MicroRNA‑376a inhibits cell proliferation and invasion in osteosarcoma via directly targeting SATB1

Guang-hong, Zhou; Jiang, Hao; Ma, Liping

doi:10.3892/mmr.2018.9344

Cited by 6 publications

(4 citation statements)

References 33 publications

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“… 29–32 miR-376a-3p, induced by TTN-AS1, mitigates the effects on colorectal cancer cell proliferation and invasion, which is a target of TTN-AS1, 33 miR-376a-3p mitigates the development of glioma by negatively regulating KLF15. 34 In addition, miR-376a-3p inhibits cell proliferation and invasion of osteosarcoma cells by directly targeting SATB1 35 In the present study, we confirmed that miR-376a-3p could affect the function of AML cells by regulating MT1X at the cellular level. Our results revealed that overexpression of miR-376a-3p evidently inhibited the proliferation, arrested in the G0/G1 phase and induced apoptosis of AML cells, and its suppressive effect could be reversed when MT1X was overexpressed, which were consistent with the trend of miR-376a-3p effects in other tumors.…”

Section: Discussionsupporting

confidence: 67%

MiR-376a-3p increases cell apoptosis in acute myeloid leukemia by targeting MT1X

Xin

Zheng

Wei

et al. 2022

Cancer Biology & Therapy

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Metallothioneins (MTs) are a group of low-molecular weight cysteine-rich proteins that play vital roles in oxidative stress, metal homeostasis, carcinogenesis and drug resistance. However, few studies have analyzed the roles of MTs in acute myeloid leukemia (AML). In this study, we revealed that the expression of metallothionein1X (MT1X), a main isoform of MTs, was highly expressed and acted as a candidate of prognostic indicator in AML patients. In vitro cell function experiments verified that silencing MT1X inhibited the proliferation of AML cells, sensitized cells to doxorubicin, and increased their apoptosis. We also showed that the downregulation of MT1X expression suppressed nuclear factor-κB (NF-κB) signaling by reducing p65, p-IκB-α, and downstream effectors. Elevated p65 and MT1X levels were indicators in AML. Moreover, we revealed that miR-376a-3p had binding sites with 3ʹ-UTR of MT1X, suggesting that MT1X was negatively regulated by miR-376a-3p. Cell functional assay results indicated that miR-376a-3p overexpression significantly inhibited the proliferation, arrested the AML cells in the G0/G1 phase and induced cell apoptosis. The rescue experiments further confirmed that miR-376a-3p could reverse the promotion of MT1X overexpression on the progress of AML cells. Taken together, our results revealed that elevated MT1X expression might be involved in the mechanism underlying AML progression, indicating that the miR-376a/MT1X axis might serve as a promising novel target for the effective treatment of patients with AML.

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Section: Discussionsupporting

confidence: 67%

MiR-376a-3p increases cell apoptosis in acute myeloid leukemia by targeting MT1X

Xin

Zheng

Wei

et al. 2022

Cancer Biology & Therapy

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“…Therefore, we focused our attention on MAPK6. Previous reports have found that MAPK6 plays an important role in many tumors [40][41][42][43]. We found that knockdown of ZNF671 up-regulated the expression level of MAPK6.…”

Section: Discussionsupporting

confidence: 51%

Decreased methylation of ZNF671 suppresses tumor progression by promoting MAPK6 transcription in laryngeal carcinoma

Zhang¹,

Liu²,

Li³

et al. 2023

Int. J. Biol. Sci.

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Background: Laryngeal squamous cell carcinoma (LSCC) is a malignant tumor of the head and neck, the exact mechanism of which has not been explored. Methods: By analyzing the GEO data, we found the highly methylated and low expression gene ZNF671. The expression level of ZNF671 in clinical samples was verified by RT-PCR, western blotting and methylation-specific PCR. The function of ZNF671 in LSCC was detected by cell culture and transfection, MTT, Edu, TUNEL assays and flow cytometry analysis. The binding sites of ZNF671 to MAPK6 promoter region were detected and verified by luciferase reporter gene and chromatin immunoprecipitation. Finally, the effect of ZNF671 on LSCC tumors was tested in vivo. Results: In this study, by analyzing GEO data GSE178218 and GSE59102, we found that zinc finger protein (ZNF671) expression was decreased, and DNA methylation level was increased in laryngeal cancer. Moreover, the abnormal expression of ZNF671 was associated with poor survival prognosis of patients. In addition, we found that overexpression of ZNF671 could inhibit the viability, proliferation, migration and invasion of LSCC cells, while promoting cell apoptosis. In contrast, the opposite effects were observed after knockdown of ZNF671. Through the prediction website and chromatin immunoprecipitation and luciferase reporter experiments, it was found that ZNF671 could bind to the promoter region of MAPK6, thereby inhibiting the expression of MPAK6. In vivo experiments confirmed that overexpression of ZNF671 could inhibit tumor growth. Conclusion:Our study found that ZNF671 expression was down-regulated in LSCC. ZNF671 up-regulates the expression of MAPK6 by binding to its promoter region, thus participating in cell proliferation, migration and invasion in LSCC. Our study may provide new ideas for early prediction and treatment of LSCC.

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“…In a recent study, Hegazy et al [9] stated that the advancement of LSCC is influenced by the alteration of miRNA expression. In particular, laryngeal cancer cells show downregulation of miR-138, which leads to less apoptosis and more cell proliferation [78]. Other miRNAs that play a relevant role in the development of laryngeal cancer (LC) are miR-195-5p and miR-206 [79].…”

Section: The Emerging Role Of Lncrnas Mirnas and Mrnasmentioning

confidence: 99%

Updates on Larynx Cancer: Risk Factors and Oncogenesis

Liberale,

Soloperto,

Marchioni

et al. 2023

IJMS

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Laryngeal cancer is a very common tumor in the upper aero-digestive tract. Understanding its biological mechanisms has garnered significant interest in recent years. The development of laryngeal squamous cell carcinoma (LSCC) follows a multistep process starting from precursor lesions in the epithelium. Various risk factors have been associated with laryngeal tumors, including smoking, alcohol consumption, opium use, as well as infections with HPV and EBV viruses, among others. Cancer development involves multiple steps, and genetic alterations play a crucial role. Tumor suppressor genes can be inactivated, and proto-oncogenes may become activated through mechanisms like deletions, point mutations, promoter methylation, and gene amplification. Epigenetic modifications, driven by miRNAs, have been proven to contribute to LSCC development. Despite advances in molecular medicine, there are still aspects of laryngeal cancer that remain poorly understood, and the underlying biological mechanisms have not been fully elucidated. In this narrative review, we examined the literature to analyze and summarize the main steps of carcinogenesis and the risk factors associated with laryngeal cancer.

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MicroRNA‑376a inhibits cell proliferation and invasion in osteosarcoma via directly targeting SATB1

Cited by 6 publications

References 33 publications

MiR-376a-3p increases cell apoptosis in acute myeloid leukemia by targeting MT1X

MiR-376a-3p increases cell apoptosis in acute myeloid leukemia by targeting MT1X

Decreased methylation of ZNF671 suppresses tumor progression by promoting MAPK6 transcription in laryngeal carcinoma

Updates on Larynx Cancer: Risk Factors and Oncogenesis

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