LIM and SH3 protein 1 induces glioma growth and invasion through PI3K/AKT signaling and epithelial-mesenchymal transition

Zhong, Chuanhong; Li, Xianglong; Tao, Bei; Peng, Lilei; Peng, Tangming; Yang, Xiaobo; Xia, Xiangguo; Chen, Ligang

doi:10.1016/j.biopha.2019.109013

Cited by 24 publications

(21 citation statements)

References 29 publications

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“…Inhibition of miR-218-5p can hinder the epithelial-mesenchymal transition LASP1 can increase tumor cell migration and invasion by promoting epithelial-mesenchymal transition(Wang et al, 2014;Zhong et al, 2019). We observed the expression and localization of LASP1 and Vimentin (a mesenchymal cell marker) in endometrial tissue.…”

mentioning

confidence: 75%

miR-218-5p in Endometrial Microenvironment Prevents the Migration of Ectopic Endometrial Stromal Cells by Inhibiting LASP1

Zhang

Wang

Zeng

et al. 2021

Preprint

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Our previous two-dimensional electrophoresis experiments showed that the expression of LASP1 in patients with endometriosis was significantly higher than that of control endometrium. However, the molecular mechanism by which LASP1 is regulated in endometriosis/adenomyosis is unknown. Herein, qPCR was performed to analysis the expression levels of LASP1 and miR-218-5p between EMs cells and control cells. Immunofluorescence in situ hybridization was carried out to measure the expression level of miR-218-5p in ectopic endometrium versus normal endometrium. After miR-218-5p mimic or inhibitor were transfected, the transwell experiment was carried out to see the effect of miR-218-5p on the migration of ESCs. EdU was used to measure cell proliferation rate. Dual-luciferase reporter assay (DR) was used to verify the binding of hsa-miR-218-5p to the 3'UTR of LASP1. Western blot and immunofluorescence analysis were carried out to identify the protein expression pattern of LASP1 and EMT markers in endometrial tissue. Our results show that high expression of LASP1 is related to the development of EMs. miR-218-5p inhibits the expression level of LASP1 by binding the 3'UTR region of LASP1. miR-218-5p is negatively correlated with the expression of LASP1 protein in endometriosis cells and tissues. Without affecting proliferation, miR-218-5p can increase the migration of ESCs. miR-218-5p is mainly secreted from blood vessels and expressed in the muscle layer around the endometrium. miR-218 also inhibits mesenchymal transition of epithelial cells by inhibiting the expression of Vimentin.

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mentioning

confidence: 75%

miR-218-5p in Endometrial Microenvironment Prevents the Migration of Ectopic Endometrial Stromal Cells by Inhibiting LASP1

Zhang

Wang

Zeng

et al. 2021

Preprint

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“…On the other hand, PI3K/AKT signaling, a classical pathway participated in tumor growth, metastasis, apoptosis and EMT, also plays a vital role in glioma development. 45 , 46 Interestingly, CXCR2 also affects tumor development by mediating PI3K/AKT signaling. 47 Here, our data revealed that miR-495-3p inhibited phosphorylated level of PI3K/Akt, while overexpressing circ_0000215 promoted the PI3K/Akt activation, which was consistent with CXCR2 expression, suggesting that circ_0000215/miR-495-3p could promote glioma progression via activating PI3K/Akt through CXCR2.…”

Section: Discussionmentioning

confidence: 99%

Circ_0000215 Increases the Expression of CXCR2 and Promoted the Progression of Glioma Cells by Sponging miR-495-3p

Mutalifu

Zhang

et al. 2020

Technol Cancer Res Treat

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Background: In recent years, accumulating studies have found that circular RNA (circRNA) exerts a great effect on tumor progression. Circ_0000215, a novel circRNA, remains largely unknown in terms of its effect and mechanism in glioma. Method: Quantitative real-time polymerase chain reaction (qRT-PCR) was carried out to detect the expressions of circ_0000215, miR-495-3p and CXCR2 in human glial cell line HEB and glioma cell lines (A172, U251, U87, SHG-44, LN-18), human glioma tissues and adjacent healthy tissues. Gain- and loss-assays of circ_0000215 were conducted. Cell proliferation ability was detected via the CCK8 assay, and cell invasion ability was examined by Transwell assay. CXCR2 expression was evaluated via RT-PCR and Western blot. Moreover, bioinformatics was applied to analyze the targeting molecules of circ_0000215 and CXCR2. Verification of the relationship between these molecules were supported through the dual-luciferase reporter gene and RNA immunocoprecipitation (RIP) assay. Results: Circ_0000215 and CXCR2 were remarkably upregulated in glioma tissues and cells. Overexpression of circ_0000215 notably promoted the proliferation, invasion and epithelial-mesenchymal transition (EMT) but inhibited apoptosis of glioma cells, while knocking down circ_0000215 had the opposite effects. Additionally, miR-495-3p, a sponge RNA of circ_0000215, inhibited the growth, invasion and EMT of glioma cells. Mechanistically, miR-495-3p targeted CXCR2 and negatively regulated CXCR2/PI3K/Akt pathway. However, the effects of miR-495-3p were all dampened by overexpression of circ_0000215. Conclusion: These data demonstrated that circ_0000215 functions as a competitive endogenous RNA by sponging miR-495-3p, thus accelerating glioma progression through CXCR2 axis.

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“…In addition, Linc00673 is also involved in the activation of the PI3K/AKT signaling pathway to promote glioma cell migration and invasion [65]. The PI3K/AKT signaling pathway has been implicated in the regulation of EMT in a variety of tissues, including gliomas [66][67][68]. Although the research reports of Linc00673 in promoting tumor progression through EMT has been well discussed, it is undeniable that Linc00673 is tissue specific.…”

Section: Involvement In the Regulation Of The Epithelial-mesenchymal mentioning

confidence: 99%

A review of linc00673 as a novel lncRNA for tumor regulation

Gong

Jiang

et al. 2021

Int. J. Med. Sci.

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Long non-coding RNAs (LncRNAs) act as regulators and play important roles in a variety of biological processes. These regulators constitute a huge information network among genes and participate in the pathophysiological process of human diseases. Increasing evidence has demonstrated that LncRNA, as an oncogene or tumor suppressor gene, is closely related to the occurrence and development of tumors. Linc00673 is a recently discovered LncRNA molecule that is dysregulated in several solid tumors. Moreover, its genetic polymorphism is believed to affect the susceptibility of a population to the corresponding cancer species. This article summarizes the role of Linc00673 in different human cancers and its molecular mechanisms with a focus on the characteristics of Linc00673 and the existing literature on it while highlighting the future research directions for Linc00673. Linc00673 has the potential to become a feasible clinical diagnostic and prognostic marker toward providing a new molecular therapeutic target for cancer patients.

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LIM and SH3 protein 1 induces glioma growth and invasion through PI3K/AKT signaling and epithelial-mesenchymal transition

Cited by 24 publications

References 29 publications

miR-218-5p in Endometrial Microenvironment Prevents the Migration of Ectopic Endometrial Stromal Cells by Inhibiting LASP1

miR-218-5p in Endometrial Microenvironment Prevents the Migration of Ectopic Endometrial Stromal Cells by Inhibiting LASP1

Circ_0000215 Increases the Expression of CXCR2 and Promoted the Progression of Glioma Cells by Sponging miR-495-3p

A review of linc00673 as a novel lncRNA for tumor regulation

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