scholarly journals Long Non-Coding RNA DANCR Participates in the Regulation of Dexamethasone and Inflammation Factors on hASC Proliferation and Migration

2021 ◽  
Author(s):  
Ran Yan ◽  
Ping Dong ◽  
Zhigang Yang ◽  
Rui Cao ◽  
Xia Liu ◽  
...  
Keyword(s):  
Cell Counting ◽  
Inflammatory Factors ◽  
Dependent Manner ◽  
Migration Ability ◽  
Non Coding Rna ◽  
Tnf Α ◽  
The Mean ◽  
And Migration ◽  
Long Non Coding Rna ◽  
Proliferation And Migration

Abstract BackgroundBoth MSC and Dexamethasone are effective methods to treat inflammatory diseases, and they are likely to be used in combination. The proliferation and migration ability is one of the main biological characteristics of MSC for repairing. However, the effect of inflammatory factors and Dex on these characteristics of MSC has not been fully understood. Therefore, this study aimed to determine the role of lncRNA DANCR in hASC proliferation and migration regulation induced by Dex and inflammatory factors, to clarify the effect and mechanism of glucocorticoids on MSC's characteristics to participate in tissue repair in an inflammatory environment. MethodshASCs were cultured and treated with dexamethasone and inflammation factors, and cell proliferation, migration abilities, and lncRNA DANCR mRNA expression were detected. Additionally, to determine the roles and mechanisms, lncRNA DANCR was knockdown or overexpressed before Dex or TNF-α treatments. MSC proliferation was tested by cell counting kit-8 and cell cycle assay. MSC migration ability was analyzed by a scratching test. Moreover, proliferation and migration-related genes were measured by a reverse transcription-polymerase chain reaction. Nuclear factor-kB (NF-κB) and PI3K-AKT-mTOR pathway proteins were investigated by western blot analysis. All values are expressed as the mean ± standard error of the mean. The differences between the groups were assessed using a two-tailed Student’s t-test. ResultsDex decreased the proliferation and migration of hASC in a dose-dependent manner. Dex could upregulate the expression of lncRNA DANCR that inhibited hASC proliferation and migration. Knockdown of DANCR reversed the inhibition of hASC proliferation and migration induced by Dex. Moreover, DANCR was decreased by inflammatory cytokines, and overexpression of DANCR alleviated the promotion of hASC proliferation and migration induced by TNF-α. Furthermore, mechanistic investigation validated that DANCR was involved in the NF-κB signaling pathway. ConclusionsWe identified a lncRNA, DANCR, involved in Dex and inflammation-affected hASC proliferation and migration, thus suggesting that concurrent application of hASCs with steroids should be avoided in clinical settings. DANCR may serve as a promising approach to regulate stem cell characteristics under an inflamed microenvironment. These findings further enrich our understanding of the functional versatility of lncRNAs in the crosstalk of inflammation conditions and stem cells. Keywords： DANCR; long non-coding RNA; Dexamethasone; TNF-α; hASC; proliferation; migration

Scutellarin combined with Lidocaine: a new combination of anti-glioma drugs

2021 ◽  
Author(s):  
Xiu-Ying He ◽  
Xiao-Ming Zhao ◽  
Qing-Jie Xia ◽  
Lei Zhou ◽  
Ting-Hua Wang
Keyword(s):  
Glioma Cells ◽  
Cell Counting ◽  
New Combination ◽  
Dependent Manner ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Migration Ability ◽  
Egfr Expression ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Glioma is the most common primary intracranial tumors. Although great achievements in the treatment have been made, the efficacy is still not satisfactory, which imposes a great burden on patients and society. Therefore, the exploration of new and effective anti-glioma drugs is urgent. Methods Human glioma cells U251 and LN229 cells were included in the study. The proliferation was detected by cell counting kit-8, plate clone formation assay, EdU incorporation assay and xCELLigence real-time cell analyzer. The cell apoptosis was evaluated by TUNEL assay and flow cytometry. The transwell assay was for assessing the migration. Moreover, Western blot was performed to detect the protein level of Epidermal growth factor receptor (EGFR). Results In present study, we found that Scutellarin(SCU) and Lidocaine suppressed the proliferation and migration, and induced the apoptosis of human glioma cells, including U251 and LN229 cells, in a dose-dependent manner. Moreover, the combination of Scutellarin and Lidocaine further restrained the proliferation and migration ability of U251 and LN229 cells, while induced their apoptosis. Mechanistically, the effect of Scutellarin and its combination with Lidocaine on glioma cells was partially associated with the downregulation of EGFR protein. Conclusions Scutellarin and Lidocaine exert a synergistic effect on suppressing the proliferation and migration and induce the apoptosis of glioma cells partly via repressing the EGFR expression.

