DEPDC1B promotes development of cholangiocarcinoma through enhancing the stability of CDK1 and regulating malignant phenotypes.

Cholangiocarcinoma (CCA) is the second most common primary tumor of the hepatobiliary system. At present, the therapeutic efficiency of cholangiocarcinoma is fairly low and the prognosis is poor. The root cause is that the molecular mechanism of the occurrence and development of CCA is largely unclear. This work intended to clarify the role of DEP domain-containing protein 1B (DEPDC1B) in the progress of CCA through cellular biology research strategies and further clarify the molecular mechanism of CCA. Clinical tissue-related detection showed that the expression level of DEPDC1B in tumor tissues was significantly higher than that in normal tissues and was positively correlated with tumor grade. Knockdown of the endogenous DEPDC1B of CCA cells can significantly inhibit cell proliferation and migration, while promoting cell apoptosis and blocking the cell cycle. DEPDC1B overexpression induced the opposite effects. Studies in animal models also showed that the downregulation of DEPDC1B can reduce the tumorigenicity of CCA cells. In addition, through gene profiling analysis and molecular biology studies, we found that CDK1 may be an important downstream mediator of DEPDC1B, the protein stability of which was significantly decreased through the ubiquitin-proteasome system in DEPDC1B knockdown cells. Moreover, knockdown of CDK1 can weaken the promotion of CCA caused by DEPDC1B overexpression. In summary, our research showed that DEPDC1B plays an important role in the development of CCA and its targeted inhibition may become one of the important methods to inhibit the progress of CCA.

Standardized nursing and clinical efficacy of OxyContin in reducing oral mucosal pain in patients with nasopharyngeal carcinoma: A randomized, double-blind, placebo-controlled study protocol.

BACKGROUND: Pain caused by oral mucositis (OM) is the main problem in the process of concurrent chemoradiotherapy for the nasopharyngeal carcinoma (NPC). This protocol aims to explore the standardized nursing and therapeutic effect of OxyContin on OM pain in the patients with NPC undergoing the concurrent chemoradiotherapy. METHODS: The experiment is a randomized clinical research, which was granted through the Research Ethics Committee of Shandong Provincial Third Hospital (No.20200802097). In this research, 90 NPC patients with OM induced by chemotherapy are enrolled, and the score of visual analogue >5 and the grade of OM >1 are evaluated. Patients with known allergy to OxyContin, the opioid abuse history, or major organ dysfunction, for instance, hepatic insufficiency, renal failure, and respiratory and heart failure, as well as a series of severe mental illness are excluded from our research. Patients in study groups receive standardized nursing and oral OxyContin. Patients in control groups only receive oral OxyContin. The analgesic effect could be assessed with the comparison of the visual analogue scale after and before the treatment. Safety evaluations contain the assessment of the vital signs, laboratory tests, as well as adverse events. The Karnofsky performance status standards of the International Cancer Control Union is utilized to evaluate the quality of life. RESULTS: The comparison of outcomes after taking OxyContin in both groups will be shown in .(Table is included in full-text article.) CONCLUSION:: The combination of OxyContin and standardized nursing care appears to improve the analgesic efficacy and life quality in NPC patients. TRIAL REGISTRATION: We registered this protocol in Research Registry (researchregistry6098).

Long noncoding RNA linc00467 plays an oncogenic role in hepatocellular carcinoma by regulating the miR-18a-5p/NEDD9 axis.

Increasing evidence has shown that numerous long noncoding RNAs (lncRNAs) play critical roles in tumorigenesis. Herein, we investigated the biological role of lncRNA linc00467 in the cancer biology of hepatocellular carcinoma (HCC). We observed that linc00467 was upregulated in HCC tissues and cells. Silencing of linc00467 using small interfering RNA interference significantly inhibited the growth and motility of HCC cells, and increased cell apoptosis through regulating the Bcl-2/Bax axis and the caspase cascade, suggesting that linc00467 exerted oncogenic functions in the progression of HCC. Moreover, we found that linc00467 could target miR-18a-5p, and NEDD9 was a target for miR-18a-5p in HCC cells. Furthermore, either the miR-18a-5p inhibitor or upregulation of NEDD9 could recover the inhibitory effects caused by silencing of linc00467. In conclusion, our data highlighted the oncogenic role of linc00467 in HCC progression by regulating the miR-18a-5p/NEDD9 axis.

Long noncoding RNA CASC21 exerts an oncogenic role in colorectal cancer through regulating miR-7-5p/YAP1 axis.

BACKGROUND: Emerging evidences show that long non-coding RNAs (lncRNAs) are widely involved in various cell processes and tumor progression. The aim of this study was to investigate the role of new lncRNA homo sapiens cancer susceptibility 21 (CASC21) in the cancer biology of colorectal cancer and explore the underlying mechanism. METHODS: We silenced the expression of CASC21 using siRNA interference in colorectal cancer cell lines HT29 and SW480, and the effects of CASC21 knockdown on cell proliferation, migration, invasion and apoptosis were assessed using CCK8, colony formation, wound-healing, Transwell and flow cytometry assays. Dual-luciferase reporter assay was performed to determine the relationship among CASC21, miR-7-5p and YAP1. Western blot analysis was used to examine expression of related proteins. RESULTS: By bioinformatics analysis, CASC21 was found to be significantly up-regulated in colorectal cancer tissues. Moreover, CASC21 knockdown displayed significant depression in cell viability, proliferation, migration, and invasion in colorectal cancer cells, as well as EMT process, while cell apoptosis was promoted by regulating the Bcl-2/Bax axis and Caspase cascade. Mechanistically, CASC21 could competently bind to miR-7-5p, resulting in increased YAP1 expression. Furthermore, up-regulation of YAP1 could rescue the inhibitory effects of CASC21 knockdown on EMT and cell invasion. CONCLUSION: Collectively, these results suggest that CASC21 functions as a ceRNA that plays an oncogenic role in the progression of colorectal cancer by regulating the miR-7-5p/YAP1 axis. LncRNA CASC21 might be a potential target for therapy of colorectal cancer.