MiR-223-5p works as an oncomiR in vulvar carcinoma by<i>TP63</i>suppression

Maia, Beatriz de Melo; Rodrigues, Iara S.; Akagi, Erica M.; Amaral, Nayra Soares do; Ling, Hui; Monroig, Paloma del C.; Soares, Fernando Augusto; Calin, George A.

doi:10.18632/oncotarget.10247

Cited by 26 publications

(19 citation statements)

References 72 publications

(96 reference statements)

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“…The current advances of its role in cancers have been summarized in a recent review [17]. More deeply, miR-223-5p, has recently evidenced to be associated with cancer pathogenesis, including vulvar carcinoma [3], non-small cell lung cancer [4] and bladder cancer [5]. However, the involvement of miR-223-5p in PCa remains obscure and worth of experimental investigation.…”

Section: Discussionmentioning

confidence: 99%

“…Recent emerging evidences support a novel concept that the passenger strand involves in the cancer pathogenesis. In particular, miR-223-5p as the aberrantly expressed lagging strand, has been reported in few solid malignant neoplasms including vulvar carcinoma [3], non-small cell lung cancer [4] and bladder cancer [5]. miR-223-5p could act as anti-tumor miRNA by targeting several oncogenic genes such as E2F8 and ANLN.…”

Section: Ivyspringmentioning

confidence: 99%

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miR-223-5p targeting ERG inhibits prostate cancer cell proliferation and migration

Wei¹,

Peng²,

He³

et al. 2020

J. Cancer

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Ectopic expression of miR-223-5p, the lagging strand of miR-223 duplex, has been reported acting as anti-tumor miRNA in many cancers. How miR-223-5p influencing prostate cancer (PCa) remains obscure and worth of experimental investigation. In this study, the expressions of miR-223-5p and ERG in common PCa cell lines were detected and compared to RWPE-1, respectively. Then luciferase reporter assay was performed to verify whether miR-223-5p could specifically target and regulate ERG. Further discovery ERG's role in the PCa oncogenesis was also conducted by up or down regulating miR-223-3p expression. We found miR-223-5p was significantly down-regulated in DU145, while it was only up-regulated in LNCaP. Similarly, ERG expression remarkably decreased in both PC-3 and DU145 than that in RWPE-1, but significantly increasing in LNCaP. Luciferase assay demonstrated slightly decreased ERG expression after miR-223-5p-mimics but significantly increased ERG expression after miR-223-5p-inhibtor. Using gene interference, we further confirmed that both ERG mRNA and protein expressions were decreased in all PCa lines transfected ERG siRNA, but increasing in both DU145 and LNCaP cells with miR-223-5p antisense oligonucleotides. MTT assay, Transwell invasion and migration assay supported the function of ERG in PCa oncogenesis. We revealed tumor suppressive abilities of miR-223-5p in PCa by negatively targeting ERG gene. It could serve as a fundamental supplement and extension of our previous study about miR-223-3p in PCa, revealing the coordinative regulation between miR-223-5p and miR-223-3p in PCa cell biological behaviors. Exploration of miR-233-duplex orientated pathway networks may help us develop novel potential therapeutic options for PCa.

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Section: Discussionmentioning

confidence: 99%

Section: Ivyspringmentioning

confidence: 99%

miR-223-5p targeting ERG inhibits prostate cancer cell proliferation and migration

Wei¹,

Peng²,

He³

et al. 2020

J. Cancer

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“…Among them, miR‐184 (Fang et al ., ), miR‐424* (Zhang et al ., ), miR‐218 (Wang et al ., ), miR‐222 (Wei et al ., ) and miR‐10a (Rong et al ., ) have been reported in relation to chemotherapy resistance in several types of tumors. Others, such as as miR‐135b* (Wang et al ., ,), miR‐223* (de Melo Maia et al ., ), miR‐135b (Han et al ., ) and miR‐196b (Ren et al ., ), have been reported as oncomiRs. The aberrant expression of miRNAs in the radioresistance of human tumors is a result of their function as negative regulators of gene expression.…”

Section: Discussionmentioning

confidence: 99%

New insights into radioresistance in breast cancer identify a dual function of miR‐122 as a tumor suppressor and oncomiR

et al. 2019

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Radioresistance of tumor cells gives rise to local recurrence and disease progression in many patients. MicroRNAs (miRNAs) are master regulators of gene expression that control oncogenic pathways to modulate the radiotherapy response of cells. In the present study, differential expression profiling assays identified 16 deregulated miRNAs in acquired radioresistant breast cancer cells, of which miR‐122 was observed to be up‐regulated. Functional analysis revealed that miR‐122 has a role as a tumor suppressor in parental cells by decreasing survival and promoting radiosensitivity. However, in radioresistant cells, miR‐122 functions as an oncomiR by promoting survival. The transcriptomic landscape resulting from knockdown of miR‐122 in radioresistant cells showed modulation of the ZNF611 , ZNF304 , RIPK1 , HRAS , DUSP8 and TNFRSF21 genes. Moreover, miR‐122 and the set of affected genes were prognostic factors in breast cancer patients treated with radiotherapy. Our data indicate that up‐regulation of miR‐122 promotes cell survival in acquired radioresistant breast cancer and also suggest that miR‐122 differentially controls the response to radiotherapy by a dual function as a tumor suppressor an and oncomiR dependent on cell phenotype.

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“…Furthermore, a miRNA sponge was also verified by them, which was most likely to appear as an efficient method for diagnosing and treating this cancer ( 12 ). It has been reported that miR-223-5p works as an oncogene by targeting p63 in vulvar cancer ( 13 ). miR-590-5p drives promotion of cellular malignant conduct with the help of the target gene TGFβRII in VSCC ( 4 ).…”

Section: Discussionmentioning

confidence: 99%

miR‑3147 serves as an oncomiR in vulvar squamous cell cancer via Smad4 suppression

Yang

Guo

2018

Mol Med Report

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The incidence of vulvar squamous cell carcinoma (VSCC) has increased annually over the last decade. MicroRNAs (miRNAs/miRs) serve an important role in tumor progression and development. Our previous microarray studies have revealed that miR-3147 was overexpressed in VSCC. However, its function and underlying mechanism in VSCC remain unknown. In the present study, it was confirmed by reverse transcription-quantitative polymerase chain reaction that the expression of miR-3147 was markedly upregulated in VSCC tissues. The increased expression of miR-3147 was positively associated with the depth of invasion. The overexpression of miR-3147 resulted in the promotion of vulvar cancer cell proliferation, migration, invasion, G1/S progression and invasion-associated gene expression. miR-3147 may participate in the process of epithelial-mesenchymal transition and reduce the expressions of downstream target genes in the transforming growth factor-β/Smad signaling pathway in A431 cells. The knockdown of Smad4 by small interfering RNA promoted malignant behaviours in A431 cells. In addition, miR-3147 regulated Smad4 by directly binding to its 3′ untranslated region. In conclusion, the results indicated that miR-3147 may serve an oncogenic role in VSCC by targeting Smad4. miR-3147 may represent a novel potential therapeutic target marker for VSCC.

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MiR-223-5p works as an oncomiR in vulvar carcinoma byTP63suppression

Cited by 26 publications

References 72 publications

miR-223-5p targeting ERG inhibits prostate cancer cell proliferation and migration

miR-223-5p targeting ERG inhibits prostate cancer cell proliferation and migration

New insights into radioresistance in breast cancer identify a dual function of miR‐122 as a tumor suppressor and oncomiR

miR‑3147 serves as an oncomiR in vulvar squamous cell cancer via Smad4 suppression

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