Long intergenic non-coding RNA 1939 inhibits proliferation and migration of human renal cell carcinoma (RCC) cells by down-regulation of miR-154

Abstract Background: Renal carcinoma (RCC) is widely accepted as a malignant tumor of urinary system. Long intergenic non-coding RNA 1939 (LINC01939) is a novel lncRNA which was found to be down-regulated in RCC. Thus, we set out to explore the effect and regulation mechanism of LINC01939 in RCC. Methods: LINC01939 and miR-154 in RCC tissues and cell lines were detected using qRT-PCR assay. Cell counting kit-8 (CCK-8) assays was exploited to examine cell viability. Flow cytometric analysis was conducted to examine apoptosis. Cell mobility was valued through wound healing assays. Western blotting was applied for examination of proteins related to proliferation, apoptosis, migration and Wnt/β-catenin/Notch. Results: LINC01939 was down-regulated in RCC tissues. LINC01939 overexpression impeded proliferation and migration, and induced apoptosis. Further study found that the overexpression of LINC01939 strongly suppressed miR-154 expression. Then, the inhibiting effect of overexpressed LINC01939 on proliferation and mobility and the promoting role of LINC01939 in apoptosis were abolished by the combination of miR-154 mimic. Finally, we found that the overexpressed LINC01939 inactivated Wnt/β-catenin and Notch through suppressing miR-154. Conclusion: The up-regulation of LINC01939 inhibited proliferation and migration of RCC cells by down-regulating miR-154.

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Long intergenic non-coding RNA 1939 inhibits proliferation and migration of human renal cell carcinoma (RCC) cells by down-regulation of miR-154

10.21203/rs.2.10547/v2 ◽

2020 ◽

Author(s):

Rongyuan Zhang ◽

Yuhua Huang ◽

Baocai Xu ◽

Chuan Lv ◽

Jianquan Hou ◽

...

Keyword(s):

Renal Cell Carcinoma ◽

Cell Carcinoma ◽

Renal Cell ◽

Down Regulation ◽

Human Renal Cell Carcinoma ◽

Non Coding Rna ◽

And Migration ◽

Journal Submission ◽

Proliferation And Migration

Abstract The authors have withdrawn the journal submission associated with this preprint and requested that the preprint also be withdrawn.

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The role of RelA (p65) threonine 505 phosphorylation in the regulation of cell growth, survival, and migration

Molecular Biology of the Cell ◽

10.1091/mbc.e11-04-0280 ◽

2011 ◽

Vol 22 (17) ◽

pp. 3032-3040 ◽

Cited By ~ 27

Author(s):

Aichi Msaki ◽

Ana M. Sánchez ◽

Li Fang Koh ◽

Benjamin Barré ◽

Sonia Rocha ◽

...

Keyword(s):

Inflammatory Responses ◽

Cellular Migration ◽

Negative Regulator ◽

Drug Induced ◽

Conserved Residues ◽

Cellular Processes ◽

And Migration ◽

Induced Apoptosis ◽

Proliferation And Migration

The NF-κB family of transcription factors is a well-established regulator of the immune and inflammatory responses and also plays a key role in other cellular processes, including cell death, proliferation, and migration. Conserved residues in the trans-activation domain of RelA, which can be posttranslationally modified, regulate divergent NF-κB functions in response to different cellular stimuli. Using rela−/−mouse embryonic fibroblasts reconstituted with RelA, we find that mutation of the threonine 505 (T505) phospho site to alanine has wide-ranging effects on NF-κB function. These include previously described effects on chemotherapeutic drug-induced apoptosis, as well as new roles for this modification in autophagy, cell proliferation, and migration. This last effect was associated with alterations in the actin cytoskeleton and expression of cellular migration–associated genes such as WAVE3 and α-actinin 4. We also define a new component of cisplatin-induced, RelA T505–dependent apoptosis, involving induction of NOXA gene expression, an effect explained at least in part through induction of the p53 homologue, p73. Therefore, in contrast to other RelA phosphorylation events, which positively regulate NF-κB function, we identified RelA T505 phosphorylation as a negative regulator of its ability to induce diverse cellular processes such as apoptosis, autophagy, proliferation, and migration.

