MicroRNA‑149‑3p inhibits cell proliferation by targeting AKT2 in oral squamous cell carcinoma

Shen, Qin; Zhu, Hong; Lei, Qiaoling; Chen, Luyuan; Yang, Dajiang; Sui, Wen

doi:10.3892/mmr.2020.11811

Cited by 15 publications

(11 citation statements)

References 42 publications

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“…miR-149 is a well-known tumor regulator that is dysregulated in various cancers, including oral squamous cell carcinoma, digestive system cancers, and lung cancer. [20][21][22] Several target genes of miR-149 have been identified, including FASLG, caspase-2, AKT1, PARP-2, and FOXM1. 23 In previous research, miRNA-149 was found to be an oncogenic regulator in ALL.…”

Section: Discussionmentioning

confidence: 99%

PI3K/AKT pathway‐related microRNA variants in childhood acute lymphoblastic leukemia

Xue

Sun

et al. 2023

Pediatric Blood & Cancer

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BackgroundDysregulation of microRNAs (miRNAs) targeting genes in the PI3K/Akt pathway has been implicated in the pathogenesis of childhood acute lymphoblastic leukemia (ALL). However, the impact of genetic variants in these miRNAs on ALL susceptibility has not been extensively explored in the Chinese population.MethodsTo address this gap, we conducted a case–control study to evaluate the association between genetic variants in five PI3K/AKT pathway‐related miRNAs (miR‐149, miR‐126, miR‐492, miR‐612, and miR‐423) and childhood ALL susceptibility in the Chinese population. Additionally, we investigated the effects of the rs2292832 mutation on ALL cell proliferation and apoptosis.ResultsOur analyses revealed that the miR‐149 rs2292832 mutant heterozygous CT genotype was more frequent in the control group than in the ALL cases, indicating a protective effect against ALL (adjusted odds ratio [OR] = 0.78, 95% confidence interval [CI] = 0.63–0.97, p = .024). Stratification analyses further revealed that the miR‐149 rs2292832 CC genotype was associated with an increased risk of childhood ALL in subgroups of older children, females, those with parents who never smoked or drank alcohol, those living in painted houses, those with B‐ALL, and those with high‐risk ALL. Finally, we observed that the rs2292832 mutation inhibited ALL cell proliferation and induced apoptosis (p = .001), providing a potential mechanism by which this genetic variant may influence ALL susceptibility.ConclusionOur study highlights the significant association between the miR‐149 rs2292832 genetic variant and childhood ALL susceptibility in the Chinese population. These findings expand our understanding of the complex genetic landscape underlying ALL and have implications for the development of personalized therapeutic strategies.

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Section: Discussionmentioning

confidence: 99%

PI3K/AKT pathway‐related microRNA variants in childhood acute lymphoblastic leukemia

Xue

Sun

et al. 2023

Pediatric Blood & Cancer

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“…Long noncoding RNA ARAP1-AS1 promotes cervical cancer progression through the regulation of miR-149-3p and POU2F2 [ 40 ]. miR-149-3p inhibits cell proliferation by targeting AKT2 in oral squamous cell carcinoma [ 41 ]. In this study, GO and KEGG analyses showed that the shared genes are involved in PI3K-Akt signaling pathway, Ras signaling pathway, AGE-RAGE signaling pathway in diabetic complications, focal adhesion, MAPK signaling pathway, proteoglycans in cancer, hypertrophic cardiomyopathy, cholinergic synapse, cocaine addiction, and protein digestion and absorption in UCEC.…”

Section: Discussionmentioning

confidence: 99%

miR-149-3p Is a Potential Prognosis Biomarker and Correlated with Immune Infiltrates in Uterine Corpus Endometrial Carcinoma

