scholarly journals U2AF2 Promote the Proliferation and Migration of Esophageal Adenocarcinoma Cells by Sustaining the Mrna Stability of SNORA21

2021 ◽  
Author(s):  
Gao Lijuan ◽  
Chen Yongshun ◽  
Li Bin
Keyword(s):  
Western Blot ◽  
Esophageal Adenocarcinoma ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Expression Level ◽  
Brdu Incorporation ◽  
Western World ◽  
Adenocarcinoma Cells ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Esophageal adenocarcinoma has gains predominance with squamous carcinoma moving to a second place in the western world. The 5-year survival rate of patients with esophageal cancer (EC) is still between 15–25%, although the treatment strategies for EC have been improved. RNA-binding proteins (RBPs) are key players in post-transcriptional events. Particularly, the U2 snRNP auxiliary (U2AF2), as a canonical RBP, has been reported to play an important role in the development, progression, and metastasis of several human cancers. However, the biological role of U2AF2 in the context of malignancies, including EC, has not yet been reported. This study is aimed to investigate the role and mechanism of U2AF2 in esophageal adenocarcinoma cell line. Methods The expression level of U2AF2 and SNORA21 was analysed by TCGA database. The expression level of U2AF2 and SNORA21 in esophageal adenocarcinoma cells was determined by Western Blot and RT-qPCR assay. The cell viability and proliferation was detected by CCK8 assay and BrdU incorporation assay. The apoptosis was examined by caspase3 immunocytofluorescense. The protein levels of Bax, Bcl-2 and E-cadherin were explored by Western Blot assay. The interaction between U2AF2 and SNORA21 was predicted by Starbase 3.0 and confirmed by RIP assay. The RNA regulated by U2AF2 was through RNA-seq analysis on the basis of downregulation of U2AF2. Results The expression of U2AF2 and SNORA21 was found to be upregulated and served as an unfavourable factor which negatively related with overall survival of esophageal adenocarcinoma patients. Silencing the expression of U2AF2 or SNORA21 could suppress the proliferation and migration of OE19 and OE33 cells and stimulate its apoptosis. Moreover, we identified that the U2AF2 could bind and interact with SNORA21 to sustain its stability. Furthermore, we show that overexpression of SNORA21 could rescue the proliferation inhibition phenotype caused by si-U2AF2. Conclusion Our study provides several lines of evidence supporting the intriguing concept that U2AF2 could promote the proliferation of OE19 and OE33 cells by directly targeting SNORA21, which might serve as a novel candidate biomarker and a new target for the treatment of esophageal adenocarcinoma.

Abstract 190: Long noncoding RNA XY11-10-11 regulates proliferation and migration of esophageal adenocarcinoma cells

2012 ◽  
Author(s):  
Xue Yang ◽  
Wenjing Wu ◽  
Nathaniel Margolies ◽  
Jee Hoon Song ◽  
Yulan Cheng ◽  
...  
Keyword(s):  
Esophageal Adenocarcinoma ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Adenocarcinoma Cells ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals The RNA-Binding Protein NELFE Promotes Gastric Cancer Growth and Metastasis Through E2F2

2021 ◽  
Vol 11 ◽  
Author(s):  
Changyu Chen ◽  
Qiang Zheng ◽  
Shubo Pan ◽  
Wenzheng Chen ◽  
Jianfeng Huang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Immune Cells ◽  
Rna Binding ◽  
Malignant Tumors ◽  
Expression Level ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
And Migration ◽  
Proliferation And Migration

Worldwide, the incidence rate of gastric cancer ranks fifth, and the mortality rate of gastric cancer ranks third among all malignant tumors. However, the pathogenesis of gastric cancer remains poorly understood. In this study, we demonstrated that the expression level of NELFE is higher in human gastric cancer tissues than in adjacent nontumor tissues. A high level of NELFE is associated with worse postoperative overall survival (OS) and relapse-free survival (RFS) rates in patients with gastric cancer. Moreover, the expression of NELFE is correlated with high tumor grade and lymph node metastasis in gastric cancer patients. Knockdown of NELFE dramatically inhibits the cell proliferation and metastasis of gastric cancer xenografts in vivo. Furthermore, we found that NELFE binding to the 3’UTR of E2F2 affects the mRNA stability of E2F2 to regulate the expression level of E2F2. In gastric cancer, E2F2 also acts as an oncogene to inhibit the proliferation and migration of gastric cancer cells by knocking down the expression level of E2F2. However, overexpressing E2F2 in cells with NELFE knockdown significantly reverses the inhibition of cell proliferation and migration induced by NELFE knockdown. Therefore, NELFE at least partially functions as an oncogene through E2F2. Moreover, CIBERSORTx analysis of the proportion of tumor-infiltrating immune cells (TICs) revealed that immune cells are correlated with NELFE and E2F2 expression, suggesting that NELFE and E2F2 might be responsible for the preservation of the immunodominant status for gastric cancer. In conclusion, NELFE acts as an oncogene in gastric cancer and can be used as a potential therapeutic target.

scholarly journals A 5′-tRNA halve, tiRNA-Gly promotes cell proliferation and migration via binding to RBM17 and inducing alternative splicing in papillary thyroid cancer