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Role of LRG1 in the Cell Proliferation, Migration, and Prognosis of Pancreatic Cancer

10.21203/rs.3.rs-733520/v1 ◽

2021 ◽

Author(s):

Jie Hua ◽

Qingcai Meng ◽

Chen Liang ◽

Miaoyan Wei ◽

Jiang Liu ◽

...

Keyword(s):

Pancreatic Cancer ◽

Cell Proliferation ◽

Rna Sequencing ◽

Cell Counting ◽

Enzyme Linked Immunosorbent Assay ◽

Cell Proliferation And Migration ◽

And Migration ◽

Proliferation And Migration

Abstract Background: The aim of this study was to explore the role of leucine-rich α2-glycoprotein 1 (LRG1) in the biological function and prognosis of pancreatic cancer.Methods: LRG1 was detected in serum and tissue specimens from patients with pancreatic cancer by enzyme-linked immunosorbent assay (ELISA), qRT-PCR, western blotting, and immunohistochemical (IHC) analysis. LRG1-overexpressing and LRG1-knockdown cell lines were established with lentiviral vectors containing LRG1-overexpression and shRNA plasmids, respectively. Colony formation, Cell Counting Kit-8 (CCK-8), wound healing, Transwell migration, and in vivo tumorigenicity assays were conducted to assess proliferation and migration of the pancreatic cancer cells. RNA sequencing was performed to identify potential downstream molecules of LRG1.Results: Serum LRG1 levels were significantly elevated in patients with pancreatic cancer compared with healthy controls. The mRNA and protein levels of LRG1 were higher in cancer tissues than in adjacent normal tissues. High LRG1 expression was significantly associated with shorter overall survival and found to be an independent risk factor for poor prognosis. Additionally, LRG1 dramatically promoted cell proliferation and migration in vitro and accelerated tumor growth in vivo. By RNA sequencing, we identified Deltex (DTX)-3-like E3 ubiquitin ligase (DTX3L) as a potential downstream molecule of LRG1. Further validation experiments confirmed a positive correlation between LRG1 and DTX3L.Conclusions: LRG1 is a valuable prognostic marker for pancreatic cancer that plays a crucial role in cell proliferation and migration. Targeting LRG1 or the downstream molecule DTX3L provides a novel strategy for the treatment of pancreatic cancer.

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MicroRNA-222 promotes the proliferation and migration of cervical cancer cells

Clinical & Investigative Medicine ◽

10.25011/cim.v37i3.21380 ◽

2014 ◽

Vol 37 (3) ◽

pp. 131 ◽

Cited By ~ 15

Author(s):

Yi Sun ◽

Bo Zhang ◽

Jiajing Cheng ◽

Yi Wu ◽

Fing Xing ◽

...

Keyword(s):

Cervical Cancer ◽

Phosphatase And Tensin Homolog ◽

Migration Assay ◽

Tensin Homolog ◽

Siha Cells ◽

Non Coding Rna ◽

Cervical Cancer Cells ◽

And Migration ◽

Proliferation And Migration

Purpose: This study aimed to investigate the role of small non-coding RNA-222 (microRNA-222; miR-222) in the development of cervical cancer (CC). Methods: Normal and CC specimens were obtained from 18 patients. HeLa and SiHa cells were grown in Dulbecco’s modified Eagle’s medium. RT–PCR, Western blot, migration assay, flow cytometry and immunofluorescence microscopy were used for analyses. Results: When compared with normal cervical tissues, miR-222 was upregulated in human CC, and the extent of up-regulation was associated with the extent and depth of CC invasion. Expression of miR-222 was inversely related to the expression of phosphatase and tensin homolog (PTEN) and p27. The reduced the expression of PTEN and p27 by miR-222 in HeLa cells and SiHa cells was associated with increased proliferation and migration of CC cells. The expression of proteins (E-cadherin and paxillin) related to the proliferation and migration was also elevated. Conclusion: MiR-222 plays an important role in the tumorigenesis of CC, possibly by specifically down-regulating p27Kip1 and PTEN. Our findings suggest that miR-222 may serve as a new therapeutic target in CC.

