMC4 was positively related to the prognosis and immunological status of sarcoma. SMC4 could be a potential biomarker for prognosis and immune cell infiltrates in sarcoma. METHODS: Several databases including ONCOMINE, GEPIA, and Kaplan-Meier Plotter were adopted to explore the expression pattern of SMC4 in sarcoma, which was confirmed by IHC. The GEPIA and TIMER datasets were adopted to investigate the associations between SMC4 and prognosis in various cancers, especially in sarcoma.

Regulation of programmed death ligand 1 (PD-L1) expression by TNF-related apoptosis-inducing ligand (TRAIL) in triple-negative breast cancer cells.

Triple-negative breast cancer (TNBC) is an aggressive form of breast cancer that lacks targeted therapies. Previous studies have shown that TNBC cells are highly sensitive to tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), making it a promising agent for treating TNBC. However, the development of TRAIL resistance limits its further clinical development, and the underlying mechanisms are not fully understood. In this study, we report the role of PD-L1 in TRAIL resistance. Specifically, we found that TRAIL treatment increases PD-L1 expression in TRAIL-sensitive cells and that basal PD-L1 expression is increased in acquired TRAIL-resistant cells. Mechanistically, we found that increased PD-L1 expression was accompanied by increased extracellular signal-regulated kinase (ERK) activation. Using both genetic and pharmacological approaches, we showed that knockdown of ERK by siRNA or inhibition of ERK activation by the mitogen-activated protein kinase kinase inhibitor U0126 decreased PD-L1 expression and increased TRAIL-induced cell death. Furthermore, we found that knockout or knockdown of PD-L1 enhances TRAIL-induced apoptosis, suggesting that PD-L1-mediated TRAIL resistance is independent of its ability to evade immune suppression. Therefore, this study identifies a noncanonical mechanism by which PD-L1 promotes TRAIL resistance, which can be potentially exploited for immune checkpoint therapy.

Combined analysis of expression, prognosis and immune infiltration of GINS family genes in human sarcoma.

OBJECTIVE: This study was undertaken to explore the expression and prognostic value of GINS family in human sarcoma, as well as the association between the expression levels of the GINS family and sarcoma immune infiltration. RESULTS: We discovered that the mRNA expression levels of GINS1, GINS2, GINS3, and GINS4 were all higher in the majority of tumor tissues than in normal samples, of course, including sarcoma. Through the CCLE, all the four members expression were observed in high levels in sarcoma cell lines. In Gene Expression Profiling Analysis (GEPIA) and Kaplan-Meier Plotter, our results indicated that the poor overall survival (OS), disease-free survival (DFS) and relapse free survival (RFS) were tightly associated with the increased expression of GINS genes. In TIMER database, we found that highly expressed GINS was significantly correlated with the low infiltration level of CD4+ T cell and macrophage. CONCLUSIONS: The four GINS family members were all the prognostic biomarkers for the prognosis of human sarcoma and can reduce the level of immune cell infiltration in the sarcoma microenvironment. METHODS: In terms of the expression levels of mRNA for GINS family members, a particular contrast in various cancers, especially human sarcoma, was conducted through ONCOMINE and GEPIA and CCLE databases. Kaplan-Meier Plotter was used to identify the prognostic value of GINS family in sarcoma. The relationship between the expression level of GINS and the infiltration of immune cells was analyzed in TIMER database.

Proteomic Analysis Identifies p62/SQSTM1 as a Critical Player in PARP Inhibitor Resistance.

