The roles of microRNA in human cervical cancer

Miao, Jingnan; Regenstein, Joe M.; Xu, Dan; Zhou, Dan; Li, Haixia; Zhang, Hua; Li, Chunfeng; Qiu, Junqiang; Chen, Xun

doi:10.1016/j.abb.2020.108480

Cited by 36 publications

(25 citation statements)

References 174 publications

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“…It is possible to group these results according to how they finally affect the EMT process. For example, there is evidence of EMT inhibition in bladder cancer ( 129 ), oral cancer ( 130 ), esophageal squamous cell carcinoma ( 131 ), lung cancer ( 132 ) and NSCLC ( 133 ), cervical cancer ( 134 ), melanoma ( 135 ), and pancreatic cancer ( 136 ), among others. Majumder et al, using the breast cancer cell line MCF-7 observed stimulation of EMT by the miR-526b ( 86 ).…”

Section: Epigenetic Modulation Of Cox-2/pge2 Axis and The Emt Transcription Factorsmentioning

confidence: 99%

The Inflammatory Profile of the Tumor Microenvironment, Orchestrated by Cyclooxygenase-2, Promotes Epithelial-Mesenchymal Transition

et al. 2021

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The tumor microenvironment (TME) corresponds to a complex and dynamic interconnection between the extracellular matrix and malignant cells and their surrounding stroma composed of immune and mesenchymal cells. The TME has constant cellular communication through cytokines that sustain an inflammatory profile, which favors tumor progression, angiogenesis, cell invasion, and metastasis. Although the epithelial-mesenchymal transition (EMT) represents a relevant metastasis-initiating event that promotes an invasive phenotype in malignant epithelial cells, its relationship with the inflammatory profile of the TME is poorly understood. Previous evidence strongly suggests that cyclooxygenase-2 (COX-2) overexpression, a pro-inflammatory enzyme related to chronic unresolved inflammation, is associated with common EMT-signaling pathways. This review article summarizes how COX-2 overexpression, within the context of the TME, orchestrates the EMT process and promotes initial metastatic-related events.

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Section: Epigenetic Modulation Of Cox-2/pge2 Axis and The Emt Transcription Factorsmentioning

confidence: 99%

The Inflammatory Profile of the Tumor Microenvironment, Orchestrated by Cyclooxygenase-2, Promotes Epithelial-Mesenchymal Transition

et al. 2021

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“…They lack protein-coding ability (19) but directly interact with the 3'-untranslated regions (3'-UTRs) of their target genes and subsequently trigger mRNA degradation and/or translational repression (20). Recently, several miRNAs have been confirmed to be dysregulated and perform important regulatory actions towards cervical cancer oncogenesis by exerting tumour-inhibiting or tumour-facilitating roles (21,22). Recently, a novel regulatory mechanism, called the competing endogenous RNA (ceRNA) theory, was uncovered, based on which lncRNAs can decoy certain miRNAs and thus indirectly affect the miRNA's target genes (23).…”

Section: Long Non-coding Rna Usp30-as1 Aggravates the Malignant Progression Of Cervical Cancer By Sequestering Microrna-299-3p And Therebmentioning

confidence: 99%

Long non‑coding RNA USP30‑AS1 aggravates the malignant progression of cervical cancer by sequestering microRNA‑299‑3p and thereby overexpressing PTP4A1