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SIRT7 Regulates the Vascular Smooth Muscle Cells Proliferation and Migration via Wnt/β-Catenin Signaling Pathway

BioMed Research International ◽

10.1155/2018/4769596 ◽

2018 ◽

Vol 2018 ◽

pp. 1-9 ◽

Cited By ~ 15

Author(s):

Jianghua Zheng ◽

Kai Chen ◽

Haifei Wang ◽

Zhilong Chen ◽

Yong Xi ◽

...

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cells ◽

Vascular Smooth Muscle Cells ◽

Muscle Cells ◽

Cell Counting ◽

Cell Proliferation And Migration ◽

And Migration ◽

Proliferation And Migration

A huge amount of evidence indicates that sirtuin 7 (SIRT7), a key mediator of many cellular activities, plays a crucial role in the pathogenesis of various diseases. However, little is known about the role of SIRT7 in atherosclerosis. This study investigated the potential role of SIRT7 in regulating the proliferation and migration of human vascular smooth muscle cells (HAVSMCs) and its possible molecular mechanism. In this study, human vascular smooth muscle cells (HAVSMCs) were induced by oxidized low-density lipoprotein (ox-LDL) to establish atherosclerosis (AS) cell model. Immunofluorescence staining and Western blot were used to detect the level of α-SMA expression, which was a marker protein in AS. In addition, RT-qPCR and Western blot assay were applied for exploring the mRNA and protein expression levels of SIRT7, Wnt, β-catenin, and cyclin D1 after knockdown or overexpression of SIRT7. And, furthermore, Cell Counting Kit-8 assay, flow cytometry, and wound-healing assay were used to assess HAVSMCs proliferation, cell cycle, and migration. Dickkopf-1 (DKK-1), a secretory glycoprotein that can block Wnt/β-catenin pathway, was used in SIRT7 overexpression HAVSMCs; subsequently cells proliferation and migration were assessed by Cell Counting Kit-8 assay, flow cytometry analysis, and wound-healing assay. We found that knockdown of SIRT7 significantly promoted cell proliferation and migration, decreased the percentages of cells in the G1 and G2 phases, and increased those in the S phase and downregulated the protein expression levels of Wnt, β-catenin, and cyclin D1, while overexpression of SIRT7 had reverse results. After treatment with Wnt/beta-catenin pathway inhibitor DKK-1 in SIRT7 overexpression HAVSMCs, cell proliferation and migration were increased, respectively. In conclusion, SIRT7 inhibited HAVSMCs proliferation and migration via enhancing Wnt/β-catenin activation, which provided a novel therapeutic strategy for antiatherosclerosis.

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The Potential Role of Cycloastragenol in Promoting Diabetic Wound Repair In Vitro

BioMed Research International ◽

10.1155/2019/7023950 ◽

2019 ◽

Vol 2019 ◽

pp. 1-10 ◽

Cited By ~ 1

Author(s):

Yi Cao ◽

Li Xu ◽

Xiaohong Yang ◽

Yuan Dong ◽

Hongbin Luo ◽

...