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Litao Han ◽  
Hejing Lai ◽  
Yichen Yang ◽  
Jiaqian Hu ◽  
Zhe Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Alternative Splicing ◽  
Papillary Thyroid Cancer ◽  
Rna Binding ◽  
Rna Binding Protein ◽  
Papillary Thyroid ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background tRNA-derived small noncoding RNAs (sncRNAs) are mainly categorized into tRNA halves (tiRNAs) and fragments (tRFs). Biological functions of tiRNAs in human solid tumor are attracting more and more attention, but researches concerning the mechanisms in tiRNAs-mediated tumorigenesis are rarely. The direct regulatory relationship between tiRNAs and splicing-related proteins remain elusive. Methods Papillary thyroid carcinoma (PTC) associated tRNA fragments were screened by tRNA fragments deep sequencing and validated by qRT-PCR and Northern Blot in PTC tissues. The biological function of tRNA fragments were assessed by cell counting kit, transwells and subcutaneous transplantation tumor of nude mice. For mechanistic study, tRNA fragments pull-down, RNA immunoprecipitation, Western Blot, Immunofluorescence, Immunohistochemical staining were performed. Results Herein, we have identified a 33 nt tiRNA-Gly significantly increases in papillary thyroid cancer (PTC) based on tRFs & tiRNAs sequencing. The ectopic expression of tiRNA-Gly promotes cell proliferation and migration, whereas down-regulation of tiRNA-Gly exhibits reverse effects. Mechanistic investigations reveal tiRNA-Gly directly bind the UHM domain of a splicing-related RNA-binding protein RBM17. The interaction with tiRNA-Gly could translocate RBM17 from cytoplasm into nucleus. In addition, tiRNA-Gly increases RBM17 protein expression via inhibiting its degradation in a ubiquitin/proteasome-dependent way. Moreover, RBM17 level in tiRNA-Gly high-expressing human PTC tissues is upregulated. In vivo mouse model shows that suppression of tiRNA-Gly decreases RBM17 expression. Importantly, tiRNA-Gly can induce exon 16 splicing of MAP4K4 mRNA leading to phosphorylation of downstream signaling pathway, which is RBM17 dependent. Conclusions Our study firstly illustrates tiRNA-Gly can directly bind to RBM17 and display oncogenic effect via RBM17-mediated alternative splicing. This fully novel model broadens our understanding of molecular mechanism in which tRNA fragment in tumor cells directly bind RNA binding protein and play a role in alternative splicing.

scholarly journals S100A6 promotes proliferation and migration of HepG2 cells via increased ubiquitin-dependent degradation of p53

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 317-326
Author(s):  
Dongqiang Song ◽  
Beili Xu ◽  
Dongmin Shi ◽  
Shuyu Li ◽  
Yu Cai
Keyword(s):  
Protein Expression ◽  
Calcium Binding ◽  
Hepg2 Cells ◽  
Expression Level ◽  
Luciferase Assay ◽  
Transcription Activator ◽  
And Migration ◽  
S100a6 Protein ◽  
Hcc Cells ◽  
Proliferation And Migration

AbstractPurposeS100A6 protein (calcyclin), a small calcium-binding protein of the S100 family, is often upregulated in various types of cancers, including hepatocellular carcinoma (HCC). The aim of this study was to illustrate the molecular mechanism of S100A6 in regulating the proliferation and migration of HCC cells.MethodsThe expressions of S100A6 in human HCC and adjacent non-tumor liver specimens were detected using immunoblotting and quantitative PCR (qPCR). The recombinant glutathione S-transferase (GST)-tagged human S100A6 protein was purified and identified. After treatment with S100A6, the proliferation of HepG2 cells was detected by the MTT and colony formation assay, and the migration of HepG2 cells was investigated by the transwell migration assay; the protein levels of cyclin D1 (CCND1), E-cadherin, and vimentin were also tested by immunoblotting. The effect of S100A6 on p21 and nuclear factor-κB pathway was verified by performing the dual luciferase assay. Then, the expression of p21 and its transcription activator, p53, was examined using immunoblotting and qPCR, the ubiquitination of which was investigated through co-immunoprecipitation.ResultsIt was found that the level of S100A6 was higher in the HCC tissues than in the adjacent non-tumor liver specimens. Exogenous overexpression of S100A6 promoted the proliferation and migration of HepG2 cells. S100A6 was observed to regulate p21 mRNA and protein expression levels and decrease p53 protein expression level, not mRNA level, by promoting the ubiquitination of p53 via the proteasome-dependent degradation pathway.ConclusionOur study indicated that S100A6 overexpression could promote the proliferation and migration of HCC cells by enhancing p53 ubiquitin-dependent proteasome degradation, ultimately regulating the p21 expression level.

