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Increased proliferation and migration of abnormal airway smooth muscle cells (ASMCs) are significantly associated with asthma. Recently, the function of long non-coding RNAs (lncRNAs) in ASMCs has been identified. Our research attempted to resolve the function of the lncRNA DGCR5 in ASMCs and focus on its in-depth mechanisms of proliferation and migration. Quantitative real-time PCR and western blotting were used to evaluate the expressions of RNA and proteins, respectively. The CCK-8 assay was used to detect cell proliferation. Transwell assays were used to assess migration. Luciferase and RNA pull-down assays were used to verify the targeting between miR-204-5p and lncRNA DGCR5 or SRSF7. LncRNA DGCR5 was upregulated in ASMCs stimulated with PDGF-BB. Knockdown of DGCR5 reversed the effect of platelet-derived growth factor BB (PDGF-BB) on the proliferation and migration of ASMCs. The results of this study showed that lncRNA DGCR5 binds to miR-204-5p, and SRSF7 is the target of miR-204-5p. Rescue experiments verified the interaction between miR-204-5p and DGCR5, as well as that between miR-204-5p and SRSF7. Overall, this study revealed that the lncRNA DGCR5/miR-204-5p/SRSF7 signalling axis has key regulatory effects on the proliferation and migration of ASMCs.

Increased proliferation and migration of abnormal airway smooth muscle cells (ASMCs) are significantly associated with asthma. Recently, the function of long non-coding RNAs (lncRNAs) in ASMCs has been identified. Our research attempted to resolve the function of the lncRNA DGCR5 in ASMCs and focus on its in-depth mechanisms of proliferation and migration. Quantitative real-time PCR and western blotting were used to evaluate the expressions of RNA and proteins, respectively. The CCK-8 assay was used to detect cell proliferation. Transwell assays were used to assess migration. Luciferase and RNA pull-down assays were used to verify the targeting between miR-204-5p and lncRNA DGCR5 or SRSF7. LncRNA DGCR5 was upregulated in ASMCs stimulated with PDGF-BB. Knockdown of DGCR5 reversed the effect of platelet-derived growth factor BB (PDGF-BB) on the proliferation and migration of ASMCs. The results of this study showed that lncRNA DGCR5 binds to miR-204-5p, and SRSF7 is the target of miR-204-5p. Rescue experiments verified the interaction between miR-204-5p and DGCR5, as well as that between miR-204-5p and SRSF7. Overall, this study revealed that the lncRNA DGCR5/miR-204-5p/SRSF7 signalling axis has key regulatory effects on the proliferation and migration of ASMCs. [ABSTRACT FROM AUTHOR]

Objective: To investigate the expression of lncRNA DGCR5 in non-small cell lung cancer (NSCLC) and its correlation with clinicopathological features. Methods: 86 patients with NSCLC who were treated surgically in the oncology department of our hospital from January 2020 to December 2021 were selected, and tumor and non tumor lung cancer tissue samples were obtained from the patients during the operation. The expression level of lncRNA DGCR5 in tumor tissues and adjacent tissues was determined by qRT PCR. To analyze the relationship between the expression level of lncRNA DGCR5 and the clinicopathological parameters of NSCLC patients, such as gender, age, clinical stage, T stage, N stage, etc. The relationship between the expression level of lncRNA DGCR5 and the prognosis of patients with total survival (OS) and progression free survival (PFS). Results: Compared with the adjacent tissues, the expression level of lncRNA DGCR5 in NSCLC tumor tissues was relatively low, and the difference was statistically significant (P<0.01). The expression of lncRNA DGCR5 was significantly correlated with tumor differentiation, TNM stage, tumor volume, lymphatic metastasis and distant metastasis (P<0.05). Kaplan Meier method was used for survival analysis. It was found that the median OS and DFS in the high expression group of lncRNA DGCR5 were significantly higher than those in the low expression group of lncRNA DGCR5 (P<0. 05). Low differentiation, clinical stage of II+IIIa, N1-N3 lymphatic metastasis, distant metastasis, and low expression of lncRNA DGCR5 were all related to the overall survival rate and progression free survival rate of NSCLC patients. Conclusion: The expression of LncRNA DGCR5 in tumor tissues of NSCLC patients is decreased. The expression level of LncRNA DGCR5 in blood of NSCLC patients is correlated with the degree of differentiation, TNM stage, lymphatic metastasis, distant metastasis and prognosis. LncRNA DGCR5 can be used as a new biomarker for early diagnosis and treatment of NSCLC. [ABSTRACT FROM AUTHOR]

