Antigallbladder Carcinoma Activity Analysis of a New Nanometer Drug Delivery System Based on Data Acquisition.

In order to solve the problem of the application of data acquisition in the new nanometer drug delivery system of microscope, a research of antigallbladder carcinoma activity analysis was proposed. Gallbladder carcinoma (GBC) is a common malignant tumor in biliary tract diseases. Due to the lack of specific clinical manifestations in the early stage, GBC has the shortcomings of the hidden onset, the difficult diagnosis, and the high misdiagnosis rate. GBC ranks in the top position among the most common tumors of the digestive system worldwide. The preoperative diagnosis rate is low, and the incidence of accidental gallbladder carcinoma is gradually increasing. Domestic gallbladder carcinoma related to cholecystectomy is not sensitive to radiotherapy and chemotherapy. Surgical resection is still the only effective method for the treatment of accidental gallbladder carcinoma.

Immune Classification and Immune Landscape Analysis of Triple-Negative Breast Cancer.

Background: To classify triple-negative breast cancer (TNBC) immunotyping using the public database, analyze the differences between subtypes in terms of clinical characteristics and explore the role and clinical significance of immune subtypes in TNBC immunotherapy. Methods: We downloaded TNBC data from the cBioPortal and GEO databases. The immune genes were grouped to obtain immune gene modules and annotate their biological functions. Log-rank tests and Cox regression were used to evaluate the prognosis of immune subtypes (IS). Drug sensitivity analysis was also performed for the differences among immune subtypes in immunotherapy and chemotherapy. In addition, dimension reduction analysis based on graph learning was utilized to reveal the internal structure of the immune system and visualize the distribution of patients. Results: Significant differences in prognosis were observed between subtypes (IS1, IS2, and IS3), with the best in IS3 and the worst in IS1. The sensitivity of IS3 to immunotherapy and chemotherapy was better than the other two subtypes. In addition, Immune landscape analysis found the intra-class heterogeneity of immune subtypes and further classified IS3 subtypes (IS3A and IS3B). Immune-related genes were divided into seven functional modules (The turquoise module has the worst prognosis). Five hub genes (RASSF5, CD8A, ICOS, IRF8, and CD247) were screened out as the final characteristic genes related to poor prognosis by low expression. Conclusions: The immune subtypes of TNBC were significantly different in prognosis, gene mutation, immune infiltration, drug sensitivity, and heterogeneity. We validated the independent role of immune subtypes in tumor progression and immunotherapy for TNBC. This study provides a new perspective for personalized immunotherapy and the prognosis evaluation of TNBC patients in the future.

Construction and Characterization of a Synergistic lncRNA-miRNA Network Reveals a Crucial and Prognostic Role of lncRNAs in Colon Cancer.

Non-coding RNAs such as long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been found to be indispensable factors in carcinogenesis and cancer development. Numerous studies have explored the regulatory functions of these molecules and identified the synergistic interactions among lncRNAs or miRNAs, while those between lncRNAs and miRNAs remain to be investigated. In this study, we constructed and characterized an lncRNA-miRNA synergistic network following a four-step approach by integrating the regulatory pairs and expression profiles. The synergistic interactions with more shared regulatory mRNAs were found to have higher interactional intensity. Through the analysis of nodes in the network, we found that lncRNAs played roles that are more central and had similar synergistic interactions with their neighbors when compared with miRNAs. In addition, known colon adenocarcinoma (COAD)-related RNAs were found to be enriched in this synergistic network, with higher degrees, betweenness, and closeness. Finally, we proposed a risk score model to predict the clinical outcome for COAD patients based on two prognostic hub lncRNAs, MEG3 and ZEB1-AS1. Moreover, the hierarchical networks of these two lncRNAs could contribute to the understanding of the biological mechanism of tumorigenesis. For each lncRNA-miRNA interaction in the hub-related subnetwork and two hierarchical networks, we performed RNAup method to evaluate their binding energy. Our results identified two important lncRNAs with prognostic roles in colon cancer and dissected their regulatory mechanism involving synergistic interaction with miRNAs.