PP7080 expedites the proliferation and migration of lung adenocarcinoma cells via sponging miR‐670‐3p and regulating UHRF1BP1

2021 ◽  
Author(s):  
Weibin Dan ◽  
Lei Shi ◽  
Li Wang ◽  
Dahe Wu ◽  
Xiaofang Huang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells ◽  
And Migration ◽  
Proliferation And Migration

FAM196B promotes proliferation and migration via regulating epithelial-mesenchymal transition in esophageal cancer

2021 ◽  
pp. 1-8
Author(s):  
Haifeng Xia ◽  
Fang Hu ◽  
Liangbin Pan ◽  
Chengcheng Xu ◽  
Haitao Huang ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Western Blot ◽  
Cox Regression ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Cox Regression Analysis ◽  
Ec Cells ◽  
And Migration ◽  
Proliferation And Migration

BACKGROUND: EC (esophageal cancer) is a common cancer among people in the world. The molecular mechanism of FAM196B (family with sequence similarity 196 member B) in EC is still unclear. This article aimed to clarify the role of FAM196B in EC. METHODS: The expression of FAM196B in EC tissues was detected using qRT-PCR. The prognosis of FAM196B in EC patients was determined by log-rank kaplan-Meier survival analysis and Cox regression analysis. Furthermore, shRNA was used to knockdown the expression of FAM196B in EC cell lines. MTT, wound healing assays and western blot were used to determine the role of FAM196B in EC cells. RESULTS: In our research, we found that the expression of FAM196B was up-regulated in EC tissues. The increased expression of FAM196B was significantly correlated with differentiation, lymph node metastasis, stage, and poor survival. The proliferation and migration of EC cells were inhibited after FAM196B-shRNA transfection in vitro and vivo. The western blot result showed that FAM196B could regulate EMT. CONCLUSION: These results suggested that FAM196B severs as an oncogene and promotes cell proliferation and migration in EC. In addition, FAM196B may be a potential therapeutic target for EC patients.

NLRP2 inhibits cell proliferation and migration by regulating EMT in lung adenocarcinoma cells

2021 ◽  
Author(s):  
Tiantian Li ◽  
Xu Li ◽  
Rongchen Mao ◽  
Lihua Pan ◽  
Yuhui Que ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Cell Proliferation And Migration ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals miR‑32‑5p suppresses the proliferation and migration of pancreatic adenocarcinoma cells by targeting TLDC1

2021 ◽  
Vol 24 (5) ◽  
Author(s):  
Peng Yuan ◽  
Chaofeng Tang ◽  
Bendong Chen ◽  
Peng Lei ◽  
Jianjun Song ◽  
...  
Keyword(s):  
Pancreatic Adenocarcinoma ◽  
Adenocarcinoma Cells ◽  
And Migration ◽  
Proliferation And Migration

Abstract 234: Interleukin 2 Promotes Proliferation and Migration in Vascular Smooth Muscle Cells

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Spencer Barnhill ◽  
Prakash Arumugam ◽  
John Matsuura ◽  
Scott Berceli ◽  
Katie Carroll ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Expression ◽  
Western Blot ◽  
Vascular Smooth Muscle Cells ◽  
Blot Analysis ◽  
Intimal Hyperplasia ◽  
Western Blot Analysis ◽  
Interleukin 2 ◽  
And Migration ◽  
Proliferation And Migration

Interleukin-2 (IL-2) is primarily known as a soluble cytokine that regulates T cell responses. We previously reported, however, that IL-2 is retained in the extracellular matrix by association with perlecan, a heparan sulfate proteoglycan (HSPG). Perlecan is the main HSPG in vascular basement membranes, and previous studies from our laboratory demonstrated that, in human arteries, vascular smooth muscle cells (VSMC) are surrounded by perlecan-bound IL-2. We also noted that IL-2 deficient mice lose SMCs with age, leading to widened esophagi and aortic aneurysms. Given this information, we hypothesized that IL-2 has a direct impact on VSMC, and that VSMC express functional IL-2 receptors (IL-2R). We therefore examined both protein and mRNA expression of each of the three IL-2R subunits (alpha, beta, gamma) on human VSMC grown from arterial explants. These VSMC expressed SMC actin, smooth muscle myosin heavy chain, and when quiescent, smoothelin. Protein expression was assessed by in cell Western and by Western blot analysis. Receptor expression was evaluated under distinct culture conditions, which yielded highly proliferative, intermediate, or quiescent VSMC. Contractile protein expression was low, intermediate, or high, respectively, consistent with the characteristics of proliferating vs quiescent SMCs. Each phenotype expressed all 3 subunits of the IL-2R. IL-2 subunits appeared to follow a cytoskeletal pattern in cells expressing high levels of contractile proteins. Western blot analysis of VSMC lysates revealed expression of all 3 receptors at molecular weights identical to lysates from a T cell line. VSMCs also expressed mRNA for each receptor subunit. Functionally, IL-2 promoted migration (using a Boyden chamber assay) and proliferation in a dose dependent fashion. Because excess proliferation and migration are critical to intimal hyperplasia, we asked whether IL-2 levels change under conditions known to generate intimal hyperplasia. In a rabbit model, IL-2 mRNA increased in venous grafts exposed to high flow for 2h. IL-2 levels, by Western blot, were also increased in human hyperplastic veins. In conclusion, these data show that VSMC have functional IL-2R, and suggest that IL-2 may contribute to the development of intimal hyperplasia.

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.

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