scholarly journals Downregulated hsa_circ_005243 induced trophoblast cell dysfunction and inflammation via β-catenin and NF-κB pathways in gestational diabetes mellitus

2020 ◽  
Author(s):  
Huiyan Wang ◽  
Wenbo Zhou ◽  
Guangtong She ◽  
Bin Yu ◽  
Lizhou Sun
Keyword(s):  
Diabetes Mellitus ◽  
Cell Proliferation ◽  
Gestational Diabetes ◽  
Pregnant Women ◽  
Inflammatory Factors ◽  
Migration Ability ◽  
Cell Proliferation And Migration ◽  
Tnf Α ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background: Gestational diabetes mellitus(GDM) is a common obstetric pregnancy complication, which poses a serious threat to the health of pregnant women and newborns. The specific etiology and pathogenesis of this disease have not been fully clarified, it is reported to be related with insulin resistance, inflammatory response and genetic factors etc. Circular RNA(circRNA) is a special kind of non-coding RNA, which have been attracted much attention in recent years. It has been reported that circRNAs may play a regulatory role in pregnancy-related diseases, including GDM. Methods: Previously we reported a circRNA, hsa_circ_005243, which was identified by RNA-sequencing. In this study we detected its expression in 20 GDM pregnant women and 20 normal controls using quantitative reverse transcription polymerase chain reaction analysis. Further in vitro experiments were conducted after hsa_circ_005243 knockdown in HTR8-S/Vneo cells, cell proliferation and migration ability was tested, the secretion of inflammatory factors (TNF-α and IL-6) were detected by ELISA. Then we detected the expression of β-catenin and increased nuclear factor kappa-B (NF-κB) signaling pathways which was related to GDM in the mechanism study. Results: We found the expression of hsa_circ_005243 was significantly reduced both in the placenta and plasma of GDM pregnant women. Knockdown of hsa_circ_005243 in trophoblast cells significantly suppressed cell proliferation and migration ability. In addition, increased secretion of inflammatory factors (TNF-α and IL-6) were observed after hsa_circ_005243 depletion. Further mechanism experiments showed that knockdown of hsa_circ_005243 reduced the expression of β-catenin and increased nuclear NF-κB p65 nuclear translocation. Conclusions: Collectively, our study showed that down-regulation of hsa_circ_005243 might be associated with the pathogenesis of GDM through regulating β-catenin and NF-κB signal pathways and suggest a new potential therapeutic target for GDM.

scholarly journals Down-regulated LncR-MALAT1 suppressed cell proliferation and migration by inactivating autophagy in bladder cancer

RSC Advances ◽  
2018 ◽  
Vol 8 (54) ◽  
pp. 31019-31027
Author(s):  
Jiude Qi ◽  
Yanfeng Chu ◽  
Guangyan Zhang ◽  
Hongjun Li ◽  
Dongdong Yang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Lung Adenocarcinoma ◽  
Tumor Cells ◽  
Cell Proliferation And Migration ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna ◽  
Proliferation And Migration

Long non-coding RNA-metastasis-associated lung adenocarcinoma transcript (LncR-MALAT) is highly expressed in a variety of tumors, which can affect the progression of tumor cells.

scholarly journals Long non-coding RNA LINC00152 regulates cell proliferation and migration by epigenetically repressing LRIG1 expression in cholangiocarcinoma