Poly (ADP-ribose) polymerase (PARP) inhibitors (PARPis) are currently being used for treating breast cancer patients with deleterious or suspected deleterious germline BRCA-mutated, HER2-negative locally advanced or metastatic diseases. Despite durable responses, almost all patients receiving PARPis ultimately develop resistance and succumb to their illness, but the mechanism of PARPi resistance is not fully understood. To better understand the mechanism of PARPi resistance, we established two olaparib-resistant SUM159 and MDA468 cells by chronically exposing olaparib-sensitive SUM159 and MDA468 cells to olaparib. Olaparib-resistant SUM159 and MDA468 cells displayed 5-fold and 7-fold more resistance over their corresponding counterparts. Despite defects in PARPi-induced DNA damage, these olaparib-resistant cells are sensitive to cisplatin-induced cell death. Using an unbiased proteomic approach, we identified 6 447 proteins, of which 107 proteins were differentially expressed between olaparib-sensitive and -resistant cells. Ingenuity pathway analysis (IPA) revealed a number of pathways that are significantly altered, including mTOR and ubiquitin pathways. Among these differentially expressed proteins, p62/SQSTM1 (thereafter p62), a scaffold protein, plays a critical role in binding to and delivering the ubiquitinated proteins to the autophagosome membrane for autophagic degradation, was significantly downregulated in olaparib-resistant cells. We found that autophagy inducers rapamycin and everolimus synergistically sensitize olaparib-resistant cells to olaparib. Moreover, p62 protein expression was correlated with better overall survival in estrogen receptor-negative breast cancer. Thus, these findings suggest that PARPi-sensitive TNBC cells hyperactivate autophagy as they develop acquired resistance and that pharmacological stimulation of excessive autophagy could lead to cell death and thus overcome PARPi resistance.

The neuroprotective effects of GPR55 against hippocampal neuroinflammation and impaired adult neurogenesis in CSDS mice.

Depression is one of the most prevalent mental illnesses in the world today, and the onset of depression is usually accompanied by neuroinflammation and impaired adult neurogenesis. As a new potential member of the endocannabinoid (eCB) system, G protein coupled receptor 55 (GPR55) has been associated with mood regulation. However, the role of GPR55 in the pathophysiology of depression remains poorly understood. Thus, a 10-day chronic social defeat stress (CSDS) paradigm was utilized as an animal model of depression to explore the potential role of GPR55 in depression. After CSDS, the protein level of GPR55 decreased significantly, but the mRNA expression did not change significantly, highlighting that although the GPR55 protein was involved in the progression of the depression- and anxiety-like phenotypes, its mRNA was not. Additionally, depression- and anxiety-like behaviors were also accompanied by neuroinflammation and impaired adult neurogenesis in the hippocampus. Interestingly, O-1602, a GPR55 agonist, remarkably prevented the development of depression- and anxiety-like behaviors as well as hippocampal neuroinflammation and neurogenesis deficits induced by CSDS. However, after electroacupuncture (EA) alleviated depression- and anxiety-like behaviors induced by CSDS, treatment with a GPR55 antagonist (CID16020046) reversed this effect. Our research demonstrated that downregulation of GPR55 expression in the hippocampus might mediate CSDS-induced depression- and anxiety-like phenotypes, and activation and upregulation of GPR55, which might be correlated with its anti-inflammatory and subsequent neuroprotective effects, could be a potential treatment for depression.

Integrative analysis of expression, prognostic significance and immune infiltration of RFC family genes in human sarcoma.

OBJECTIVE: To reveal the expression and prognostic value of replication factor C family genes (RFCs) in patients with sarcoma. RESULTS: The results showed that the mRNA expression levels of RFC2, RFC3, RFC4, and RFC5 were increased in sarcoma tissues. In addition, Cancer Cell Line Encyclopedia (CCLE) dataset analysis indicated that RFC1, RFC2, RFC3, RFC4, and RFC5 were elevated expressed in sarcoma cell lines. Moreover, Gene Expression Profiling Interactive Analysis (GEPIA) and Kaplan-Meier Plotter showed that highly expressed RFC2-5 were associated with poor overall survival (OS) or relapse-free survival (RFS) in sarcoma patients. The results of the Tumor Immune Estimation Resource (TIMER) database indicated that the expression of RFCs was negatively correlated with the infiltration of CD4+ T cells and macrophages. CONCLUSIONS: There were significant differences in the expression of RFCs between normal tissue and sarcoma tissue, and RFC2, RFC3, RFC4, and RFC5 might be promising prognostic biomarkers for sarcoma. METHODS: The expression of RFCs was analyzed using the ONCOMINE dataset and GEPIA dataset. CCLE dataset was used to assess the expression of RFCs in the cancer cell line. The prognostic value of RFCs was evaluated by GEPIA and Kaplan-Meier analysis. Furthermore, the association between RFCs and their co-expressed genes were explored via ONCOMINE and GEPIA datasets. We used the TIMER dataset to analyze the immune cell infiltration of RFCs in sarcoma.