Bin Li,1 Zhirui Guo,2 Quan Liang,1 Huiling Zhou,3 Yanping Luo,4 Shuyun He,2 Zhe Lin1 1Department of Urology, The First Peoples’ Hospital of Foshan, Foshan City, Guangdong Province 528000, People’s Republic of China; 2Department of Radiology, The First Peoples’ Hospital of Foshan, Foshan City, Guangdong Province 528000, People’s Republic of China; 3Department of Infectious Disease, The First Peoples’ Hospital of Foshan, Foshan City, Guangdong Province 528000, People’s Republic of China; 4Department of Anesthesiology Surgery, The First Peoples’ Hospital of Foshan, Foshan City, Guangdong Province 528000, People’s Republic of ChinaCorrespondence: Zhe LinDepartment of Urology, The First Peoples’ Hospital of Foshan, Foshan City, Guangdong Province 528000, People’s Republic of ChinaEmail 18038866138@163.comBackground: Long non-coding RNA (lncRNA) DiGeorge syndrome critical region gene 5 (DGCR5) plays different roles in different types of human cancer, but its role in prostate cancer (PC) has not been reported.Methods: DGCR5 and TGF-β1 expression in paired tumor and adjacent healthy tissues from 64 PC patients was analyzed by performing RT-qPCR. A 5-year follow-up study was performed to analyze the prognostic value of DGCR5 for PC. The interaction between DGCR5 and TGF-β1 was analyzed by overexpression experiments. Cell stemness was analyzed by cell stemness assay.Results: In our study, we found that DGCR5 was down-regulated in tumor tissues than in adjacent healthy tissues of PC patients, but TGF-β1 was up-regulated in the tumor tissues. DGCR5 expression was not affected by clinical stages, but low DGCR5 level in the tumor was correlated with poor survival. DGCR5 and TGF-β1 were inversely correlated in tumor tissues but not in adjacent healthy tissues. DGCR5 over-expression resulted in down-regulation of TGF-β1, while TGF-β1 treatment did not significantly affect DGCR5 expression. DGCR5 over-expression led to decreased stemness of PC cells, but TGF-β1 treatment played a reverse role and attenuated the effects of DGCR5 over-expression. DGCR5 may decrease the stemness of PC cells by down-regulating TGF-β1.Keywords: prostate cancer, lncRNA DGCR5, TGF-β1, stemness

Glioma is one of the most commonly diagnosed brain malignancies with a high cancer-related death rate in humans. The prognosis of glioma patients is still unsatisfactory. In the present study, we attempted to identify lncRNAs and miRNAs that might be related to NF-κB-mediated epithelial-mesenchymal transition in glioma cells based on online microarray expression profiles, and investigate the specific effects of lncRNA-miRNA-mRNA axes on glioma cell phenotypes. Herein, we identified lncRNA DGCR5 as a downregulated lncRNA in glioma that was negatively regulated by NF-κB1 in an NF-κB1 RE-dependent manner. LncRNA DGCR5 overexpression significantly inhibited the capacity of glioma cells to proliferate, migrate, and invade, whereas promoted the apoptosis of glioma cells. Moreover, lncRNA DGCR5 overexpression upregulated the epithelial marker E-cadherin while downregulating the mesenchymal marker VIM, as well as Snai2 and TWIST. Regarding the underlying molecular mechanisms, lncRNA DGCR5 could inhibit miR-21 and miR-23a expression, and miR-21 or miR-23a overexpression significantly reversed the tumor-suppressive effects of lncRNA DGCR5 overexpression. LncRNA DGCR5 exerted its tumor-suppressive effects through the DGCR5/miR-21/Smad7 and DGCR5/miR-23a/PTEN axes. In conclusion, lncRNA DGCR5 suppresses the capacity of glioma cells to migrate and invade via miR-21/Smad7, whereas it inhibits the proliferation and enhances the apoptosis of glioma cells through miR-23a/PTEN.