Lü

Wang

et al. 2022

International Journal of Endocrinology

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Background. Endocrine disruption is an important factor in the development of endometrial cancer. Expression of miR-149-3p is observed in some cancer types, while its role in uterine corpus endometrial carcinoma (UCEC) is unclear. Methods. The clinical and genomic data and prognostic information on UCEC were obtained for patients from the TCGA database. The Kruskal–Wallis test, Wilcoxon signed-rank test, and logistic regression were used to analyze the relationship between clinical characteristics and miR-149-3p expression. Kaplan–Meier survival curve analysis was used to study the influence of miR-149-3p expression and miR-149-3p target genes on the prognosis of UCEC patients. The TargetScan, PicTar, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were used to determine the involvement of miR-149-3p target genes in function. Immune infiltration analysis was used to analyze the functional involvement of miR-149-3p. QRT-PCR was used to validate the expression of miR-149-3p in UCEC cell lines. Results. High expression of miR-149-3p in UCEC was significantly associated with age ( P < 0.001 ), histological type ( P < 0.001 ), histological grade ( P < 0.001 ), tumor invasion ( P = 0.014 ), and radiation therapy ( P = 0.011 ). High miR-149-3p expression predicted poorer overall survival (OS) (HR: 2.56; 95% CI: 1.64–4.00; P < 0.001 ), progression-free interval (PFI) (HR: 1.85; 95% CI: 1.29–2.65; P = 0.001 ), and disease-specific survival (DSS) (HR: 2.33; 95% CI: 1.37–3.99; P = 0.002 ). Low expressions of miR-149-3p target genes, including ADCYAP1R1, CGNL1, CHST3, CYGB, DNAH9, ESR1, HHIP, HIC1, HOXD11, IGF1, INMT, LSP1, MTMR10, NFIC, PLCE1, RARA, SNTN, SPRYD3, and ZBTB7A, were associated with poor OS in UCEC. MiR-149-3p may be involved in the occurrence and development of UCEC via pathways including PI3K-Akt signaling pathway, Ras signaling pathway, AGE-RAGE signaling pathway in diabetic complications, focal adhesion, and MAPK signaling pathway. miR-149-3p may inhibit the function of CD8 T cells, cytotoxic cells, eosinophils, iDC, mast cells, neutrophils, NK CD56bright cells, NK CD56dim cells, pDC, T cells, T helper cells, TFH, Th17 cells, and Treg. miR-149-3p was significantly upregulated in UCEC cell lines compared with endometriotic stromal cells. Conclusion. High expression of miR-149-3p was significantly associated with poor survival in UCEC patients. It may be a promising biomarker of prognosis and response to immunotherapy for UCEC patients.

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“…Therefore, the overexpression of QKI and miR-200 is capable of inhibiting EMT in HNSCCs, despite the migratory capacity induced in miR-200 by ZEB1. Another important miRNA related to the tumor microenvironment is miR-149-3p, whose overexpression has been associated with a reduction in tumor neovascularization and a decrease in fibroblast growth factor-2 (FGF-2) signaling, playing an important role in the tumor microenvironment and the reduction in hypoxia, inhibiting the proliferation of OSCC cells, inducing apoptosis via the activation of caspase 3 [ 163 , 164 , 165 ], and possibly acting against EMT. Li et al observed that the overexpression of miR-625 is capable of inducing the inhibition of EMT by the increase in the expression of E-cadherin and the decrease in the levels of N-cadherin and Vimentin.…”

Section: Inhibition Of Emt Is Important In the Treatment Of Hnsccmentioning

confidence: 99%

Epithelial–Mesenchymal Transition Associated with Head and Neck Squamous Cell Carcinomas: A Review

González-González

Ortiz-Sarabia

Molina-Frechero

et al. 2021

Cancers

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Head and neck squamous cell carcinomas (HNSCCs) are aggressive, recurrent, and metastatic neoplasms with a high occurrence around the world and can lead to death when not treated appropriately. Several molecules and signaling pathways are involved in the malignant conversion process. Epithelial–mesenchymal transition (EMT) has been described in HNSCCs, a major type of aggressive carcinoma. EMT describes the development of epithelial cells into mesenchymal cells, which depends on several molecular interactions and signaling pathways that facilitate mesenchymal conversion. This is related to interactions with the microenvironment of the tumor, hypoxia, growth factors, matrix metalloproteinases, and the presence of viral infections. In this review, we focus on the main molecules related to EMT, their interactions with the tumor microenvironment, plasticity phenomena, epigenetic regulation, hypoxia, inflammation, their relationship with immune cells, and the inhibition of EMT in the context of HNSCCs.

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MicroRNA‑149‑3p inhibits cell proliferation by targeting AKT2 in oral squamous cell carcinoma

Cited by 15 publications

References 42 publications

PI3K/AKT pathway‐related microRNA variants in childhood acute lymphoblastic leukemia

PI3K/AKT pathway‐related microRNA variants in childhood acute lymphoblastic leukemia

miR-149-3p Is a Potential Prognosis Biomarker and Correlated with Immune Infiltrates in Uterine Corpus Endometrial Carcinoma

Epithelial–Mesenchymal Transition Associated with Head and Neck Squamous Cell Carcinomas: A Review

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