The role of miRNAs in the invasion and metastasis of cervical cancer

Wang, Jinyan; Chen, Lijuan

doi:10.1042/bsr20181377

Cited by 69 publications

(49 citation statements)

References 167 publications

(200 reference statements)

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“…miRNAs have regularly been found to be dysregulated in cervical cancer (31). Indeed, the dysregulation of miRNAs has been reported to contribute to a number of processes associated with cancer pathophysiology, including cell proliferation, cell cycle, apoptosis, epithelial-mesenchymal transition, metastasis, angiogenesis and resistance to chemoand radiotherapy (32)(33)(34).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑889‑3p targets FGFR2 to inhibit cervical cancer cell viability and invasion

et al. 2019

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MicroRNAs (miRNAs) are frequently dysregulated in cervical cancer, and the aberrant regulation of miRNAs may be involved in the regulation of various cancer-associated biological processes. Therefore, further exploration of the specific roles of dysregulated miRNAs in cervical cancer and their associated mechanism may promote the development of effective therapeutic approaches. miRNA-889-3p (miR-889) serves crucial roles in esophageal squamous cell carcinoma and hepatocellular carcinoma. However, to the best of our knowledge, no studies concerning the relationship between miR-889 and cervical cancer were performed. The aims of this study were to measure miR-889 expression in cervical cancer and to examine the potential effects of miR-889 in cervical cancer development on a molecular level to provide potential clinical insight. The present study revealed that miR-889 was downregulated in cervical cancer tissues and cell lines. Reduced miR-889 expression was significantly associated with International Federation of Gynecology and Obstetrics cancer staging and with lymph node metastasis. In addition, miR-889 overexpression reduced cervical cancer cell viability and invasive ability. Using bioinformatics analysis, fibroblast growth factor receptor 2 (FGFR2) was predicted to be a potential target of miR-889, which was confirmed using luciferase reporter assay. Reverse transcription-quantitative PCR and western blot analysis results suggested that miR-889 overexpression decreased FGFR2 expression in cervical cancer cells at the mRNA and the protein level, respectively. Conversely, FGFR2 silencing using small interfering RNA imitated the tumor suppressive effects of miR-889 overexpression in cervical cancer cells, which was successfully reversed by plasmid-facilitated FGFR2 overexpression. These observations demonstrated that miR-889 may serve tumor suppressive roles in cervical cancer by directly targeting FGFR2, which indicated that this miRNA may be a promising therapeutic target for patients with cervical cancer.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‑889‑3p targets FGFR2 to inhibit cervical cancer cell viability and invasion

et al. 2019

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“…Even though E1, E2, L1 and L2 are always encountered in all HPVs, the other genes may vary (Stubenrauch et al, 2007;Nobre et al, 2009). The major oncogenes are considered to be E5, E6 and E7, which are also known for altering a variety of signaling pathways, such as Wnt, Notch, PI3K/Akt, MAPK, IFN and NF-κB and others (Gupta et al, 2018;Xu et al, 2018;Wang and Chen, 2019). However, studies have demonstrated that the HPV infection could alter the interaction between miRNAs and some of these pathways.…”

Section: Microrna Signaling In Hpv Infectionmentioning

confidence: 99%

MicroRNA Involvement in Signaling Pathways During Viral Infection

Barbu

Condrat

Thompson

et al. 2020

Front. Cell Dev. Biol.

123

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“…They may act as tumor suppressors or oncogenes by regulating the expression of various target genes (2,3). MiR-21 has been reported to be associated with a wide variety of human cancers, including cervical cancer (4,5). The upregulation of miR-21 has been observed in cervical cancer cell lines and clinical specimens (6,7).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑21 promotes cell metastasis in cervical cancer through modulating epithelial‑mesenchymal transition

et al. 2020

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MicroRNA (miR)-21 is known to act as an oncogene in cervical cancer by promoting cell proliferation and migration; however, the underlying molecular mechanisms have remained to be fully elucidated. The present study revealed that the gene expression levels of miR-21 and epithelial-mesenchymal transition (EMT)-associated transcription factor Zinc finger E-box-binding homeobox 1 (ZEB1), in cervical cancer and lymphatic metastatic carcinoma tissues were significantly higher than those in normal tissues (P<0.05). Furthermore, the gene expression levels of miR-21 and ZEB1 were positively associated with muscular infiltration depth, parametrical invasion and lymph node metastasis in patients with cervical cancer. Immunohistochemistry assays indicated that the expression levels of ZEB1 and the mesenchymal cell marker Vimentin in cervical cancer tissues were significantly higher than those in normal cervical tissues (P<0.05). Overexpression of miR-21 in HeLa and SiHa cells caused the upregulation of the mesenchymal cell markers Vimentin and N-cadherin, and downregulation of the epithelial cell marker E-cadherin at the proteins level. In addition, overexpression of miR-21 enhanced the invasiveness of HeLa and SiHa cells. These results demonstrated that miR-21 was upregulated in cervical cancer tissues and promoted cell metastasis through modulating EMT. A better understanding of the role of miR-21 and EMT may lead to the development of more effective therapies for patients with cervical cancer.

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The role of miRNAs in the invasion and metastasis of cervical cancer

Cited by 69 publications

References 167 publications

MicroRNA‑889‑3p targets FGFR2 to inhibit cervical cancer cell viability and invasion

MicroRNA‑889‑3p targets FGFR2 to inhibit cervical cancer cell viability and invasion

MicroRNA Involvement in Signaling Pathways During Viral Infection

MicroRNA‑21 promotes cell metastasis in cervical cancer through modulating epithelial‑mesenchymal transition

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