miR‐454 performs tumor‐promoting effects in oral squamous cell carcinoma via reducing NR3C2

Guo, Jingyu; Wang, Yukun; Lv, Bo; Jin, Hong

doi:10.1111/jop.13015

Cited by 19 publications

(13 citation statements)

References 27 publications

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“…15 Nevertheless, the precise mechanism of miR-454-3p in OSCC is blurry. In accordance with the result that has been reported, 28 we attested that the level of miR-454-3p was incremental in OSCC tissues and cells. Simultaneously, the abundances of miR-454-3p and circGDI2 in OSCC tissues were reversely related.…”

Section: Discussionsupporting

confidence: 93%

“…14,15 Guo et al certified that miR-454 was upregulated and facilitated OSCC cells growth by sponging NR3C2. 16 The transcription regulator forkhead box F2 (FOXF2) is a critical molecule that participates in embryogenesis and tumorigenic processes. 17 FOXF2 level was lessened in OSCC tissues and FOXF2 silence signally accelerated OSCC cells progression.…”

Section: Introductionmentioning

confidence: 99%

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CircGDI2 Regulates the Proliferation, Migration, Invasion and Apoptosis of OSCC via miR-454-3p/FOXF2 Axis

Shi¹,

Li²,

Zhang³

et al. 2021

CMAR

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Background: Aberrant expression of circular RNA (circRNA) is involved in the occurrence and development of multifarious cancers, including oral squamous cell carcinoma (OSCC). However, the biological role of circGDI2 and the action mechanism in OSCC remain largely unclear. Methods: The expression levels of circGDI2, miR-454-3p and forkhead box F2 (FOXF2) were examined by quantitative real-time PCR (qRT-PCR) or Western blot. The stability of circGDI2 was confirmed by Ribonuclease R (RNase R) assay. Cell Counting Kit 8 (CCK8) assay, colony formation and transwell assay were used to detect cell proliferation, migration or invasion. Cell apoptosis was tested by flow cytometry. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were employed to verify the interaction between miR-454-3p and circGDI2 or FOXF2. Moreover, xenograft mouse models were constructed to assess tumor growth in vivo. Results: CircGDI2 was a stable circRNA and was low expressed in OSCC tissues and cells. CircGDI2 overexpression could effectively inhibit the proliferation, migration, invasion and promote apoptosis in OSCC cells, and suppress OSCC tumor growth in nude mice in vivo. MiR-454-3p could be sponged by circGDI2, and its overexpression could mitigate the suppressive effects of circGDI2 overexpression on OSCC progression. In addition, FOXF2 was a target of miR-454-3p, and miR-454-3p silence could impede the cell growth of OSCC cells by enhancing FOXF2 expression. Meanwhile, circGDI2 positively regulated FOXF2 expression by targeting miR-454-3p. Conclusion: CircGDI2 served as a repressor to restrain OSCC malignancy via miR-454-3p/ FOXF2 axis, which might be a novel biomarker for targeted OSCC therapy.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

CircGDI2 Regulates the Proliferation, Migration, Invasion and Apoptosis of OSCC via miR-454-3p/FOXF2 Axis

Shi¹,

Li²,

Zhang³

et al. 2021

CMAR

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“…Dysregulation of NR3C2 has been shown to be implicated in the development, progression, and prognosis of several tumors. [ 8 ] Understanding the molecular mechanism underlying the effect of NR3C2 in cancer progression might contribute to investigating novel therapeutic strategies. [ 11 ] In this study, we discovered that NR3C2 expression was significantly downregulated in breast cancer samples and suppressed the growth and aggressiveness abilities in breast cancer cells.…”

Section: Discussionmentioning

confidence: 99%

“…For instance, in oral squamous cell carcinoma, NR3C2 was downregulated and regarded as the target of miR‐454 to regulate cancer cell behaviors. [ 8 ] And a high expression of NR3C2 showed a better prognosis of colon adenocarcinoma patients and was regulated by miR‐4709 to inhibit cell malignant behaviors. [ 25 ] In step with these findings, we discovered that NR3C2 was significantly downregulated in breast cancer samples, and its lower expression was related to the worse overall survival of breast cancer patients in various stages.…”

Section: Discussionmentioning

confidence: 99%

“…For example, recent research uncovered that NR3C2 functioned as a potential tumor suppressor in oral squamous cell carcinoma. [ 8 ] Furthermore, knockdown of NR3C2 was discovered to contribute to angiogenesis in colorectal cancer. And underexpression of NR3C2 in some malignant tumors is connected with disease recurrence and overall survival, such as colorectal cancer, [ 9 ] non‐small cell lung cancer, [ 10 ] and renal cell carcinoma.…”