Keyword(s):

Wound Healing ◽

Wound Repair ◽

Cell Counting ◽

Migration Ability ◽

Cell Growth And Migration ◽

Cell Based Therapy ◽

And Migration ◽

Proliferation And Migration

Background. Refractory wound healing is a severe complication of diabetes with a significant socioeconomic burden. Whereas current therapies are insufficient to accelerate repair, stem cell-based therapy is increasingly recognized as an alternative that improves healing outcomes. The aim of the present study is to explore the role of cycloastragenol (CAG), a naturally occurring compound in Astragali Radix, in ameliorating refractory cutaneous wound healing in vitro, which may provide a new insight into therapeutic strategy for diabetic wounds. Methods. Human epidermal stem cells (EpSCs) obtained from nine patients were exposed to CAG, with or without DKK1 (a Wnt signaling inhibitor). A lentiviral short hairpin RNA (shRNA) system was used to establish the telomerase reverse transcriptase (TERT) and β-catenin knockdown cell line. Cell counting kit-8, scratch wound healing, and transwell migration assay were used to determine the effects of CAG in cell growth and migration. The activation of TERT, β-catenin, and c-Myc was determined using real-time qPCR and western blot analysis. Chromatin immunoprecipitation (ChIP) was performed to evaluate the associations among CAG, TERT, and Wnt/β-catenin signals. Results. CAG not only promoted the proliferation and migration ability of EpSCs but also increased the expression levels of TERT, β-catenin, c-Myc. These effects of CAG were most pronounced at a dose of 0.3 μM. Notably, the CAG-promoted proliferative and migratory abilities of EpSCs were abrogated in TERT and β-catenin-silenced cells. In addition, the ChIP results strongly suggested that CAG-modulated TERT was closely associated with the activation of Wnt/β-catenin signaling. Conclusion. Our data indicate that CAG is a TERT activator of EpSCs and is associated with their proliferation and migration, a role it may play through the activation of Wnt/β-catenin signaling.

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Knockdown of long non-coding RNA OIP5-AS1 suppresses cell proliferation and migration in ox-LDL-induced human vascular smooth muscle cells (hVMSCs) through targeting miR-152-3p/PAPPA axis

RSC Advances ◽

10.1039/c9ra06614d ◽

2019 ◽

Vol 9 (56) ◽

pp. 32499-32509 ◽

Cited By ~ 1

Author(s):

Xiangya Yang ◽

Zhongrui Li ◽

Lei Zhang ◽

Xiaoshan Wu ◽

Qixin Kang ◽

...

Keyword(s):

Cell Proliferation ◽

Smooth Muscle ◽

Smooth Muscle Cells ◽

Vascular Smooth Muscle Cells ◽

Cell Proliferation And Migration ◽

Non Coding Rna ◽

And Migration ◽

Long Non Coding Rna ◽

Proliferation And Migration

Knockdown of OIP5-AS1 suppressed ox-LDL-treated hVMSCs proliferation and migration; overexpression of miR-152 played the similar role of OIP5-AS1 knockdown; OIP5-AS1 functioned as ceRNA to regulate PAPPA expression through sponging miR-152.

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Mechanism and Role of the Neuropeptide LGI1 Receptor ADAM23 in Regulating Biomarkers of Ferroptosis and Progression of Esophageal Cancer

Disease Markers ◽

10.1155/2021/9227897 ◽

2021 ◽

Vol 2021 ◽

pp. 1-15

Author(s):

Chen Chen ◽

Jun Zhao ◽

Jing-ni Liu ◽

Chenyu Sun

Keyword(s):