The association between Ki-67 expression and the clinical pathological characteristics of colorectal cancer: A protocol for a systematic review and meta-analysis.

BACKGROUND: This study will explore the association between Ki-67 expression and clinical pathological characteristics (CPC) of colorectal cancer (CC). METHODS: We will search relevant studies from electronic databases (Cochrane Library, PUBMED, EMBASE, Scopus, Cumulative Index to Nursing and Allied Health Literature, China Biology Medicine, and China National Knowledge Infrastructure) from beginning to April 1, 2020 without language and publication time limitations. We will consider all case-controlled studies (CCSs) or randomized controlled studies (RCSs) investigating the association between Ki-67 expression and CPC of CC. We will appraise study quality of CCSs by Newcastle-Ottawa Scale, and RCSs by Cochrane risk of bias tool. Statistical analysis will be carried out by Review Manager 5.3 software. RESULTS: The present study will explore the association between Ki-67 expression and CPC of CC. CONCLUSION: Its findings may summarize scientific evidence of the association between Ki-67 expression and CPC of CC, and may provide helpful evidence for clinical practice.Systematic review registration: PROSPERO CRD42020173795.

Effects of oxymatrine on the proliferation of human liver cancer Bel-7404 cells: A protocol of systematic review and meta-analysis.

BACKGROUND: This study will examine the effects of oxymatrine on the proliferation of human liver cancer Bel-7404 cells (HLCBC). METHODS: This study will search electronic bibliographic databases available in PUBMED, EMBASE, Cochrane Library, Scopus, Cumulative Index to Nursing and Allied Health Literature, China Biology Medicine, and China National Knowledge Infrastructure. We attempt to search case-controlled studies (CCSs) or randomized controlled studies (RCSs) pertaining to HLCBC from their inception to the February 29, 2020 without limitations of language and publication time. We will include any CCSs or RCSs on exploring oxymatrine on the proliferation of HLCBC. We will assess the methodological quality of CCSs by Newcastle-Ottawa Scale, and RCSs by Cochrane risk of bias tool. Review Manager 5.3 software will be utilized for statistical analysis. RESULTS: The current study will summarize most recent eligible studies to investigate the effects of oxymatrine on the proliferation of HLCBC. CONCLUSION: Its results may provide reliable scientific evidence on effects of oxymatrine on the proliferation of HLCBC. SYSTEMATIC REVIEW REGISTRATION: INPLASY202040026.

Effects of artemisinin on proliferation and apoptosis of human liver cancer HepG2 cells: A protocol of systematic review and meta-analysis.

BACKGROUND: This study will examine the effects of artemisinin on proliferation and apoptosis of human liver cancer HepG2 cells (HLCHG-2C). METHODS: This study will systematically retrieve potential literatures in MEDLINE, Scopus, Web of Science, Cochrane Library, EMBASE, WANGFANG, and China National Knowledge Infrastructure from their initiation to the February 29, 2020. There are not limitations related to the language and publication time. All case-controlled studies (CCSs) or randomized controlled studies (RCSs) will be included in this study which investigated the effects of artemisinin on proliferation and apoptosis of HLCHG-2C. Two independent investigators will examine searched records, collect data from included studies, and will identify their methodological quality. Any divergences will be disentangled by discussion with another investigator. RevMan 5.3 software will be placed to pool the data and to carry out data analysis. RESULTS: This study will summarize all eligible studies to test the effects of artemisinin on proliferation and apoptosis of HLCHG-2C. CONCLUSION: The results of this study will exert evidence to examine the effects of artemisinin on proliferation and apoptosis of HLCHG-2C, and it may benefit further research, patients, and healthcare providers. SYSTEMATIC REVIEW REGISTRATION: INPLASY202040075.

