scholarly journals LncRNA XIST promotes extracellular matrix synthesis, proliferation and migration by targeting miR-29b-3p/COL1A1 in human skin fibroblasts after thermal injury

2019 ◽  
Vol 52 (1) ◽  
Author(s):  
Wei Cao ◽  
Youping Feng
Keyword(s):  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Wound Healing ◽  
Western Blot ◽  
Thermal Injury ◽  
Human Skin Fibroblasts ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Long noncoding RNAs (lncRNAs) have been reported to be associated with dermis process during burn wound healing. This study aimed to investigate the role of lncRNA X-inactive specific transcript (XIST) in human skin fibroblasts (HSF) and extracellular matrix (ECM) as well as the regulatory network of XIST/microRNA-29b-3p (miR-29b-3p)/collagen 1 alpha 1 (COL1A1). Methods The wound samples were collected from 25 patients with deep partial thickness burn at day 5 after burn. The thermal injured model was established using HSF cells. The expressions of XIST, miR-29b-3p and COL1A1 were measured by quantitative real-time polymerase chain reaction and western blot. ECM synthesis, cell proliferation and migration were detected by western blot, cell counting kit-8 and trans-well assays, respectively. The interaction between miR-29b-3p and XIST or COL1A1 was explored by bioinformatics analysis and luciferase reporter assay. Results The expressions of XIST and COL1A1 were enhanced but miR-29b-3p expression was decreased after thermal injury. XIST overexpression promoted ECM synthesis, cell proliferation and migration in thermal injured HSF cells. However, XIST knockdown played an opposite effect. miR-29b-3p overexpression inhibited ECM synthesis, cell proliferation and migration, which was reversed by XIST. COL1A1 silence suppressed ECM synthesis, cell proliferation and migration by miR-29b-3p targeting. Moreover, COL1A1 up-regulation weakened the effect of XIST silence on ECM synthesis and HSF cell function. Conclusion XIST promoted ECM synthesis, cell proliferation and migration by sponging miR-29b-3p and targeting COL1A1 in HSF cells after thermal injury, indicating the promoting role of XIST in wound healing.

scholarly journals MicroRNA-708 targeting ZNF549 regulates colon adenocarcinoma development through PI3K/AKt pathway

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Zhidong Zhao ◽  
Xianju Qin
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Cell Lines ◽  
Colon Adenocarcinoma ◽  
Signal Pathway ◽  
Luciferase Reporter ◽  
Mesenchymal Transition ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract Colon adenocarcinoma (COAD) is the most common type of gastrointestinal cancer and is still the third leading cause of cancer-related mortality worldwide. Therefore, finding new and promising drugs to eradicate cancer may be a feasible method to treat COAD patients. Cys2-His2 zinc finger proteins (ZFPs) is one of the largest transcription factor family and many of them are highly involved in regulation of cell differentiation, proliferation, apoptosis, and neoplastic transformation. In this study, we identified a tumor-inhibiting factor, ZNF549, which expressed lowly in COAD tissues and COAD cell lines (HT29, HCT116, SW480, LoVo, and SW620). Overexpression of ZNF549 inhibit the ability of COAD cell proliferation and migration. On the contrary, decreasing the ZNF549 expression level promote the ability of COAD cell proliferation and migration. Through bioinformatics analysis, we found that ZNF549 was a potential target of hsa-miR-708-5p (miR-708-5p). Furthermore, we verified the possibility of miR-708-5p targeting the ZNF549 gene, and miR-708-5p inhibited the expression of ZNF549 by luciferase reporter assays, qRT-PCR and western blot assays. Moreover, the relationship between miR-708-5p and phosphatidylinositol 3-kinase/AKt (PI3K/AKt) signal pathway was elucidated. Overexpression and inhibition of miR-708-5p resulted in increased and decreased expression of p-AKt and p-PI3K in HCT116 cells, respectively. RT-qPCR and western blot assays results demonstrated that miR-708-5p regulated COAD cells development by promoting the process of Epithelial-mesenchymal transition (EMT) through PI3K/AKt signaling pathway. In summary, our findings demonstrated that ZNF549, the target gene of miR-708-5p, functions as a tumor suppressor to inhibit COAD cell lines proliferation and migration through regulate the PI3K/AKt signal pathway.

scholarly journals Biological and Clinical Significance of the CCR5/CCL5 Axis in Hepatocellular Carcinoma

Cancers ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 883 ◽  
Author(s):  
Santosh K. Singh ◽  
Manoj K. Mishra ◽  
Brian M. Rivers ◽  
Jennifer B. Gordetsky ◽  
Sejong Bae ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Clinical Significance ◽  
Treatment Options ◽  
Biological Significance ◽  
Improve Patient Survival ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Despite the improvement in survival for patients with liver cancer (LCa) in recent decades, only one in five patients survive for 5 years after diagnosis. Thus, there is an urgent need to find new treatment options to improve patient survival. For various cancers, including LCa, the chemokine CCL5 (RANTES) facilitates tumor progression and metastasis. Since the function of the CCR5/CCL5 interaction in LCa cell proliferation and migration is poorly understood, the present study was undertaken to investigate the role of the CCR5/CCL5 axis in these processes. Flow cytometry, RT-PCR, Western blot, and immunofluorescence techniques were used to quantify the expression of CCR5 and CCL5 in LCa cells. To determine the biological significance of CCR5 expressed by LCa cell lines, a tissue microarray of LCas stained for CCR5 and CCL5 was analyzed. The results showed higher expression (p < 0.001) of CCR5 and CCL5 in hepatocellular carcinoma (HCC) tissues compared to non-neoplastic liver tissues. Furthermore, to delineate the role of the CCR5/CCL5 interaction in LCa cell proliferation and migration, various LCa cells were treated with maraviroc, a CCR5 antagonist, in the presence of CCL5. These data demonstrated the biological and clinical significance of the CCR5/CCL5 axis in LCa progression. The targeting of this axis is a promising avenue for the treatment of LCa.

Role of ephrin B2 in human retinal endothelial cell proliferation and migration

2003 ◽  
Vol 15 (11) ◽  
pp. 1011-1017 ◽  
Author(s):  
Jena J. Steinle ◽  
Cynthia J. Meininger ◽  
Usha Chowdhury ◽  
Guoyao Wu ◽  
Harris J. Granger
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Endothelial Cell Proliferation ◽  
Cell Proliferation And Migration ◽  
Retinal Endothelial Cell ◽  
And Migration ◽  
Proliferation And Migration

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

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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