The NF‐κB‐modulated miR‐19a‐3p enhances malignancy of human ovarian cancer cells through inhibition of IGFBP‐3 expression

Bai, Ru; Cui, Zhenhua; Ma, Yongjing; Wu, Yang; Wang, Ning-Ping; Huang, Ling; Yao, Qing; Sun, Jianmin

doi:10.1002/mc.23113

Cited by 34 publications

(33 citation statements)

References 45 publications

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“…For instance, experiments in ovarian cancer cells have shown that miR−19a−3p suppresses the levels of IGF binding protein−3 (IGFBP−3), thus promoting the growth and migration of these cells. Notably, the expression of this miRNA can be modulated by NF−κB (Bai et al, 2019). Shastri et al have demonstrated the inhibitory effects of the miR-29 family on IGF-1.…”

Section: Igf-associated Mirnas In Human Disordersmentioning

confidence: 99%

The Interplay Between Non-coding RNAs and Insulin-Like Growth Factor Signaling in the Pathogenesis of Neoplasia

Ghafouri‐Fard

Abak

Mohaqiq

et al. 2021

Front. Cell Dev. Biol.

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The insulin-like growth factors (IGFs) are polypeptides with similar sequences with insulin. These factors regulate cell growth, development, maturation, and aging via different processes including the interplay with MAPK, Akt, and PI3K. IGF signaling participates in the pathogenesis of neoplasia, insulin resistance, diabetes mellitus, polycystic ovarian syndrome, cerebral ischemic injury, fatty liver disease, and several other conditions. Recent investigations have demonstrated the interplay between non-coding RNAs and IGF signaling. This interplay has fundamental roles in the development of the mentioned disorders. We designed the current study to search the available data about the role of IGF-associated non-coding RNAs in the evolution of neoplasia and other conditions. As novel therapeutic strategies have been designed for modification of IGF signaling, identification of the impact of non-coding RNAs in this pathway is necessary for the prediction of response to these modalities.

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Section: Igf-associated Mirnas In Human Disordersmentioning

confidence: 99%

The Interplay Between Non-coding RNAs and Insulin-Like Growth Factor Signaling in the Pathogenesis of Neoplasia

Ghafouri‐Fard

Abak

Mohaqiq

et al. 2021

Front. Cell Dev. Biol.

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“…Gestational diabetes mellitus (GDM) is defined as "diabetes diagnosed in the second or third trimester of pregnancy that is not clearly overt diabetes prior to gestation" (1)(2)(3). It is among the most common metabolic disease during pregnancy.…”

Section: Introductionmentioning

confidence: 99%

Hyperglycemia aggravates monocyte-endothelial adhesion in human umbilical vein endothelial cells from women with gestational diabetes mellitus by inducing Cx43 overexpression

Zhang¹,

Wu²,

Sun³

et al. 2021

Ann Transl Med

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Background: Gestational diabetes mellitus (GDM) is among the most common metabolic diseases during pregnancy and inevitably leads to maternal and fetal complications. Hyperglycemia results in injury to vascular endothelial cells, including monocyte-endothelial adhesion, which is considered to be the initiating factor of vascular endothelial cell injury. Connexin 43 (Cx43) plays a key role in this adhesion process.Therefore, this study aimed to explore the effects of Cx43 on monocyte-endothelial adhesion in GDMinduced injury of vascular endothelial cells. Methods: Human umbilical vein endothelial cells (HUVECs) were isolated from umbilical cords from pregnant women with and without GDM. THP-1 cells (a human leukemia monocytic cell line) adhering to HUVECs, related molecules [intracellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1)], and the activity of the phosphoinositide 3-kinase/protein kinase B/Nuclear factorkappa B (PI3K/AKT/NF-κB) signaling pathway were compared between the normal and GDM-HUVECs. Oleamide and specific small interfering ribonucleic acids (siRNAs) were used to inhibit Cx43 expression in GDM-HUVECs to observe the effects of Cx43 on the adhesion of THP-1 cells and HUVECs. Results: A much higher number of THP-1 cells adhered to GDM-HUVECs than to normal HUVECs. This was accompanied by an increased expression of Cx43, ICAM-1, and VCAM-1, as well as activation of the PI3K/AKT/NF-κB signaling pathway. After the inhibition of Cx43 expression in GDM-HUVECs with oleamide and specific siRNA, THP-1-HUVEC adhesion, ICAM-1 and VCAM-1 expression, and activation of PI3K/AKT/NF-κB signaling pathway were all attenuated. Hyperglycemia was able to increase expression of Cx43 in HUVECs. Conclusions: For the first time, Cx43 expression was found to be substantially higher in GDM-HUVECs than in normal HUVECs. Hyperglycemia caused the overexpression of Cx43 in HUVECs, which resulted in the activation of the PI3K/AKT/NF-κB signaling pathway and the increase of its downstream adhesion molecules, including ICAM-1 and VCAM-1, ultimately leading to increased monocyte-endothelial adhesion.

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“…In addition, miR-19a-3p was reported to promote hepatocellular carcinoma metastasis and chemoresistance through the PTEN/Akt signaling (Qi et al 2018). miR-19a-3p participated in so many biology processes, pathways and diseases (Wang, Li and Xue 2019, Bai et al 2019. TEK was identi ed to participate in PI3K/Akt signaling in our bioinformatics analyses process; however, we did not study how TEK regulated PI3K/Akt signaling at this stage of our research.…”

Section: Discussionmentioning

confidence: 97%

TEK Suppresses Lung Adenocarcinoma Cell Phenotypes by Interacting with miR-19a-3p

Peng

Yang

Sun

et al. 2020

Preprint

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Abstract Background: We identified TEK as a key gene that that participates in lung adenocarcinoma cell migration and adhesion, and miR-19a-3p a potential upstream regulator of TEK. Both TEK and miR-19a-3p have been reported during lung cancer development. However, how TEK/miR-19a-3p interactome regulates lung adenocarcinoma remains unraveled. We herein aim to report a novel TEK/miR-19a-3p interactome in lung adenocarcinoma.Methods: The mRNA and protein expression of TEK in tissues and cell lines were determined using qPCR and Western blot, respectively. CCK-8 assay, EDU assay, flow-cytometry cell apoptosis assay, scratch assay, and cell-to-extracellular matrix adhesion assay were performed to detect the proliferation, apoptosis, migration, and adhesion of A549 and H1975 cell lines. Results：Both mRNA and protein levels of TEK were down-regulated in tumor tissues and cell lines. Compared with the control, the transfection of TEK overexpression plasmids into H1975 and A549 cells led to the significant inhibition of cancerous phenotypes. On the other hand, miR-19a-3p promoted lung adenocarcinoma cancerous cell phenotypes by downregulating TEK.Conclusions: TEK can be a potential LUAD tumor suppressor by interacting with miR-19a-3p. This novel interactome can be used as a novel therapy target for LUAD.

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The NF‐κB‐modulated miR‐19a‐3p enhances malignancy of human ovarian cancer cells through inhibition of IGFBP‐3 expression

Cited by 34 publications

References 45 publications

The Interplay Between Non-coding RNAs and Insulin-Like Growth Factor Signaling in the Pathogenesis of Neoplasia

The Interplay Between Non-coding RNAs and Insulin-Like Growth Factor Signaling in the Pathogenesis of Neoplasia

Hyperglycemia aggravates monocyte-endothelial adhesion in human umbilical vein endothelial cells from women with gestational diabetes mellitus by inducing Cx43 overexpression

TEK Suppresses Lung Adenocarcinoma Cell Phenotypes by Interacting with miR-19a-3p

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