Esophageal Cancer ◽

Cell Lines ◽

Noncoding Rna ◽

The Cancer Genome Atlas ◽

Cell Counting ◽

Luciferase Reporter ◽

Cerna Network ◽

And Migration ◽

Proliferation And Migration

Background. According to recent studies, ferroptosis is closely related to the efficacy and prognosis of tumour treatment. However, the role of ferroptosis in esophageal squamous cell carcinoma (ESCC) has not been explored comprehensively. Materials and Methods. The esophageal cancer (EC) transcriptome data was downloaded from The Cancer Genome Atlas (TCGA), then analyzed, to obtain the differentially expressed messenger RNA (mRNA), microRNA (miRNA), and long noncoding RNA (lncRNA) between groups with the low and high Ferroptosis Potential Index (FPI) and construct a ferroptosis-associated ceRNA network. In addition, the expression of ARHGEF26-AS1 and miR-372-3p in ESCC cell lines was assessed, and the appropriate cell lines were selected. The interaction between ARHGEF26-AS1, miR-372-3p, and ADAM23 was also determined through a dual-luciferase reporter assay. Moreover, the Western blot, Cell Counting Kit-8 (CCK-8), wound healing, cell viability, and cell death assays were conducted to establish the biological functions of the ARHGEF26-AS1/miR-372-3p/ADAM23 pathway in ESCCs. Results. An FPI scoring model reflecting the activity of the ferroptosis pathway was constructed, and a ferroptosis-associated ceRNA network was established. The findings revealed that low expression of ADAM23 and ARHGEF26-AS1 as well as high expression of miR-372-3p was associated with poor prognosis and a lower FPI score in EC patients. Functionally, overexpression of ADAM23 and ARHGEF26-AS1 and the miR-372-3p inhibitor not only promoted ferroptosis in ESCC cells in vitro but also inhibited the proliferation and migration of cells. Mechanistically, ARHGEF26-AS1 upregulated the expression of ADAM23 by competitively binding to miR-372-3p. Conclusions. The study showed that the lncRNA, ARHGEF26-AS1 acts as a miR-372-3p sponge that regulates the neuropeptide LGI1 receptor ADAM23 expression. This in turn not only inhibits the proliferation and migration of ESCC cells but also upregulates the ferroptosis pathway. A neuropeptide-related ferroptosis regulatory pathway was identified in this study.

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PPP2R3A Affects the Function and Mechanism of Heterogeneous Fibroblasts in Pulmonary Fibrosis

10.21203/rs.3.rs-952433/v1 ◽

2021 ◽

Author(s):

Xiaoni Shi ◽

Shaoqi Yang ◽

Wei Luo ◽

Sha Wang ◽

Jie Huang ◽

...

Keyword(s):

Pulmonary Fibrosis ◽

Physiological Saline ◽

Cell Counting ◽

Lesion Area ◽

And Migration ◽

Remodeling Of Extracellular Matrix ◽

Interfering Rna ◽

Tgf Β1 ◽

Proliferation And Migration

Abstract Background: Fibroblasts have important roles in the synthesis and remodeling of extracellular matrix (ECM) proteins during pulmonary fibrosis. However, the spatiotemporal distribution of heterogeneous fibroblasts during disease progression remains unknown. Methods: Physiological saline and silica were used to generate a chronic pulmonary fibrosis model in mice, and single-cell sequencing, spatial transcriptome sequencing, real-time fluorescent quantitative PCR, immunohistochemistry and immunofluorescence were performed to identify fibroblast subtypes. Small interfering RNA was used to specifically knockdown the target protein, and western blotting, bromodeoxyuridine (BrdU), Cell Counting Kit-8 (CCK-8) and wound healing assays were used to detect the role of GREM1/PPP2R3A in a newly identified fibroblast subtype. Results: Fibroblasts of the new subtype were mainly located in the lesion area and coexpressed inflammation- and proliferation-related genes; they were termed inflammatory-proliferation fibroblasts. Grem1 was the most highly expressed gene in this subtype, as confirmed in HPF-a cells after TGF-β1 treatment. We characterized the downstream mechanism of GREM1/PPP2R3A: these factors mediated the increases in cell viability, proliferation and migration induced by TGF-β1 in fibroblasts. Conclusion: This new subtype of inflammatory, proliferative fibroblasts plays a pivotal role during pulmonary fibrosis, and PPP2R3A, as a downstream regulatory target of GREM1, is involved in pulmonary fibrosis, providing new insights for the prevention and treatment of silicosis.

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