The circular RNA ciRS-7 has been reported to be involved in the pathogenesis of various tumors, including gastric and colorectal cancer. However, the role of ciRS-7 in esophageal squamous cell carcinoma (ESCC) remains unsolved. In this study, we found that the ciRS-7 expression was significantly upregulated in ESCC cancer tissues compared with matched normal tissues and associated with poor patient survival. Overexpression of ciRS-7 abrogated the tumor-suppressive roles of miR-7 including cell proliferation, migration and invasion in vitro as well as tumor growth and lung metastasis in vivo. Mechanistically, ciRS-7 functioned as the sponge of miR-7 and reactivated its downstream HOXB13-mediated NF-κB/p65 pathway. Conclusively, our findings demonstrate how ciRS-7 induces malignant progression of ESCC and that ciRS-7 may act as a novel prognostic marker and therapeutic target for this lethal disease.

The long non-coding RNA (lncRNA) NKILA (nuclear transcription factor NF-κB interacting lncRNA) functions as a suppressor in human breast cancer and tongue cancer. However, the clinical significance and biological roles of NKILA in esophageal squamous cell carcinoma (ESCC) remain unknown. In this study, we showed that NKILA was downregulated in ESCC tissues and cancer cells compared with their normal counterparts. Low NKILA expression correlated with large tumor size and advanced TNM stage, and predicted poor overall and disease-free survival of ESCC patients. Further loss- and gain-of-function assays indicated that NKILA inhibited proliferation and migration of ESCC cells in vitro, suppressed tumor growth and lung metastasis in vivo. Mechanistically, NKILA could inhibit phosphorylation of IκBα, suppress p65 nuclear translocation and downregulate the expression of NF-κB target genes in ESCC cells. These results suggest NKILA could suppress malignant development of ESCC via abrogation of the NF-κB signaling and may potentially serve as a prognostic marker for ESCC.

Administration of ginsenoside Rg1 enhances the resistance of HSC/HPCs to ionizing radiation-induced senescence in mice by inhibiting the oxidative stress reaction, reducing DNA damage, and regulating the cell cycle.

Satisfactory outcome was observed in one mild case and one severe case of COVID-19 pneumonia after the use of the online/offline multidisciplinary quarantine observation form, online monitoring, and classified diagnosis and treatment, as well as strict compliance with quarantine measures. Conditions of both patients were improved, and cross-infection and disease onset clustering were not observed. The multidisciplinary selfquarantine model provides early judgment, identification, and treatment of disease, improves compliance with early rehabilitation, increases confidence in recovery, and enhances self-management capabilities. This model is applicable to the current novel coronavirus pneumonia epidemic and can actively promote the management of suspected or confirmed mild cases, monitoring of critical cases, and self-management of discharged patients. The application of this new management model is worthy of being promoted in our specialized treatment facilities and in countries with severe epidemics.

MicroRNAs (miRNAs) are a class of small non-coding RNAs approximately 18-22 nucleotides in length, which play an important role in malignant transformation. The roles of miR-192 as an oncogene or tumor suppressor in solid tumors have been previously reported. However, little is known about the role of miR-192 in human acute myeloid leukemia. The results of the present study indicate that miR-192 is significantly downregulated in specimens from acute myeloid leukemia patients. Functional assays demonstrated that overexpression of miR-192 in NB4 and HL-60 cells significantly inhibited cell proliferation compared with that in control cells, and induced G0/G1 cell cycle arrest, cell differentiation, and apoptosis in vitro. Dual-luciferase reporter gene assays showed that miR-192 significantly suppressed the activity of a reporter gene containing the wild type 3'-UTR of CCNT2, but it did not suppress the activity of a reporter gene containing mutated 3'-UTR of CCNT2. QRT-PCR and Western blot assays showed that miR-192 significantly downregulated the expression of CCNT2 in human leukemia cells. Exogenous expression of CCNT2 attenuated the cell cycle arrest induced by miR-192 in NB4 and HL-60 cells. Collectively, miR-192 inhibits cell proliferation and induces G0/G1 cell cycle arrest in AML by regulating the expression of CCNT2.

Background Accumulating evidence highlights the critical roles of fibroblast growth factors (FGFs) in regulating the progression of multiple human cancers, including non-small cell lung cancer (NSCLC). In this study, we investigated the role of FGF11 in the progression of NSCLC. Methods Previously published transcriptomic data (GSE75037 and GSE81089) were used to compare FGF11 expression level between NSCLC tumor tissues and adjacent normal tissues. 100 cases of NSCLC tumor tissues and 30 cases of matched adjacent normal tissues were used to validate FGF11 expression at mRNA and protein level by qPCR and immunohistochemistry. Bioinformatics analysis and dual luciferase reporter analysis were performed to confirm the regulatory effect of miR-525-5p on FGF11 expression. CCK-8 assay and transwell migration assay were employed to examine cellular proliferation, migration and invasion. Gene set enrichment analysis (GSEA) was performed to identify the signaling pathway associated with FGF11 expression. Finally, the functional role of FGF11 in NSCLC tumor growth was evaluated by in vivo study. Results FGF11 was upregulated in NSCLC tumor tissues and tumor cell lines. High FGF11 expression was associated with a poor prognosis in NSCLC patients. In vitro loss- and gain-of function experiments demonstrated that FGF11 knockdown inhibited, whereas FGF11 overexpression promoted the proliferation, migration and invasion of NSCLC cells. Dual luciferase reporter assay confirmed that FGF11 was downregulated by miR-525-5p, and the effect of FGF11 on cell proliferation, migration and invasion could be interfered by miR-525-5p. GSEA analysis further revealed that FGF11 expression was enriched with genes in hypoxia signaling pathway and the oncogenic function of FGF11 could be suppressed by knocking down HIF-1α in NSCLC cells. Moreover, FGF11 knockdown suppressed NSCLC tumor growth whereas FGF11 overexpression promoted tumor growth in vivo. Conclusions Our study showed that FGF11 functions as an oncogene in tumor NSCLC progression. miR-525-5p seems to negatively regulate FGF11 and the oncogenic role of FGF11 is dependent on the upregulation of HIF-1α. Our study suggests that targeting FGF11 and HIF-1α may serve as novel strategies for the treatment of NSCLC.

Background: The aim of the present study was to investigate the effect of over-expressing circular RNA (circ_0003645) on cell functions and its molecular mechanism in breast cancer. Methods: The expression profile of circ_0003645, breast cancer cell lines, and the transcription levels of circular RNA, miRNA and HMGB1 gene were detected by qRT-PCR. Flow cytometry analysis was manipulated to evaluate cancer cell proliferation and cell apoptosis. The correlation between miR-139p-3p and circular_0003645 or HMGB1 was predicted by GEO, and TCGA was confirmed using the dual-luciferase reporter assay. Results: Circ_0003645 expression was conspicuously increased in both the breast cancer tissues and cell lines. Circ_0003645 knockdown inhibited cell proliferation and induced the apoptosis of breast cancer cells in vitro and in vivo. By sponging miR-139-3p, circ_0003645 promoted the breast cancer cells progression and positively regulated HMGB1 gene. Conclusion: Circ_0003645 functions as a ceRNA for miR-139-3p, which could upregulate HMGB1 and further promote cell proliferation in breast cancer.

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