Comprehensive analysis of expression and prognosis for LMNB family genes in human sarcoma.

ABSTRACT: Previous studies indicated that lamin proteins were thought to be related to gene expression, chromatin structure, and unclear stability. There are 2 types of vertebrate lamins, including A and B. The 2 B type proteins are encoded by lamin B1 (LMNB1) and lamin B2 (LMNB2). The LMNBs factor has been found to be associated with the development of multiple tumors, but its association with sarcoma has been barely mentioned.The transcription levels of LMNBs were analyzed via Oncomine database. Gene Expression Profiling Interactive Analysis (GEPIA) dataset was adopted to analyze the differential expression of LMNBs in sarcoma. Cancer Cell Line Encyclopedia dataset was used to explore the expression of LMNBs in sarcoma cell line. We analyzed the prognostic value of LMNBs in GEPIA and Kaplan-Meier Plotter. Oncomine and GEPIA datasets were also used to detect the relationship between LMNBs and their co-expressed genes. We used the Database for Annotation, Visualization and Integrated Discovery to conduct the Gene Ontology analysis of LMNBs and their co-expressed genes. Kyoto Encyclopedia of Genes and Genomes was also used to analyze the pathway of LMNBs.LMNB1 and LMNB2 were reported to be hyperexpressed in sarcoma. The expression of LMNBs was elevated in various sarcoma cell lines. According to the results, we observed that LMNBs were connected to the poor overall survival, recurrence-free survival, and disease-free survival of sarcoma patients.This study indicated that hyperexpression of LMNBs was significantly related to worse outcome of sarcoma, LMNB1 and LMNB2 were expected to become potential biomarkers for human.

Prognostic significance of long non-coding RNA five prime to XIST in various cancers.

BACKGROUND: To observe the clinicopathological and prognostic value of long non-coding RNA five prime to X inactive specific transcript (lncFTX) in multiple tumors. METHODS: Eligible studies for lncFTX were identified by searching PubMed, Embase, Web of Science and Cochrane Library databases from inception to December 01, 2020. Stata 12.0 software was used to calculate the odds ratio (OR)/hazard ratio (HR) and 95% confidence interval (95% CI). We used The Cancer Genome Atlas (TCGA) dataset to further investigate the differential expression and prognostic value of lncFTX. RESULTS: We included 11 studies involving a total of 1633 patients. The results showed that the expression of lncFTX was positively associated with advanced TNM stage (III-IV versus I-II) (OR = 2.30, 95% CI: 1.74-3.03, P < 0.05), lymph nodes metastasis (OR = 3.01, 95% CI: 2.00-4.52, P < 0.05), distant metastasis (OR = 3.68, 95% CI: 2.13-6.34, P < 0.05), and cancer mortality (HR = 1.83, 95% CI: 1.20-2.81, P < 0.05). However, the expression of lncFTX was not associated with tumor differentiation (poor differentiation versus well or moderate differentiation) and vessel invasion of cancer. Subgroup analysis showed that the higher lncFTX expression was associated with shorter overall survival in cancer patients, regardless of the sample size and cancer type. No publication bias was found, and the sensitivity analysis results suggested that the main findings were robust. Elevated expression and prognostic significance of FTX were confirmed using TCGA dataset. CONCLUSIONS: This study found that the expression of lncFTX was positively associated with advanced tumor node metastasis (TNM) stage, lymph nodes, distant metastasis and, cancer mortality, suggesting that lncFTX might be a potential prognostic biomarker for tumors.

The rise of developmental biology in China.

Developmental biology research in China started from experimental embryology, in particular from studies on aquatic and reptile animals. The recent growth of the developmental biology community in China parallels the increased governmental funding support and the recruitment of overseas talents. This flourishing field in China embraces the activities of developmental biology-related societies, national meetings, key research initiatives and talented scientists. The first Development paper from China, published in 2000, marked the beginning of a new era. More recently, the second decade in the 21st century witnessed the blossoming of developmental biology research in China. Significant research spotlights, technical advances, and up-and-coming areas will be discussed in this overview.