Hepatocellular carcinoma (HCC) is an invasive malignant tumour and the second major cause of cancer‐related deaths over the world. CRNDE and miR‐217 are non‐coding RNAs which play critical roles in cell growth, proliferation, migration. Mitogen‐activated protein kinase 1 (MAPK1) also participates in cancer cell process. Hence, this study aimed at investigating the effect of CRNDE on migration and invasion of HCC and figuring out the role of miR‐217 and MAPK1 in this process. The overexpression of CRNDE was demonstrated by a microarray‐based lncRNA profiling study. CRNDE expression in HCC was verified by qRT‐PCR. MTT assay and BrdU staining were applied to detect cell proliferation level. Transwell assay was utilized to examine cell migration and invasiveness abilities. Wound healing assay was performed for further exploration of cell migration capacity. MiR‐217 was predicted by bioinformatics. The dual luciferase reporter assay was performed to corroborate the targeting relationship between CRNDE, miR‐217 and MAPK1. MAPK1, the downstream target of miR‐217, was predicted using bioinformatics and was further confirmed by qRT‐PCR and Western blot. The interaction between CRNDE, miR‐217 and MAPK1 was studied by qRT‐PCR, Western blot, MTT, BrdU, transwell assay and wound healing assay. CRNDE was up‐regulated in HCC tissues and HCC cell lines. The high expression of CRNDE facilitated cell proliferation, migration and invasion, while the inhibited one affected on the contrary. MiR‐217, negatively correlated with CRNDE expression, was the target of CRNDE and was more lowly expressed in HCC. With the high expression of miR‐217, HCC cell proliferation, migration and invasion were suppressed. MAPK1, the possible target of miR‐217, was negatively correlated with miR‐217 but positively correlated with CRNDE and had the same effect in HCC formation process as CRNDE. Long non‐coding RNA CRNDE promotes the proliferation, migration and invasion of HCC cells through miR‐217/MAPK1 axis.

Hepatocellular carcinoma (HCC) is a main cause of cancer‐related deaths globally. Long non‐coding RNAs (lncRNAs) play important roles in diverse cancers. Our previous microarray‐based lncRNA profiling showed that LINC00467 was highly expressed in HCC. Here, we further explored the expression, role and functional mechanism of lncRNA LINC00467 in HCC. Our findings revealed that LINC00467 was up‐regulated in HCC tissues and HCC cell lines. Increased expression of LINC00467 was positively associated with tumour size and vascular invasion. In vitro functional experiments revealed that LINC00467 accelerated HCC cell proliferation, cell cycle progression and migration and reduced HCC cell apoptosis. In vivo functional assays revealed that LINC00467 drove HCC xenograft growth and HCC cell proliferation and repressed HCC cell apoptosis in vivo. Moreover, LINC00467 inhibited NR4A3 post‐transcriptionally via interacting with NR4A3 mRNA to form double‐stranded RNA, which was further degraded by Dicer. The expression of NR4A3 was inversely associated with LINC00467 in HCC tissues. Functional rescue assays found that restore of NR4A3 expression blocked the oncogenic roles of LINC00467 in HCC. Taken together, our results demonstrated that lncRNA LINC00467 was a novel highly expressed and oncogenic lncRNA in HCC via inhibiting NR4A3. Targeting LINC00467 or enhancing NR4A3 may be potential therapeutic strategies against HCC.

Background At present, the coronavirus disease 2019 (COVID-19) is spreading all over the world. The occurrence of spontaneous pneumothorax in these patients might be higher than the fact, and we should pay high clinical attention to them. Method Data regarding clinical investigation, laboratory investigation, diagnosis, and treatment measures of 21 COVID-19 patients with spontaneous pneumothorax from January to March of 2020 were collected and analyzed in this study. Results Seven patients had a history of basic lung diseases. All patients used different methods of oxygen therapy before the occurrence of spontaneous pneumothorax according to the severity of the COVID-19, including 18 patients with ventilator-assisted breathing, 2 patients with bilevel positive airway pressure assisted breathing, and 1 patient with mask oxygen inhalation. All patients were confirmed cases of COVID-19 by chest CT (computed tomography) and virus nucleic acid detection and were found to have spontaneous pneumothorax through physical examination, bedside X-ray, and/or bedside ultrasound. 13 of 21 patients combined with pleural effusion at the same time. All the patients underwent closed thoracic drainage for spontaneous pneumothorax and the pleural effusion, if any. Nine patients died, and 12 patients recovered smoothly. Conclusion Spontaneous pneumothorax might be an overlooked complication of COVID-19 patients and may be associated with poor prognosis.