LASP2 is downregulated in human liver cancer and contributes to hepatoblastoma cell malignant phenotypes through MAPK/ERK pathway.

LASP2 was recently demonstrated to serve as multifaceted roles in several types of cancers. However, its underlying mechanism in the progression of human liver cancer has not been explored. The aims of the current study were to detect LASP2 expression in a liver tissue microarray, and to determine whether LASP2 contributes to malignant phenotypes of HepG2 human hepatoblastoma cells. Our results revealed that LASP2 expression was downregulated in liver cancer tissues relative to normal non-cancerous tissues, and its downregulated expression was closely correlated with malignant process of liver cancer. In vitro, upregulation of LASP2 expression by transfection with LASP2 vector significantly suppressed HepG2 cells viability, colony formation and migration activities. Conversely, the viability, colony formation and migration abilities of HepG2 cells were increased when downregulating LASP2 expression by transfection with small interfering RNA targeting LASP2. Interaction study showed that silencing of LASP2 in HepG2 cells triggered high expression of Cyclin D1, ERK and p-ERK, and low expression of Bax, respectively. In addition, LASP2 silencing-induced malignant phenotypes were further attenuated after HepG2 cells treatment with ERK1/2 blocker PD98059. Collectively, our data suggest a link between LASP2 and MAPK/ERK axis in the development of hepatoblastoma and LASP2 may be a potential marker for assessment of liver cancer prognosis and staging.

CXCL3 overexpression promotes the tumorigenic potential of uterine cervical cancer cells via the MAPK/ERK pathway.

CXCL3 belongs to the CXC-type chemokine family and is known to play a multifaceted role in various human malignancies. While its clinical significance and mechanisms of action in uterine cervical cancer (UCC) remain unclear. This investigation demonstrated that the UCC cell line HeLa expressed CXCL3, and strong expression of CXCL3 was detected in UCC tissues relative to nontumor tissues. In addition, CXCL3 expression was strongly correlated with CXCL5 expression in UCC tissues. In vitro, HeLa cells overexpressing CXCL3, HeLa cells treated with exogenous CXCL3 or treated with conditioned medium from WPMY cells overexpressing CXCL3, exhibited enhanced proliferation and migration activities. In agreement with these findings, CXCL3 overexpression was also associated with the generation of HeLa cell tumor xenografts in athymic nude mice. Subsequent mechanistic studies demonstrated that CXCL3 overexpressing influenced the expression of extracellular signal-regulated kinase (ERK) signaling pathway associated genes, including ERK1/2, Bcl-2, and Bax, whereas the CXCL3-induced proliferation and migration effects were attenuated by exogenous administration of the ERK1/2 blocker PD98059. The data of the current investigation support that CXCL3 appears to hold promise as a potential tumor marker and interference target for UCC.

MicroRNA­584 directly targets CCND1 and inhibits cell proliferation and invasion in pancreatic cancer.

Multiple previous studies have demonstrated that the dysregulation of microRNAs (miRNAs) is implicated in the occurrence and development of pancreatic cancer. Therefore, a further characterisation of deregulated miRNAs in pancreatic cancer may provide novel insight into the oncogenesis and progression of pancreatic cancer, which may facilitate the identification of effective therapeutic targets for treating patients with this disease. In the present study, reverse transcription­quantitative polymerase chain reaction analysis demonstrated that the expression level of miRNA­584­5p (miR­584) was significantly decreased in pancreatic cancer tissues and cell lines. It was demonstrated that restoration of miR­584 expression significantly suppressed the proliferative and invasive ability of pancreatic cancer cells. Bioinformatics analysis predicted that cyclin D1 (CCND1) was a putative target of miR­584. Subsequent experiments demonstrated that CCND1 was a direct target gene of miR­584 in pancreatic cancer cells. Furthermore, the inhibition of CCND1 mimicked the suppressive effect of miR­584 overexpression in pancreatic cancer cells. The restoration of CCND1 expression significantly abolished the inhibitory effects of miR­584 overexpression on pancreatic cancer cells. Collectively, the present results demonstrated that miR­584 inhibited the development of pancreatic cancer by directly targeting CCND1, suggesting that this miRNA may represent a potential therapeutic target for this fatal disease.

