Results By performing qRT-PCR from CRC tissues and paired adjacent normal mucosa tissues, we identified that circRUNX1 expression was significantly upregulated in CRC tissues and positively related with lymph node metastasis, distant metastasis and advanced tumor-node-metastasis tumor stage in patients. Functionally, circRUNX1 knockdown inhibited cell proliferation and migration and promoted apoptosis, whereas its overexpression exerted opposite effects. In vivo, circRUNX1 promoted tumor growth and metastasis. Mechanically, circRUNX1 shared miRNA response elements with IGF1. circRUNX1 competitively bound to miR-145-5p and prevented miR-145-5p from decreasing the expression of IGF1, which facilitated tumor growth. Conclusion Our studies verified that circRUNX1 functions as a tumor promotor in CRC cells by targeting the miR-145-5p/IGF1 signaling pathway and may have potential use as a prognostic indicator and therapeutic target in CRC patients.Renal cell carcinoma (RCC) is among the 10 most common cancers in the USA. One-third of the patients diagnosed with this cancer present with locally advanced or metastatic disease. In the past, advanced disease conferred poor survival outcomes; however, the treatment paradigm for RCC has been revolutionized twice since 2005. The initial wave of revolution came with the emergence of vascular endothelial growth factor (VEGF) inhibitors and a second wave arose more recently with the emergence and unprecedented success of checkpoint inhibitors in RCC. A third wave combining these two strategies is well underway and likely represents the new paradigm to improve survival outcomes for afflicted patients. In this review, we discuss the current treatment landscape for patients with advanced RCC, focusing on approved VEGF and checkpoint inhibitors in the first-line setting as well as highlighting landmark combination clinical trials.[This corrects the article DOI 10.2147/OTT.S31387.].Purpose Exosomes participate in cellular communications by transmitting active molecules, including long noncoding RNAs (lncRNAs) and are regarded as suitable candidates for disease diagnosis. This study aimed to identify gastric cancer (GC)-specific exosomal lncRNA and investigate the potential diagnostic value of plasma exosomal lncRNA in GC. Patients and methods Exosomes from the culture media (CM) of four GC cells (GCCs) and human gastric epithelial cells were isolated. Exosomal RNA was extracted, and lncRNA microarray assay was performed to identify GC-specific exosomal lncRNAs. The expression levels of the candidate exosomal lncRNAs were validated in 120 subjects via quantitative reverse transcription PCR (qRT-PCR). The receiver operating characteristic (ROC) curve and area under curve were used to estimate the diagnostic capacity. We investigated the potential relationship between plasma exosomal lncRNA expression and the clinicopathological parameters of GC. Results A total of 199 exosomal lncRNAs were expressed at considerable higher levels in GCCs than those in normal controls, among which the top 10 upregulated lncRNAs were selected for further validation in cell, CM, and plasma. qRT-PCR revealed that lnc-SLC2A12-101 was remarkably upregulated in exosomes derived from patients with GC and GCCs. The area under the ROC curve was 0.776, which was higher than the diagnostic accuracies of CEA, CA 19-9, and CA72-4.  https://www.selleckchem.com/products/tat-beclin-1-tat-becn1.html  The expression level of exosomal lnc-SLC2A12-101 was also significantly correlated with tumor size, TNM stage, lymph node metastasis, and degree of differentiation. The postoperative expression levels of exosomal lnc-SLC2A12-101 were lower compared with those of preoperative levels. Conclusion Our study suggested that exosomal lnc-SLC2A12-101 may be a potential noninvasive biomarker for the diagnosis and prognosis monitoring of GC. Further large-scale studies are necessary to validate its performance in GC progression.Background Solute carrier family 39 member 4 (SLC39A4) has been reported to play an oncogenic role in several cancers. However, the role of SLC39A4 in esophageal squamous cell carcinoma (ESCC) remains unclear. In this study, we aimed to explore the clinical significance and function of SLC39A4 in ESCC. Methods The Cancer Genome Atlas and Gene Expression Omnibus databases were analyzed to assess the level of SLC39A4 in ESCC. The expression level of SLC39A4 was measured by RT-qPCR and immunohistochemistry in a cohort of 73 patients aged 45-65 years with ESCC. Kaplan-Meier analysis was used to identify the correlation between SLC39A4 and the prognosis of ESCC patients. In vitro experiments were conducted to explore the biological function of SLC39A4 in ESCC cell line TE-1 and TE-10. Results The mRNA level of SLC39A4 was significantly enhanced in ESCC specimens, which was in line with the outcome of online databases analysis. Moreover, the aberrant expression of SLC39A4 was positively correlated with clinical stage, T categories and lymph node metastasis. Kaplan-Meier analysis indicated that elevated SLC39A4 expression predicted poor prognosis of patients with ESCC. Furthermore, the in vitro experiments showed that SLC39A4 knockdown not only impaired the proliferation and motility capacities of ESCC cells but also enhanced the sensitivity to cisplatin treatment. Conclusion Our findings suggest that SLC39A4 could serve as a novel prognosis biomarker to promote ESCC progression; however, the mechanism of SLC39A4 in ESCC remains to be further explored.Introduction Long non-coding RNA (lncRNA) was reported to be a crucial regulator in cancer. In this work, our purpose is to explore the biological roles of nuclear paraspeckle assembly transcript 1 (NEAT1) in gastric cancer (GC). Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect NEAT1 expression in GC cells and normal cells. GC cell behaviors after NEAT1 overexpression or downregulation were analyzed by Cell Counting Kit-8 assay, colony formation assay, wound-healing assay, and flow cytometry assay. Bioinformatic tools were used to analyze the significance of NEAT1 in GC. The involvement of microRNA-365a-3p (miR-365a-3p) and ATP-binding cassette subfamily C member 4 (ABCC4) in the biological roles of NEAT1 in GC progression was validated by luciferase activity reporter assay and rescue experiments. Results We found NEAT1 increased expression in both GC tissues and cells and correlated with poorer overall survival of cancer patients. We found NEAT1 overexpression promotes, while its knockdown inhibits GC cell proliferation, colony formation, invasion, and cell cycle progression in vitro.