miR‑152 may function as an early diagnostic and prognostic biomarker in patients with cervical intraepithelial neoplasia and patients with cervical cancer

Yang, Dongmei; Zhang, Qiu-Mei

doi:10.3892/ol.2019.10233

Cited by 14 publications

(24 citation statements)

References 34 publications

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“…Chen et al ( 14 ) reported that miR-499a promotes the proliferation, cell cycle progres-sion, colony formation, migration and invasion of CC cells by targeting SRY-box transcription factor 6. In addition, several miRNAs serve as diagnostic biomarkers in patients with CC, such as miR-152 and miR-365 ( 15 , 16 ). Despite the aforementioned findings, the roles of miRNAs in the development of CC require further investigation.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑15a‑5p‑targeting oncogene YAP1 inhibits cell viability and induces cell apoptosis in cervical cancer cells

et al. 2020

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MicroRNAs (miRNAs) have been reported to have important regulatory roles in the progression of several types of cancer, including cervical cancer (CC). However, the biological roles and regulatory mechanisms of miRNAs in CC remain to be fully elucidated. The aim of the present study was to examine the functions of miRNAs in CC and the possible mechanisms. Using a microarray, it was identified that miRNA-15a-5p (miR-15a-5p) was one of the most down-regulated miRNAs in CC tissues compared with adjacent noncancerous tissues. The low expression of miR-15a-5p was observed in CC tumor tissues with distant metastasis and in CC cell lines. In addition, the effects of miR-15a-5p upregulation on cell viability, apoptosis, invasion and migration of CC cells were investigated using CCK-8, flow cytometry, Transwell and wound healing assays, respectively. It was demonstrated that upregulation of miR-15a-5p significantly suppressed the viability, migration and invasion, and promoted the apoptosis of SiHa and C-33A cells. Furthermore, yes-associated protein 1 (YAP1), a well-known oncogene, was confirmed to be directly targeted by miR-15a-5p and was found to be negatively regulated by miR-15a-5p. Further correlation analysis indicated that miR-15a-5p expression was negatively correlated with YAP1 expression in CC tissues. Notably, overexpression of YAP1 abrogated the tumor suppressive effects of miR-15a-5p in CC cells. Taken together, these present findings indicated that the miR-15a-5p/YAP1 axis may provide a novel strategy for the clinical treatment of CC.

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Section: Introductionmentioning

confidence: 99%

MicroRNA‑15a‑5p‑targeting oncogene YAP1 inhibits cell viability and induces cell apoptosis in cervical cancer cells

et al. 2020

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“…Wei et al [8] reported that miR-221-3p promoted CC metastasis by directly targeting twist homolog 2 (TWIST2). Additionally, some miRNAs, such as miR-365 and miR-152, have become potential diagnostic biomarkers in patients with CC [12,13]. Therefore, identifying more miRNAs that are aberrantly expressed in CC and addressed their underlying molecular mechanisms can be beneficial for therapeutic approaches for CC.…”

Section: Introductionmentioning

confidence: 99%

The promotional effect of microRNA-103a-3p in cervical cancer cells by regulating the ubiquitin ligase FBXW7 function

et al. 2022

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MicroRNAs (miRNAs) have been reported to be involved in the initiation and progression of human tumors including cervical cancer (CC). However, the mechanisms underlying of their actions in CC remain to be fully elucidated. Herein, the differentially expressed miRNAs that were screened based on GSE55940 microarray data retrieved from Gene Expression Omnibus (GEO), and miR-103a-3p was significantly upregulated in CC tissues which was selected as the target miRNA for further research. We also found that high expression of miR-103a-3p was closely associated with histological grades, FIGO stage and distant metastasis as well as reflected poor overall survival. Moreover, miR-103a-3p inhibition decreased the growth capacity of SiHa and HeLa cells by inducing cell apoptosis. And F-box and WD repeat-domain containing protein 7 (FBXW7), a well-known tumor suppressor in many cancer types, was identified as a direct target of miR-103a-3p. It was further found that FBXW7 was significantly downregulated in CC tissues, and it was inversely correlated with miR-103a-3p expression levels. Further investigation demonstrated that FBXW7 upregulation could simulate the roles of miR-103a-3p knockdown in cell viability and apoptosis. Moreover, FBXW7 knockdown efficiently abrogated the influences of CC cells proliferation caused by miR-103a-3p inhibition. Notably, miR-103a-3p could block FBXW7 mediated the downstream transcription factor pathways. Taken together, these findings suggest that miR-103a-3p functions as an oncogene in CC by targeting FBXW7.

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“…miR-153 has been previously reported to regulate radiosensitivity ( 8 , 9 ), as well as other processes, in various types of cancer. For example, miR-153 was reported to mediate cell proliferation and apoptosis in renal cancer ( 13 ), inhibit migration in breast ( 14 , 15 ) and lung cancer ( 16 ), act as a prognostic marker for gastric ( 17 ) and cervical cancer ( 18 ), mediate immune escape from natural killer cells in pancreatic cancer ( 19 ), and enhance chimeric antigen receptor T cell immunotherapy in colon cancer ( 20 ). In pancreatic cancer, miR-153 mainly has antitumour properties.…”

Section: Discussionmentioning

confidence: 99%

miR-153 enhances the therapeutic effect of radiotherapy by targeting JAG1 in pancreatic cancer cells

et al. 2021

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Pancreatic cancer is one of the deadliest diseases, due to the lack of early symptoms and resistance to current therapies, including radiotherapy. However, the mechanisms of radioresistance in pancreatic cancer remain unknown. The present study explored the role of microRNA-153 (miR-153) in radioresistance of pancreatic cancer. It was observed that miR-153 was downregulated in pancreatic cancer and positively correlated with patient survival time. Using stably-infected pancreatic cancer cells that overexpressed miR-153 or miR-153 inhibitor, it was found that miR-153 overexpression sensitized pancreatic cancer cells to radiotherapy by inducing increased cell death and decreased colony formation, while cells transfected with the miR-153 inhibitor promoted radioresistance. Further investigation demonstrated that miR-153 promoted radiosensitivity by directly targeting jagged canonical Notch ligand 1 (JAG1). The addition of recombinant JAG1 protein in the cell cultures reversed the therapeutic effect of miR-153. The present study revealed a novel mechanism of radioresistance in pancreatic cancer and indicated that miR-153 may serve as a potential therapeutic target for radioresistance.

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miR‑152 may function as an early diagnostic and prognostic biomarker in patients with cervical intraepithelial neoplasia and patients with cervical cancer

Cited by 14 publications

References 34 publications

MicroRNA‑15a‑5p‑targeting oncogene YAP1 inhibits cell viability and induces cell apoptosis in cervical cancer cells

MicroRNA‑15a‑5p‑targeting oncogene YAP1 inhibits cell viability and induces cell apoptosis in cervical cancer cells

The promotional effect of microRNA-103a-3p in cervical cancer cells by regulating the ubiquitin ligase FBXW7 function

miR-153 enhances the therapeutic effect of radiotherapy by targeting JAG1 in pancreatic cancer cells

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