Effect of neuromuscular electrical stimulation for fatigue management in patients with advanced laryngeal cancer receiving chemoradiotherapy.

This study retrospectively investigated the effect of neuromuscular electrical stimulation (NMES) for fatigue management in patients with advanced laryngeal cancer (ALC) receiving chemoradiotherapy.A total of 60 eligible patients with ALC receiving chemoradiotherapy were included. These patients were assigned equally to a treatment group and a control group. Patients in the treatment group received NMES therapy and were treated for a total of 8 weeks, while the patients in the control group did not receive NMES therapy. The primary outcome was fatigue, measured by the multidimensional fatigue inventory (MFI). The secondary outcomes included anxiety and depression, measured by the Hospital Anxiety and Depression Scale (HADS), and sleep quality, measured by the Pittsburgh Sleep Quality Index (PSQI). All outcomes were evaluated before and after 8-week NMES treatmentAfter 8-week NMES treatment, the patients in the treatment group did not exert better effect than patients in the control group in fatigue relief, measured by the MFI score, anxiety and depression decrease, assessed by HADS, and sleep quality improvement, evaluated by PSQI.The results of this study demonstrate that NMES may not benefit for fatigue relief in patients with ALC receiving chemoradiotherapy. Future studies should still focus on this topic and warrant these results.

Downregulation of TBC1 Domain Family Member 24 (BC1D24) Inhibits Breast Carcinoma Growth via IGF1R/PI3K/AKT Pathway.

BACKGROUND TBC1 domain family member 24 (TBC1D24) pathogenic mutations affect its binding to ARF6 and then result in severe impairment of neuronal development. However, there are no reports about the expression and function of TBC1D24 in cancer. The aim of the present study was to evaluate the effect of proliferation, migration, and invasion after silencing TBC1D24 expression in breast cancer MCF-7 cells, and to elucidate the potential mechanism of TBC1D24 in breast cancer. MATERIAL AND METHODS The expression of TBC1D24 in breast cancer tissues and the adjacent non-tumor tissues was determined by S-P immunohistochemistry. The malignant behavior, including proliferation, migration, and invasion ability, was determined after silencing TBC1D24 in breast cancer MCF-7 cells. The expression of IGF1R was determined after silencing TBC1D24. The expression of TBC1D24 and IGF1R was detected after transfecting miR-30a mimics or inhibitors. The effect of TBC1D24 on MCF-7 cells growth in vivo was evaluated by a tumor xenograft study. RESULTS TBC1D24 expression was elevated and was associated with poor outcome in breast carcinoma. TBC1D24 high expression was significantly correlated with unfavorable OS and RFS for breast cancer patients (p<0.05). Silencing TBC1D24 inhibited the proliferation, migration, and invasion ability of MCF-7 cells. TBC1D24 and IGF1R expression were decreased when transfected with miR-30a mimics. However, TBC1D24 and IGF1R expression were increased when transfected with miR-30a inhibitors (p<0.05). Knockdown of TBC1D24 inhibited the expression of IGF1R, PI3K, and p-AKT (p<0.05). Knockdown of TBC1D24 abolished tumorigenicity of MCF-7 cells. The average volume and weight of tumors was lower after silencing TBC1D24 expression (P<0.05). CONCLUSIONS Silencing TBC1D24 inhibited MCF-7 cells growth in vitro and in vivo. TBC1D24 promoted breast carcinoma growth through the IGF1R/PI3K/AKT pathway. TBC1D24 is a potential therapeutic target for breast cancer.