Section: Introductionmentioning

confidence: 99%

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miR‐301b and NR3C2 co‐regulate cells malignant properties and have the potential to be independent prognostic factors in breast cancer

Peng

et al. 2020

J Biochem & Molecular Tox

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This study intends to address the function of miR‐301b/nuclear receptor subfamily 3 group C member 2 (NR3C2) in breast cancer. The Cancer Genome Atlas database was processed to investigate the expression of miR‐301b/NR3C2 in breast cancer samples, as well as the relationship between their expression and the prognosis of the patients. Cox regression analysis was performed to determine whether miR‐301b/NR3C2 was an independent predictor of the patient's prognosis. Associations between miR‐301b and NR3C2 were analyzed by prediction website, dual‐luciferase assay, and Pearson correlation coefficient. Quantitative polymerase chain reaction and Western blot analyses were implemented to detect gene expression. The relevant biological characteristics of MCF7 and BCAP‐37 cells were tested by cell counting kit‐8, colony formation, and transwell assays. Lower expression of NR3C2, which was closely related to the bad prognosis of breast cancer patients, was presented in breast cancer samples and can be used as an independent predictor. miR‐301b, as an upstream regulator of NR3C2, was highly expressed in breast cancer samples and can be used as an independent predictor as well. Notably, a higher level of miR‐301b and lower level of NR3C2 were related to the reduced overall survival in patients with breast cancer. The proliferative and migratory behaviors of cells were elevated or blocked after overexpression of miR‐301b or NR3C2, respectively. However, the above situation was attenuated after together upregulation of miR‐301b and NR3C2. The present data afforded evidence that miR‐301b may be a tumor‐promoting miRNA in breast cancer, and that miR‐301b/NR3C2 axis mediated tumor development from cell proliferation and migration.

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Identification of NR3C2 as a functional diagnostic and prognostic biomarker and potential therapeutic target in non‐small cell lung cancer

Sun,

Gao,

Guo

et al. 2024

Cancer Innovation

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BackgroundNon‐small cell lung cancer (NSCLC), including the lung squamous cell carcinoma (LUSC) and lung adenocarcinoma (LUAD) subtypes, is a malignant tumor type with a poor 5‐year survival rate. The identification of new powerful diagnostic biomarkers, prognostic biomarkers, and potential therapeutic targets in NSCLC is urgently required.MethodsThe UCSC Xena, UALCAN, and GEO databases were used to screen and analyze differentially expressed genes, regulatory modes, and genetic/epigenetic alterations in NSCLC. The UCSC Xena database, GEO database, tissue microarray, and immunohistochemistry staining analyses were used to evaluate the diagnostic and prognostic values. Gain‐of‐function assays were performed to examine the roles. The ESTIMATE, TIMER, Linked Omics, STRING, and DAVID algorithms were used to analyze potential molecular mechanisms.ResultsNR3C2 was identified as a potentially important molecule in NSCLC. NR3C2 is expressed at low levels in NSCLC, LUAD, and LUSC tissues, which is significantly related to the clinical indexes of these patients. Receiver operating characteristic curve analysis suggests that the altered NR3C2 expression patterns have diagnostic value in NSCLC, LUAD, and especially LUSC patients. Decreased NR3C2 expression levels can help predict poor prognosis in NSCLC and LUAD patients but not in LUSC patients. These results have been confirmed both with database analysis and real‐world clinical samples on a tissue microarray. Copy number variation contributes to low NR3C2 expression levels in NSCLC and LUAD, while promoter DNA methylation is involved in its downregulation in LUSC. Two NR3C2 promoter methylation sites have high sensitivity and specificity for LUSC diagnosis with clinical application potential. NR3C2 may be a key participant in NSCLC development and progression and is closely associated with the tumor microenvironment and immune cell infiltration. NR3C2 co‐expressed genes are involved in many cancer‐related signaling pathways, further supporting a potentially significant role of NR3C2 in NSCLC.ConclusionsNR3C2 is a novel potential diagnostic and prognostic biomarker and therapeutic target in NSCLC.

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miR‐454 performs tumor‐promoting effects in oral squamous cell carcinoma via reducing NR3C2

Cited by 19 publications

References 27 publications

CircGDI2 Regulates the Proliferation, Migration, Invasion and Apoptosis of OSCC via miR-454-3p/FOXF2 Axis

CircGDI2 Regulates the Proliferation, Migration, Invasion and Apoptosis of OSCC via miR-454-3p/FOXF2 Axis

miR‐301b and NR3C2 co‐regulate cells malignant properties and have the potential to be independent prognostic factors in breast cancer

Identification of NR3C2 as a functional diagnostic and prognostic biomarker and potential therapeutic target in non‐small cell lung cancer

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