MicroRNA-374b Suppresses Proliferation and Promotes Apoptosis in T-cell Lymphoblastic Lymphoma by Repressing AKT1 and Wnt-16

Dong, Qian; Chen, Kailin; Deng, Huimin; Rao, Hui‐Lan; Huang, Hui Qiang; Liao, Yiji; Sun, Xiaofei; Lü, Suying; Xie, Dan; Cai, Qingqing

doi:10.1158/1078-0432.ccr-14-2947

Cited by 54 publications

(31 citation statements)

References 47 publications

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“…Accumulating evidence has illustrated that miR‐374b is associated with cancerogenesis, in instances such as colorectal cancer study, where the expression of miR‐374b has been reported to be down‐regulated highlighting it as a potential biomarker for colorectal cancer (Wu et al, ). Qian et al () discussed that miR‐374b inhibits cell proliferation and induce cell apoptosis by suppressing the levels of AKT1 and Wnt‐16 in the AKT signaling pathway in patients with T‐cell lymphoblastic lymphoma. Lu et al () provided an analysis indicative of the notion that miRNA‐374b may affect the development of triple‐negative breast cancer through its regulation of certain central pathways, involving that of fibroblast growth factor and transforming growth factor.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐374b inhibits cervical cancer cell proliferation and induces apoptosis through the p38/ERK signaling pathway by binding to JAM‐2

Cao²,

et al. 2018

Journal Cellular Physiology

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Cervical cancer (CC) remains a highly prevalent cancer and mortality globally among women globally. The aim of the present study was to assess the ability of miR-374b to regulate CC cells through JAM-2, whilst exploring whether the underlying mechanism and its relation to the p38/ERK signaling pathway. During the study, microRNA-374b (miR-374b) was observed to have been expressed at a low level among CC tissues. Hence, a series of miR-374b mimics, miR-374b inhibitors, siRNA against JAM-2, SB202190 (an inhibitor for p38), and PD98059 (an inhibitor for ERK) were introduced to treat CC Siha cells and normal cervical Ect1/E6E7 cells. MTT, flow cytometry, scratch test, and transwell assays were applied to determine cell viability, apoptosis, migration, and invasion. The inhibitory role of the p38/ERK signaling pathway was observed in the CC cells treated with miR-374b mimics or siRNA against JAM-2. miR-374b mimic exposure was found to reduce cell viability, migration, and invasion, but induce apoptosis. MiR-374b inhibitor exposure was observed to have induced effects on the CC cells in a contrary manner to those induced by that of the miR-374b mimics. The key findings of the study demonstrated that miR-374b significantly inhibits cell proliferation, migration, and invasion through the blockade of the p38/ERK signaling pathway activation, as well as negatively binding to JAM-2, highlighting its potential as a therapeutic target for CC.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‐374b inhibits cervical cancer cell proliferation and induces apoptosis through the p38/ERK signaling pathway by binding to JAM‐2

Cao²,

et al. 2018

Journal Cellular Physiology

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“…Generally, miRNAs bind to messenger RNAs’ (mRNAs) 3′ untranslated region (3′ UTR), which result in the degradation or translated inhibition of mRNA [5]. Emerging evidence suggests that altered expressions of miRNAs are implicated in various tumor biological process, such as cell growth, proliferation, angiogenesis, migration, invasion and so forth, via regulating targeted genes, [6–8].…”

Section: Introductionmentioning

confidence: 99%

miR-509-3-5P inhibits the invasion and lymphatic metastasis by targeting PODXL and serves as a novel prognostic indicator for gastric cancer

Zhang

Zhu

Sheng³

et al. 2017

Oncotarget

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BackgroundOur study aimed to investigate the clinicopathological feature and prognostic role of miR-509-3-5P in gastric cancer, to determine the invasive and metastatic role of miR-509-3-5P in vitro and in vivo and to explore the molecular mechanism between miR-509-3-5P and PODXL.ResultsStrikingly lower miR-509-3-5P expression was detected in gastric cancer tissues with advanced tumor stage, poor differentiation and advanced pT stage, and was regarded as an independent prognostic role for poor prognosis. MiR-509-3-5P expression was markedly down-regulated in gastric cancer cell lines and tissues comparing with normal gastric cell and adjacent normal tissues, respectively. Decreased expression of miR-509-3-5P promoted the colony, migration and invasion abilities of gastric cancer cells in vitro as well as tumorigenesis and lymph node metastasis in vivo. Based on the luciferase assay and tissue microarray, PODXL was regarded as a target gene of miR-509-3-5P.Materials and MethodsThe expression of miR-509-3-5P in gastric cancer patients and its clinicopathological relationships as well as prognostic role was studied employing tissue microarray; qRT-PCR was applied to explore miR-509-3-5P expression in gastric cancer cell lines and samples. Moreover, public database was used to analyze the expression of miR-509-3-5P and PODXL. Functional and molecular mechanism experiments were performed in vitro and in vivo.ConclusionsOverexpression of miR-509-3-5P inhibits the invasion and metastasis of gastric cancer in vitro and in vivo, functioning as a tumor suppressor, by targeting PODXL. More importantly, miR-509-3-5P was downregulated in gastric cancer tissues and may serve as a novel prognostic indicator for gastric cancer.

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“…Here, it was found that miR‐374b overexpression promoted p53 expression in NSCLC. At the same time, many studies have shown that miR‐374b exerts its effect by inhibiting the expression of target genes, such as AKT1 and PTEN . In this study, it was found that miR‐374b directly targets ITGB1.…”

Section: Discussionmentioning

confidence: 55%

MicroRNA‐374b mediates the initiation of non‐small cell lung cancer by regulating ITGB1 and p53 expressions

et al. 2020

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Background: Previous studies have shown that microRNAs (miRNAs) play important roles in the pathogenesis of human cancers. This study aims to clarify the role of miR-374b in non-small cell lung cancer (NSCLC). Methods: In this study, RT-qPCR and western blot analysis were used to measure mRNA and protein expression. The regulatory mechanism of miR-374b/ ITGB1 was investigated by dual-luciferase reporter, CCK-8, and transwell assays. Results: MiR-374b expression was reduced in NSCLC tissues and associated with lymph node metastasis, tumor stage and prognosis in NSCLC patients. Functionally, overexpression of miR-374b inhibited cell viability and metastasis in NSCLC. In addition, miR-374b blocked EMT and promoted p53 expression in NSCLC. MiR-374b was found to directly target ITGB1. Furthermore, upregulation of ITGB1 weakened the antitumor effect of miR-374b in NSCLC. Conclusions: MiR-374b inhibits the tumorigenesis of NSCLC by downregulating ITGB1 and upregulating p53.

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MicroRNA-374b Suppresses Proliferation and Promotes Apoptosis in T-cell Lymphoblastic Lymphoma by Repressing AKT1 and Wnt-16

Cited by 54 publications

References 47 publications

MicroRNA‐374b inhibits cervical cancer cell proliferation and induces apoptosis through the p38/ERK signaling pathway by binding to JAM‐2

MicroRNA‐374b inhibits cervical cancer cell proliferation and induces apoptosis through the p38/ERK signaling pathway by binding to JAM‐2

miR-509-3-5P inhibits the invasion and lymphatic metastasis by targeting PODXL and serves as a novel prognostic indicator for gastric cancer

MicroRNA‐374b mediates the initiation of non‐small cell lung cancer by regulating ITGB1 and p53 expressions

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