BackgroundColorectal cancer (CRC) is a common malignant tumor with high metastatic and recurrent rates. This study probes the effect and mechanism of long non-coding RNA MIR31HG on the progression of CRC cells.Materials and MethodsQuantitative real-time PCR (qRT-PCR) was used to analyze the expression of MIR31HG and miR-361-3p in CRC tissues and normal tissues. Gain- or loss-of-function assays were conducted to examine the roles of MIR31HG, miR-361-3p and YY1 transcription factor (YY1) in the CRC progression. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and colony formation experiment were conducted to test CRC cell proliferation. CRC cell invasion was determined by Transwell assay. The glucose detection kit and lactic acid detection kit were utilized to monitor the levels of glucose and lactate in CRC cells. The glycolysis level in CRC cells was examined by the glycolytic stress experiment. Western blot was performed to compare the expression of glycolysis-related proteins (PKM2, GLUT1 and HK2) and angiogenesis-related proteins (including VEGFA, ANGPT1, HIF1A and TIMP1) in HUVECs. The binding relationships between MIR31HG and miR-361-3p, miR-361-3p and YY1 were evaluated by the dual-luciferase reporter assay and RNA immunoprecipitation (RIP).ResultsMIR31HG was up-regulated in CRC tissues and was associated with poorer prognosis of CRC patients. The in-vitro and in-vivo experiments confirmed that overexpressing MIR31HG heightened the proliferation, growth, invasion, glycolysis and lung metastasis of CRC cells as well as the angiogenesis of HUVECs. In addition, MIR3HG overexpression promoted YY1 mRNA and protein level, and forced overexpression of YY1 enhanced MIR31HG level. Overexpressing YY1 reversed the tumor-suppressive effect mediated by MIR31HG knockdown. miR-361-3p, which was inhibited by MIR31HG overexpression, repressed the malignant behaviors of CRC cells. miR-361-3p-mediated anti-tumor effects were mostly reversed by upregulating MIR31HG. Further mechanism studies illustrated that miR-361-3p targeted and negatively regulated the expression of YY1.ConclusionThis study reveals that MIR31HG functions as an oncogenic gene in CRC via forming a positive feedback loop of MIR31HG-miR-361-3p-YY1.
Numerous studies have shown that the expression of circular RNA (circRNA) is closely related to the malignant progression of cancer. However, the role of circ-MFN2 in colorectal cancer (CRC) is unclear. Our study aims to explore the role and mechanism of circ-MFN2 in CRC progression. The relative expression levels of circ-MFN2, microRNA (miR)-574-3p and insulin-like growth factor 1 receptor (IGF1R) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was determined using 3-(4, 5-dimethyl-2 thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay. The colony number and radioresistance of cells were assessed using colony formation assay. Moreover, the migration and invasion of cells were measured using transwell assay. Tumor xenograft model was constructed to evaluate the effect of circ-MFN2 knockdown on CRC tumor growth. Furthermore, dual-luciferase reporter assay was used to verify the interaction between miR-574-3p and circ-MFN2 or IGF1R. In addition, the protein level of IGF1R was evaluated by western blot (WB) analysis. Circ-MFN2 expression was elevated in CRC tissues and cells. Knockdown of circ-MFN2 restrained the proliferation, migration, invasion, and radioresistance of CRC cells in vitro. Furthermore, silenced circ-MFN2 also reduced the tumor volume and weight of CRC in vivo. MiR-574-3p could be sponged by circ-MFN2, and its inhibitor reversed the suppression effect of circ-MFN2 silencing on CRC progression. Moreover, IGF1R was a target of miR-574-3p, and its overexpression reversed the inhibition effect of miR-574-3p mimic on CRC progression. In addition, circ-MFN2 could positively regulate IGF1R expression by sponging miR-574-3p. Our results revealed that circ-MFN2 promoted the proliferation, metastasis and radioresistance of CRC through regulating the miR-574-3p/IGF1R axis, suggesting that circ-MFN2 might be a novel therapeutic biomarker for CRC.
Li3V2(PO4)3 (LVP) is one of the candidates for high-energy-density cathode materials matching lithium metal batteries due to its high operating voltage and theoretical capacity. However, the inevitable side reactions of LVP with a traditional liquid-state electrolyte under high voltage, as well as the uncontrollable growth of lithium dendrites, worsen the cycling performance. Herein, a hybrid solid-state electrolyte is prepared by the confinement of a lithium-containing ionic liquid with a mesoporous SiO2 scaffold, and used for a LVP-cathode-based lithium metal battery. The solid-state electrolyte not only exhibits a high ionic conductivity of 3.14 × 10−4 S cm−1 at 30 °C and a wide electrochemical window of about 5 V, but also has good compatibility with the LVP cathode material. Moreover, the cell paired with a solid-state electrolyte exhibits good reversibility and can realize a stable operation at a voltage of up to 4.8 V, and the discharge capacity is well-maintained after 100 cycles, which demonstrates excellent capacity retention. As a contrast, the cell paired with a conventional liquid-state electrolyte shows only an 87.6% discharge capacity retention after 100 cycles. In addition, the effectiveness of a hybrid solid-state electrolyte in suppressing dendritic lithium is demonstrated. The work presents a possible choice for the use of a hybrid solid-state electrolyte compatible with high-performance cathode materials in lithium metal batteries.
Papillary thyroid carcinoma (PTC) is the most common type of thyroid malignancy but shows excellent prognosis. We investigated the clinical significance of cyclin-dependent kinase 9 (CDK9) in patients with PTC.This prospective observational study included 192 patients with PTC, who visited our hospital between August 2018 and February 2020. We obtained 93 tissue samples from patients with benign thyroid disease during the same period as controls. Immunohistochemical evaluation and reverse transcription-quantitative polymerase chain reaction assay were performed to evaluate CDK9 expression. Patients' demographic and clinical characteristics were analyzed.Delphian lymph node (DLN) metastasis in patients with PTC was associated with clinicopathological characteristics. CDK9 expression was up-regulated in patients with PTC, and those with DLN metastasis showed higher CDK9 expression. We also observed that tumor size, capsule invasion, tumor-node-metastasis classification (TNM) stage, and multifocality were the risk factors for DLN metastasis in patients with PTC. Additionally, CDK9 expression was strongly associated with tumor size, capsule invasion, TNM stage, and multifocality and weakly associated with the number of metastatic DLN.CDK9 is up-regulated in patients with PTC and associated with prognosis in these patients.Abbreviations: BTD = benign thyroid disease, CDK9 = cyclin-dependent kinase 9, DLN = Delphian lymph node, LN = lymph node, PTC = papillary thyroid carcinoma, RT-qPCR = reverse transcription-quantitative polymerase chain reaction.
Pleomorphic adenomas (PAs) are the most common benign salivary neoplasms. PAs are generally slow-growing but may sometimes become aggressive and grow rapidly within a short period of time. Here, we report the case of an 83-year-old Chinese woman with an anterior neck mass that had been growing over the past 30 years. She felt uncomfortable because the mass had grown quite rapidly in the past year. The final diagnosis of a PA of the left submandibular gland was confirmed by histopathological and immunohistochemical examinations after surgical resection. Our patient recalled a history of an excision of a neck mass 40 years prior to presentation at another hospital. Based on our imaging findings and surgical findings, we speculate that the neck mass 40 years prior may also have been a PA. Our case reminds us the rare recurrence possibility of PAs, and early and thorough resection may have a good prognosis. In addition, to the best of our knowledge, this is the largest PA of the submandibular gland reported to date.
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