Clinical Value of PET.CT Based on Big Data in Colorectal and Peritoneal Metastatic Cancer.

This study focuses on the evaluation of the clinical utility of PET-CT imaging in peritoneal metastases and colorectal cancer. One hundred patients with colorectal peritoneal metastases, who underwent whole-body PET-CT imaging from January 2015 to December 2019, were selected as the experimental group, and 20 healthy individuals were selected as the control group. The SUVmax of the two groups of patients was 5.73 ± 3.84 and 2.70 ± 2.32, respectively, and the difference was statistically significant. The SUVmax AUC was 0.720, and the AUC of serum AFP, CEA, CA125, and CA199 were 0.596, 0.677, 0.642, and 0.696, respectively. Conclusion. 100 patients with colorectal and peritoneal metastatic cancer underwent PET/CT examination. The follow-up or other imaging examinations confirmed the diagnosis. Analysis of the ROC curve in this study found that with a peritoneal SUVmax> 3.2 as the diagnostic index for colorectal peritoneal metastatic cancer, the sum of sensitivity and specificity reached the maximum.

A retrospective study based on SEER database: not all high-risk factors are equal for stage II colon cancer.

Background: For stage II colon cancer, understanding of high-risk factors (HRFs) that affect the overall survival (OS) and the benefit of chemotherapy is limited. Meanwhile, no stable predictor can effectively predict OS of stage II colon cancer to date. Our study is aimed to identify HRFs associated with OS of stage II colon cancer, to quantify the risk conferred by each HRF, and to evaluate OS benefit gained by chemotherapy. Meanwhile, we attempt to establish a nomogram model for stage II colon cancer. Methods: The clinical variables of patients with stage II colon cancer between 2000 and 2018 were retrieved from the Surveillance, Epidemiology, and End Results (SEER) database. Univariate and multivariate analysis were performed to filtered out all the HRFs. We calculated the hazard ratios (HR) and evaluated the survival benefit of adjuvant chemotherapy for each HRF and combinations of HRFs. Then, a nomogram model based on all HRFs was established and verified. Results: A total of 39,103 patients with stage II colon cancer were included. T4b tumors were the highest risk for reduced OS [HR =2.821; 95% confidence interval (CI): 1.949-4.082], mucin-producing tumors (HR =2.412; 95% CI: 1.326-4.388) the second, and lymph node (LN) examined less than 12 (HR =2.200; 95% CI: 1.786-2.710) the third. T4 tumors (HR =0.790; 95% CI: 0.542-1.151), poorly/undifferentiated tumors (HR =0.468; 95% CI: 0.237-0.924), and some combinations of HRFs containing either could benefit from adjuvant chemotherapy. Meanwhile, we established an effective nomogram model based on the identified HRFs. Conclusions: The study has identified several novel HRFs for stage II colon cancer. Adjuvant chemotherapy has considerable OS benefit for stage II colon cancers with some specific HRFs, and treatment plans need to be individualized. Type and number of HRFs should be taken into consideration when recommending adjuvant chemotherapy. Our new nomogram model has better predictive ability and stability than the tumor-node-metastasis (TNM) stage system of American Joint Committee on Cancer (AJCC) staging system.

CircPRMT5 circular RNA promotes proliferation of colorectal cancer through sponging miR-377 to induce E2F3 expression.

CircPRTM5 is associated with cell proliferation and migration in many kinds of malignancies. However, the functions and mechanisms of CircPRTM5 in CRC progression remain unclear. We explored the role and the mechanisms of CircPRTM5 in the development of CRC. Tissues of CRC patients and matched adjacent non-tumour tissues were collected to evaluate the expression of CircPRTM5. The expression of CircPRTM5 in CRC tissues was significantly higher than that in adjacent tissues. The biological functions of CircPRTM5 in CRC were determined by overexpression and down-regulation of CircPRTM5 in CRC cells in vitro and in vivo. The results indicate that knockdown of CircPRTM5 can significantly inhibit the proliferation of CRC cells. The potential mechanisms of CircPRTM5 in CRC development were identified by RT-qPCR, Western blotting analysis and luciferase reporter assay. CircPRTM5 competitively regulates the expression of E2F3 by capillary adsorption of miR-377. CircPRMT5 regulates CRC proliferation by regulating the expression of E2F3, which affects the expression of the cell cycle-associated proteins cyclinD1 and CDK2. CircPRTM5 exerts critical regulatory role in CRC progression by sponging miR-377 to induce E2F3 expression.

Silencing of long noncoding RNA UCA1 inhibits colon cancer invasion, migration and epithelial-mesenchymal transition and tumour formation by upregulating miR-185-5p in vitro and in vivo.

