Early diagnostic value of ECT whole-body bone imaging combined with PINP and ß-CTX for bone metastasis of lung cancer.

OBJECTIVE: This research was aimed at investigating the early diagnostic value of emission computed tomograph (ECT) whole-body bone imaging combined with PINP and ß-CTX for bone metastasis of lung cancer. METHODS: Case data of 86 lung cancer patients were categorized into lung cancer with bone metastasis (LCWBM, 46 cases) and lung cancer without bone metastasis (LCWOBM, 40 cases) groups according to the presence or absence of bone metastasis. Patients' general information were collected. ECT whole-body bone imaging was used to detect bone metastases and the grading of the extent of disease (EOD) in both groups, and electrochemiluminescence was utilized to detect the serum levels of PINP and ß-CTX. Spearman correlation analysis was employed to evaluate the correlation between EOD grading and PINP and ß-CTX levels. Logistic univariate and multivariate regression was implemented to analyze the risk factors of bone metastasis of lung cancer. Receiver operating characteristic (ROC) curve was applied to analyze the diagnostic efficacy of the single test of ECT whole-body bone imaging, PINP, or ß-CTX and the combination of the three tests. RESULTS: The differences in pathological type, clinical stage and EOD grading, the number of positive ECT cases, and the expression levels of PINP and ß-CTX between the LCWBM and LCWOBM groups were statistically significant. In LCWBM patients with different EOD grading, the trends of the expression of PINP and ß-CTX were grade 3 > grade 2 > grade 1 and grade 0. Further correlation analyses revealed that EOD grading showed a significant positive correlation with the PINP and ß-CTX expression levels. Univariate logistic regression analysis demonstrated that adenocarcinoma, TNM stage IV, ECT positivity, and high expression of PINP and ß-CTX were associated with bone metastasis of lung cancer, and multivariate logistic regression analysis indicated that ECT positivity, high expression of PINP and ß-CTX were independent risk factors for bone metastasis of lung cancer. The area under the curve (AUC) of ECT, PINP, and ß-CTX alone for the diagnosis of bone metastasis of lung cancer were 0.872, 0.888, and 0.874, respectively, and the AUC for the combined diagnosis of the three was 0.963, which was greater than that of any one of the individual indices, with a sensitivity of 86.96% and a specificity of 97.50% at a Youden index of 0.845. CONCLUSION: ECT whole-body bone imaging combined with PINP and ß-CTX has high diagnostic value for bone metastasis of lung cancer.

TCL1A acts as a tumour suppressor by modulating gastric cancer autophagy via miR-181a-5p-TCL1A-Akt/mTOR-c-MYC loop.

Gastric cancer is the third most commonly cause of tumour-related death worldwide and one of the most prevalent malignancies in China. TCL1A, TCL1 family Akt coactivator A, can active Akt/mTOR pathway and regulate the autophagy. However, the action of TCL1A in gastric cancer is not well understood. The present study is investigating the mechanism of action of TCL1A in gastric cancer. TCL1A was lowly expressed in gastric cancer tissues. Subsequent experiments demonstrated that miR-181a-5p can regulate c-MYC through the TCL1A-Akt/mTOR pathway and c-MYC can in turn affect the expression of miR-181a-5p, thus confirming the existence of the miR-181a-5p-TCL1A-Akt/mTOR-c-MYC loop. Flow cytometric apoptosis assay and mRFP-eGFP-LC3 autophagy assay demonstrated that both miR-181a-5p and TCL1A can affect autophagy and apoptosis of gastric cancer cells through the loop. In vivo experiments confirmed that TCL1A can affect the proliferation of gastric cancer. These results illustrate that TCL1A can exert tumour suppressive effects and affect gastric cancer autophagy and progression via the miR-181a-5p-TCL1A-Akt/mTOR-c-MYC loop, which could be a potential therapeutic target for gastric cancer.

Application of Enhanced T1WI of MRI Radiomics in Glioma Grading.

Objective: To explore the application value of the radiomics method based on enhanced T1WI in glioma grading. Materials and Methods: A retrospective analysis was performed using data of 114 patients with glioma, which was confirmed using surgery and pathological tests, at our hospital between January 2017 and November 2020. The patients were randomly divided into the training and test groups in a ratio of 7 : 3. The Analysis Kit (AK) software was used for radiomic analysis, and a total of 461 tumor texture features were extracted. Spearman correlation analysis and the least absolute shrinkage and selection (LASSO) algorithm were employed to perform feature dimensionality reduction on the training group. A radiomics model was then constructed for glioma grading, and the validation group was used for verification. Results: The area under the ROC curve (AUC) of the proposed model was calculated to identify its performance in the training group, which was 0.95 (95% CI = 0.905-0.994), accuracy was 84.8%, sensitivity was 100%, and specificity was 77.8%. The AUC of the validation group was 0.952 (95% CI = 0.871-1.000), accuracy was 93.9%, sensitivity was 90.0%, and specificity was 95.6%. Conclusions: The radiomics model based on enhanced T1WI improved the accuracy of glioma grading and better assisted clinical decision-making.