2020 ◽  
Author(s):  
Ni Wang ◽  
Yang Yu ◽  
Boming Xu ◽  
Chunmei Zhang ◽  
Jie Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Biological Function ◽  
Rna Seq ◽  
Normal Tissues ◽  
Qrt Pcr ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna ◽  
Proliferation And Migration

Abstract Background: Recently, long non-coding RNAs (lncRNAs) have been verified to have significant regulatory roles in multiple human cancer processes. Long non-coding RNA LINC00152, located on chromosome 2p11.2, was identified as an oncogenic lncRNA in various cancers. However, the biological function and molecular mechanism of LINC00152 in cholangiocarcinoma (CCA) are still unknown.Methods: Bioinformatic analysis was performed to determine LINC00152 expression levels in the CCA and normal tissues by using raw microarray data downloaded from Gene Expression Omnibus (GSE76297) and The Cancer Genome Atlas (TCGA). Quantitative reverse transcription PCR (qRT-PCR) was used to validate LINC00152 expression in the CCA tissues compared with that in the paired normal tissues. CCK8, colony formation, Edu assays, transwell assays, flow cytometry, and in vivo tumor formation assays were performed to investigate the biological function of LINC00152 on CCA cell phenotypes. RNA-seq was carried out to identify the downstream target gene which was further examined by qRT-PCR, western bolt and rescue experiments. RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assays were performed to reveal the factors involved in the mechanism of LINC00152 functions in CCA.Results: LINC00152 is significantly upregulated in cholangiocarcinoma. LINC00152 regulated the proliferation and migration of cholangiocarcinoma cells both in vitro and in vivo. RNA-seq revealed that LINC00152 knockdown preferentially affected genes linked with cell proliferation, cell differentiation and cell adhesion. Furthermore, mechanistic investigation validated that LINC00152 could bind EZH2 and modulate the histone methylation of promoter of leucine rich repeats and immunoglobulin like domains 1 (LRIG1), thereby affecting cholangiocarcinoma cells growth and migration.Conclusion: Taken together, these results demonstrated the significant roles of LINC00152 in cholangiocarcinoma and suggested a new diagnostic and therapeutic direction of cholangiocarcinoma.

scholarly journals Long Non-coding RNA X-Inactive Specific Transcript Mediates Cell Proliferation and Intrusion by Modulating the miR-497/Bcl-w Axis in Extranodal Natural Killer/T-cell Lymphoma

2020 ◽  
Vol 8 ◽  
Author(s):  
Qinhua Liu ◽  
Ruonan Ran ◽  
Zhengsheng Wu ◽  
Xiaodan Li ◽  
Qingshu Zeng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Natural Killer T Cell ◽  
Cell Proliferation And Migration ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna ◽  
Killer T Cell ◽  
Proliferation And Migration

The present study was directed toward laying new findings for Extranodal natural killer/T-cell lymphoma (ENKL)-oriented therapy with a focus on long non-coding RNA (lncRNA)–microRNAs (miRNAs)–mRNA interaction. The expression and function of XIST (X-inactive specific transcript) were analyzed both in vivo and in vitro. The online database of lncRNA-miRNA interaction was used to screen the target of XIST, and miR-497 was selected. Next, the predicted binding between XIST and miR-497, and the dynamic effect of XIST and miR-497 on downstream Bcl-w was evaluated. We found that XIST dramatically increased in the blood of ENKL patients and cell lines. XIST knockdown suppressed the cell proliferation and migration in vivo and in vitro. Herein, we confirmed the negative interaction between XIST and miR-497. Moreover, XIST knockdown reduced the protein levels of Bcl-w, a downstream target of miR-497. XIST sponges miR-497 to promote Bcl-w expression, and finally modulating ENKL cell proliferation and migration. To be interested, inhibition of Bcl-w by ABT737 can overcome the high expression of XIST, and suppressed the ENKL proliferation and migration by inducing apoptosis. This study provided a novel experimental basis for ENKL-oriented therapy with a focus on the lncRNA–miRNA–mRNA interaction.

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