Colon cancer is the third most common malignancy in the world. Long-chain noncoding RNA urothelial carcinoma-associated 1 (UCA1) was abnormally expressed in colon cancer and participated in colon cancer by regulating multiple miRNAs. This study further explored the molecular mechanism of UCA1 in the development of colon cancer from both in vitro and in vivo. The results showed that UCA1 was highly expressed in colon cancer cells, while miR-185-5p was low expressed. Bioinformatics analysis showed that miR-185-5p was a target of UCA1, while MAPK14 was a target of miR-185-5p. Knockdown of UCA1 with shRNA (sh-UCA1) resulted in a significant increase in miR-185-5p and a significant decrease in MAPK14. In addition, sh-UCA1 inhibited invasion, migration and epithelial-mesenchymal transformation of colon cancer cells. Western blotting also showed that sh-UCA1 inactivated the MAPKAPK2/HSP27 pathway. Furthermore, animal studies have revealed that sh-UCA1 inhibited tumour formation in vivo and improved the survival rate of mice. Collectively, these results suggest that silencing UCA1 may inhibit the carcinogenesis and metastasis of colon cancer in vitro and in vivo by modulating miR-185-5p/MAPK14/MAPKAPK2/HSP27 axis. SIGNIFICANCE OF THE STUDY: Colon cancer is the third largest malignant tumour worldwide. This study elucidated the role of urothelial carcinoma-associated 1 (UCA1) in colon cancer cells and its molecular mechanism. The present study suggests that silencing UCA1 may inhibit the invasion, migration, epithelial-mesenchymal transformation and tumour formation of colon cancer by upregulating miR-185-5p in vitro and in vivo. In summary, this study provides a new strategy for targeted therapy of colon cancer.

Albumin exfoliated titanium disulfide nanosheet: a multifunctional nanoplatform for synergistic photothermal/radiation colon cancer therapy.

PURPOSE: TiS2-HSA-FA, a nanoagent based on titanium disulfide (TiS2), human serum albumin (HSA), and folic acid (FA), was synthesized for potential use in synergistic photothermal/radiation therapy for colon cancer. METHODS: TiS2 nanosheets were synthesized through a HSA-assisted exfoliation method and then modified with PEGylated FA. The morphology, size, zeta potential, stability, cellular uptake, cytotoxicity, biodistribution, and in vitro and in vivo biocompatibility of the nanoparticles as well as their suitability for synergistic photothermal/radiation colon cancer therapy were investigated. RESULTS: The as-synthesized TiS2-HSA-FA nanoparticles showed excellent physiological stability, as well as high absorption values in the near-infrared (NIR) and X-ray regions, giving them superb activity as a photothermal and radiation sensitizer. In vitro and in vivo experiments indicated that TiS2-HSA-FA showed high tumor targeting selectivity, blood circulation time, biocompatibility, and suitability for synergistic tumor photothermal radiotherapy. CONCLUSION: A multifunctional nanoplatform based on TiS2 was developed and found to be potentially suitable for synergistic photothermal/radiation therapy for colon cancer.

LINC01303 functions as a competing endogenous RNA to regulate EZH2 expression by sponging miR-101-3p in gastric cancer.

Long non-coding RNA (lncRNA) is one of the important regulators of many malignancies. However, the biological function and clinical significance of a large number of lncRNAs in gastric cancer remain unclear. Therefore, we analysed the TCGA data to find that LINC01303 is significantly up-regulated in gastric cancer tissues. However, the biological function of LINC01303 in GC remains unknown. In our study, we found that the expression of LINC01303 was significantly higher in GC tissues than in adjacent tissues by real-time quantitative PCR. We can significantly inhibit the malignant proliferation, migration and invasion of GC cells by silencing LINC01303 expression. In addition, LINC01303 knockdown can also inhibit GC growth in vivo. After the bioinformatics analysis, we found that LINC01303 can be used as a miR-101-3p sponge to competitively adsorb miR-101-3p with EZH2. Therefore, our results indicate that LINC01303 promotes the expression of EZH2 by inhibiting miR-101-3p activity and promotes GC progression. In summary, in this study, we demonstrated for the first time that the LINC01303/miR-101-3p/EZH2 axis promotes GC progression.

miR-221 and miR-222 Simultaneously Target RECK and Regulate Growth and Invasion of Gastric Cancer Cells.

BACKGROUND: Although Helicobacter pylori infection is necessary for development of gastric adenocarcinoma (GAC), the underlying mechanism remains poorly defined. This study aimed to explore how miR-221 and miR-222 are dysregulated after H. pylori infection and how these 2 miRNAs are involved in pathological development of gastric cancer. MATERIAL AND METHODS: qRT-PCR analysis was performed to quantify miR-221 and miR-222 expression in patients with H. pylori - induced chronic gastritis, H. pylori-negative healthy controls, and in gastric cancer tissues and the corresponding adjacent normal tissues. Cell models were used to verify the expression profile. Dual luciferase assay was performed to verify putative binding between miR-221 or miR-222 and RECK. A loss-and-gain function study was performed to assess the miR-221/miR-222-RECK axis in gastric cancer cells. RESULTS: H. pylori infection leads to significantly higher miR-221 and miR-222 expression. MiR-221 and miR-222 can bind the same sequence of RECK 3'UTR, thereby modulating its expression. Through simultaneous regulation over RECK, miR-221 and miR-222 can promote gastric cancer cell growth and invasion. CONCLUSIONS: The miR-221/miR-222-RECK axis might be an important path modulating H. pylori infection-related gastric cancer development.