Chen

Chi²,

Chen

et al. 2021

Oncol Lett

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USP30 antisense RNA 1 (USP30-AS1) has been studied in bladder urothelial carcinoma. However, the detailed role of USP30-AS1 in cervical cancer remains to be elucidated. Therefore, the present study determined whether USP30-AS1 is implicated in cervical cancer malignancy, and investigated relevant molecular mechanisms. USP30-AS1 expression was measured via reverse transcription-quantitative PCR. Functional experiments, including the Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and mouse tumour model, were performed in order to elucidate the roles of USP30-AS1. The target of USP30-AS1 was predicted using bioinformatics analysis, which was further verified via RNA immunoprecipitation and luciferase reporter assays. Herein, USP30-AS1 overexpression was detected in cervical cancer sample data from The Cancer Genome Atlas and our cohort. Patients with cervical cancer expressing high levels of USP30-AS1 exhibited shorter overall survival than those with low USP30-AS1 expression. In vitro and in vivo experiments revealed that USP30-AS1 interference promoted cell apoptosis; restrained cell proliferation, migration and invasion in vitro, and hindered tumour growth in vivo. Mechanistically, USP30-AS1 competed for microRNA-299-3p (miR-299-3p) in cervical cancer and lowered the regulatory actions of miR-299-3p on protein tyrosine phosphatase type IVA (PTP4A1), resulting in PTP4A1 overexpression. Furthermore, rescue experiments confirmed that miR-299-3p interventions or exogenous PTP4A1 could counteract the cancer-inhibiting actions of USP30-AS1 silencing on cervical cancer cells. In conclusion, the miR-299-3p/PTP4A1 axis is the downstream effector of USP30-AS1 in cervical cancer, forming the USP30-AS1/miR-299-3p/PTP4A1 pathway. This newly identified competing endogenous RNA pathway may offer a novel theoretical and experimental basis for developing promising new strategies for the targeted therapy of cervical cancer.

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“…These molecules play a role in post-transcriptional gene regulation by base pairing with the 3'-untranslated regions of their target genes to ultimately trigger translational suppression and/or mRNA degradation (15). The abnormal expression of miRNAs is a hallmark of cancer, including cervical cancer (16). miRNAs are crucial regulators during the genesis and development of cervical cancer (17,18).…”

Section: Introductionmentioning

confidence: 99%

Long non‑coding RNA LINC01006 exhibits oncogenic properties in cervical cancer by functioning as a molecular sponge for microRNA‑28‑5p and increasing PAK2 expression

et al. 2021

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As previously reported, long intergenic non-protein-coding RNA 1006 (LINc01006) plays crucial roles in prostate, pancreatic and gastric cancers. However, whether it plays important roles in cervical cancer remains unclear. The present study thus aimed to determine the precise role of LINc01006 in cervical cancer and elucidate its regulatory mechanisms. The expression of LINc01006 in cervical cancer was examined by reverse transcription-quantitative polymerase chain reaction. Cell proliferation assay, flow cytometric analysis, Transwell migration and invasion assays, and tumor xenograft model experiments were performed to elucidate the roles of LINc01006 in cervical cancer. Bioinformatics analysis, luciferase reporter assay, RNA immunoprecipitation and rescue experiments were performed for mechanistic analyses. The expression of LINc01006 was found to be upregulated in cervical cancer and to be associated with a poor prognosis. The absence of LINc01006 inhibited the proliferation, migration and invasion of cervical cancer cells, whereas it promoted cell apoptosis in vitro. The downregulation of LINc01006 impeded tumor growth in vivo. LINc01006 was verified as an endogenous 'sponge' that competed for microRNA-28-5p (miR-28-5p), which resulted in the upregulation of the miR-28-5p target P21-activated kinase 2 (PAK2). Rescue experiments revealed that the suppression of miR-28-5p expression or the overexpression of PAK2 abrogated the effects of LINc01006 downregula-tion on malignant cellular functions in cervical cancer. On the whole, the present study demonstrates that LINc01006 exhibits tumor-promoting functions in cervical cancer via the regulation of the miR-28-5p/PAK2 axis. These findings may provide the basis for the identification of LINC01006-targeted clinical therapy.

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The roles of microRNA in human cervical cancer

Cited by 36 publications

References 174 publications

The Inflammatory Profile of the Tumor Microenvironment, Orchestrated by Cyclooxygenase-2, Promotes Epithelial-Mesenchymal Transition

The Inflammatory Profile of the Tumor Microenvironment, Orchestrated by Cyclooxygenase-2, Promotes Epithelial-Mesenchymal Transition

Long non‑coding RNA USP30‑AS1 aggravates the malignant progression of cervical cancer by sequestering microRNA‑299‑3p and thereby overexpressing PTP4A1

Long non‑coding RNA LINC01006 exhibits oncogenic properties in cervical cancer by functioning as a molecular sponge for microRNA‑28‑5p and increasing PAK2 expression

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