USP11 induce resistance to 5-Fluorouracil in Colorectal Cancer through activating autophagy by stabilizing VCP.

Chemotherapy plays an important role in the treatment of patients with colorectal cancer (CRC). However, the resistance to chemotherapy severely affects the prognosis of CRC patients and the mechanisms are still poorly understood. Our study investigated the role of ubiquitin-specific protease 11 (USP11) in CRC chemotherapy and found that USP11 could induce resistance to 5-fluorouracil by activating autophagy. A series of in vitro and in vivo experiments revealed that USP11 promoted autophagy through AMPK/Akt/mTOR pathway via stabilizing valosin-containing protein (VCP). Overall, our study demonstrated that USP11 might be valuable to predict the chemotherapeutic sensitivity and improve the prognosis of CRC patients.

5-Lipoxygenase promotes epithelial-mesenchymal transition through the ERK signaling pathway in gastric cancer.

BACKGROUND AND AIM: 5-Lipoxygenase has been reported to enhance cell proliferation, migration, and invasion. Epithelial-mesenchymal transition is considered an important process for tumor metastasis and invasion. METHODS: The 5-lipoxygenase expression levels and the prognoses in patients with gastric cancer were evaluated by immunohistochemistry and by the log-rank test on Kaplan-Meier curves. We established 5-lipoxygenase-overexpressed and 5-lipoxygenase-silenced gastric cancer cells and measured migration, invasion, and epithelial-mesenchymal transition makers to examine the role of 5-lipoxygenase in gastric cancer in vitro. In vivo, 5-lipoxygenase-overexpressed gastric cancer cells were administered into mice by subcutaneous injection, intraperitoneal injection or splenic intravenous injection to study the proliferation or metastasis of 5-lipoxygenase in mice. Using the extracellular signal-regulated kinase pathway inhibitor U0126 and activator tumor growth factor-ß, we investigated the mechanism of epithelial-mesenchymal transition induced by 5-lipoxygenase in gastric cancer cells. RESULTS: 5-Lipoxygenase was upregulated in gastric cancer tissues and was related to poor overall survival in gastric cancer patients. 5-Lipoxygenase promoted gastric cancer cell proliferation, migration, and invasion and induced the process of epithelial-mesenchymal transition in gastric cancer cells. In the nude mouse model, mice with gastric cancer tumors overexpressing 5-LOX had a faster tumor growth rate and more severe abdominal and liver metastases than the control group. Inhibition of extracellular signal-regulated kinase signaling by U0126 or activation by tumor growth factor-ß neutralized the effect of 5-LOX overexpression or silencing on epithelial-mesenchymal transition. CONCLUSION: 5-Lipoxygenase promotes epithelial-mesenchymal transition in gastric cancer by activating the extracellular signal-regulated kinase signaling pathway.

MicroRNAs for Diagnosis and Treatment of Colorectal Cancer.

Colorectal cancer (CRC) is the third most common cancer worldwide, with high morbidity and mortality rates. The diagnosis and treatment of CRC have the most significant value for disease- free survival. Early diagnosis and early surgical resection are generally considered to be the most effective ways to reduce CRC mortality. In the past few years, many researchers have focused on the role of microRNAs in different tumors, making the functions of microRNAs gradually clear. The present study reviews the role of microRNAs in the diagnosis and treatment of colorectal cancer. Compared with the usual diagnosis methods and biomarker, circulating microRNAs can be promising new effective biomarkers for CRC diagnosis and treatment.

PCDHGA9 represses epithelial-mesenchymal transition and metastatic potential in gastric cancer cells by reducing ß-catenin transcriptional activity.

Gastric cancer (GC) has a high mortality rate, and metastasis is the main reason for treatment failure. It is important to study the mechanism of tumour invasion and metastasis based on the regulation of key genes. In a previous study comparing the expression differences between GES-1 and SGC-7901 cells, PCDHGA9 was selected for further research. In vitro and in vivo experiments showed that PCDHGA9 inhibited invasion and metastasis. A cluster analysis suggested that PCDHGA9 inhibited epithelial-mesenchymal transition (EMT) through the Wnt/ß-catenin and TGF-ß pathways. Laser confocal techniques and western blotting revealed that PCDHGA9 inhibited the nuclear translocation of ß-catenin, regulated T cell factor (TCF)/ /lymphoid enhancer factor (LEF) transcriptional activity, directly impacted the signal transmission of the TGF-ß/Smad2/3 pathway, strengthened the adhesion complex, weakened the effects of TGF-ß, and blocked the activation of the Wnt pathway. In addition, PCDHGA9 expression was regulated by methylation, which was closely related to poor clinical prognosis. The aim of this study was to elucidate the molecular mechanism by which PCDHGA9 inhibits EMT and metastasis in GC to provide a new theoretical basis for identifying GC metastasis and a new target for improving the outcome of metastatic GC.