MicroRNA-24 induces cisplatin resistance by targeting PTEN in human tongue squamous cell carcinoma

Zheng, Xiangqian; Li, Jiansen; Chen, Peng; Zhao, Jingzhu; Chi, Jiadong; Meng, Xiangrui; Yun, Xinwei; Li, Dapeng; Yu, Yang; Gao, Ming; Li, Yigong

doi:10.1016/j.oraloncology.2015.08.002

Cited by 39 publications

(29 citation statements)

References 29 publications

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“…Several other studies also revealed an oncogenic role for miR-24-3p in other types of cancers, including gastric cancer, 36 pancreatic carcinoma, 39 and tongue squamous cell carcinoma. 40 On the other hand, tumor suppressor activity has also been reported for miR-24-3p in breast cancer, cervical cancer, 41 and gastric cancer. 42 Kui et al Q17 showed abundant expression of miR-24-3p in HL cell lines; however, in our study, the levels were more average (average rank, 84 of 453 miRNAs expressed).…”

Section: Discussionmentioning

confidence: 99%

miR-24-3p Is Overexpressed in Hodgkin Lymphoma and Protects Hodgkin and Reed-Sternberg Cells from Apoptosis

Yuan

Kluiver

Koerts

et al. 2017

The American Journal of Pathology

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miRNAs play important roles in biological processes, such as proliferation, metabolism, differentiation, and apoptosis, whereas altered expression levels contribute to diseases, such as cancers. We identified miRNAs with aberrant expression in Hodgkin lymphoma (HL) and investigated their role in pathogenesis. Small RNA sequencing revealed 84 significantly differentially expressed miRNAs in HL cell lines as compared to germinal center B cells. Three up-regulated miRNAs-miR-23a-3p, miR-24-3p, and miR-27a-3p-were derived from one primary miRNA transcript. Loss-of-function analyses for these miRNAs and their seed family members resulted in decreased growth on miR-24-3p inhibition in three HL cell lines and of miR-27a/b-3p inhibition in one HL cell line. Apoptosis analysis indicated that the effect of miR-24-3p on cell growth is at least in part caused by an increase of apoptotic cells. Argonaute 2 immunoprecipitation revealed 1142 genes consistently targeted by miRNAs in at least three of four HL cell lines. Furthermore, 52 of the 1142 genes were predicted targets of miR-24-3p. Functional annotation analysis revealed a function related to cell growth, cell death, and/or apoptosis for 15 of the 52 genes. Western blotting of the top five genes showed increased protein levels on miR-24-3p inhibition for CDKN1B/P27 and MYC. In summary, we showed that miR-24-3p is up-regulated in HL and its inhibition impairs cell growth possibly via targeting CDKN1B/P27 and MYC.

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Section: Discussionmentioning

confidence: 99%

miR-24-3p Is Overexpressed in Hodgkin Lymphoma and Protects Hodgkin and Reed-Sternberg Cells from Apoptosis

Yuan

Kluiver

Koerts

et al. 2017

The American Journal of Pathology

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“…Upregulation of miR-24 has been observed in a number of cancers (25)(26)(27), including OSCC (28,29). Our previous study demonstrated that frequent upregulation of miR-24 occurred in TSCC, and miR-24 induced cell survival and cisplatin resistance in vitro (29).…”

Section: Introductionmentioning

confidence: 92%

miR-24 promotes the proliferation, migration and invasion in human tongue squamous cell carcinoma by targeting FBXW7

Zhao

Chi

et al. 2016

Oncology Reports

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Recent studies suggest that aberrant expression of miR-24 is linked to various human cancers, including tongue squamous cell carcinoma (TSCC). F-box and WD-40 domain protein 7 (FBXW7), a tumor-suppressor gene, is responsible for the degradation of several proto-oncogenes. However, the function and mechanism of miR-24 and FBXW7 in TSCC remains unclear. In the present study, we found that miR-24 was increased in TSCC tissues and cell lines, and that upregulation of miR-24 was associated with advanced clinical stage and a shorter overall survival of TSCC patients. Inhibition of miR-24 significantly suppressed the proliferation, migration and invasion of TSCC cells in vitro. Furthermore, miR-24 repressed FBXW7 expression by directly binding to the 3-untranslated region of FBXW7. Moreover, the suppression of FBXW7 increased the proliferation, migration and invasion of TSCC cells, and the restoration of FBXW7 substantially attenuated the oncogenic effects of miR-24. In conclusion, our results demonstrated that upregulation of miR-24 was associated with tumor progression and poor prognosis in TSCC patients, and that overexpression of miR-24 was correlated with the proliferation, migration and invasion of TSCC cells in vitro, at least partially through regulation of its functional target FBXW7. Thus, miR-24 may serve as a novel potential biomarker for the prognosis of TSCC patients.

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“…MiR-24-3p has been recognized as an oncogenic gene in some cancers, such as gastric cancer, pancreatic carcinoma, and tongue squamous cell carcinoma H. Zhang et al, 2016;Zheng et al, 2015). MiR-320a…”

Section: Discussionmentioning

confidence: 99%

Identification of microRNAs related to myocardial ischemic reperfusion injury

Liu

Zhou

et al. 2018

Journal Cellular Physiology

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Previous studies have suggested that microRNAs (miRNAs) are associated with the progression of myocardial ischemic reperfusion (I/R) injury. However, inconsistent results have been obtained due to the differences in sequencing platform, control selection, and filtering conditions. To explore the key miRNAs in the pathogenesis of myocardial I/R injury and develop miRNA diagnostic biomarkers for myocardial I/R injury prevention, we performed a systematic analysis of publicly available myocardial I/R injury miRNA expression data and investigated the function of the signature miRNA. A total of 17 representative myocardial I/R injury miRNA datasets were extracted from the Google Scholar website and a systematic bioinformatics analysis was done. TargetScan software was used to predict the miRNA target genes, and functional enrichment and transcription factor binding analyses were performed on the target genes using the DAVID and Tfacts databases. In this study, a total of 10 signature miRNAs associated with myocardial I/R injury were identified, which included eight significantly upregulated miRNAs (miR‐let‐7b‐3p, miR‐let‐7c‐3p, miR‐15b‐3p, miR‐195‐3p, miR‐21‐5p, miR‐214‐5p, miR‐24‐3p, and miR‐320a) and two significantly downregulated miRNAs (miR‐126‐5p and miR‐499a‐5p). They had different influences on myocardial I/R injury. The upregulated target gene‐expressing signature messenger RNAs (mRNAs) were mainly involved in the transcriptional regulation process of GO: 0000122, negative regulation of transcription from RNA polymerase II promoter, and so on, while downregulated expression of signature mRNAs was mainly involved in GO:0070534, protein K63‐linked ubiquitination, and so forth. To summarize, 10 signature miRNAs of myocardial I/R injury pathogenesis were identified and their target genes and transcription factors were revealed, suggesting the potential novel therapeutic targets for myocardial I/R injury.

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MicroRNA-24 induces cisplatin resistance by targeting PTEN in human tongue squamous cell carcinoma

Cited by 39 publications

References 29 publications

miR-24-3p Is Overexpressed in Hodgkin Lymphoma and Protects Hodgkin and Reed-Sternberg Cells from Apoptosis

miR-24-3p Is Overexpressed in Hodgkin Lymphoma and Protects Hodgkin and Reed-Sternberg Cells from Apoptosis

miR-24 promotes the proliferation, migration and invasion in human tongue squamous cell carcinoma by targeting FBXW7

Identification of microRNAs related to myocardial ischemic reperfusion injury

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