miR-448 is a novel prognostic factor of lung squamous cell carcinoma and regulates cells growth and metastasis by targeting DCLK1

Shan, Changting; Fan, Fei; Li, Fengzhu; Zhuang, Bo; Zheng, Yulong; Wan, Yufeng; Chen, Jianhui

doi:10.1016/j.biopha.2017.02.017

Cited by 30 publications

(21 citation statements)

References 27 publications

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“…A previous study reported that miR-448 levels were significantly higher in plasma samples from patients with NSCLC compared with those from healthy volunteers, and that it may serve as a potential biomarker (27). Another recent study demonstrated that miR-448 was decreased in lung SCC tissues and cell lines (17). In the present study, it was observed that miR-448 was able to suppress the progression of NSCLC through targeting SIRT1.…”

Section: Discussionsupporting

confidence: 62%

“…miR-448 has been identified as a tumor suppressor in several cancer types, including breast, hepatocellular and colorectal cancer (14)(15)(16). A recent study reported that low expression of miR-448 predicted poor prognosis of lung squamous cell carcinoma (SCC), a subtype of NSCLC, and it suppressed SCC cell proliferation and metastasis via targeting DCLK1 (17).…”

Section: Introductionmentioning

confidence: 99%

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miR‑448 promotes progression of non‑small‑cell lung cancer via targeting SIRT1

Qi¹,

Wang

Pang³

2019

Exp Ther Med

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Deregulation of microRNAs (miRs) has been demonstrated to be involved in both the initiation and the development of non-small-cell lung cancer (NSCLC). miR-448 has been identified as a tumor suppressor in several cancer types. The aim of the present study was to explore the role of miR-448 in NSCLC. Tumor tissues and paired normal tissues were obtained from patients with NSCLC. The viability and migration of A549 cells were determined by the Cell Counting kit-8 and wound-healing assays, respectively. Gene and protein levels were detected by reverse transcription-quantitative polymerase chain reaction analysis and western blotting, respectively. The interaction between the 3' untranslated region of sirtuin1 (SIRT1) and miR-448 was predicted by TargetScan and verified by dual luciferase reporter assay. miR-448 levels were revealed to be decreased whereas SIRT1 levels were increased in NSCLC tissues compared with normal tissues. Pearson's correlation analysis demonstrated that there was a negative correlation between miR-448 and SIRT1 mRNA levels. Overexpression of miR-448 led to reduced growth and migration ability of A549 cells. In addition, overexpression of miR-448 decreased SIRT1 mRNA and protein levels, thereby inhibiting epithelial-mesenchymal transition (EMT) and affecting EMT-associated molecules, including vimentin and E-cadherin. Dual luciferase reporter assay confirmed that SIRT1 was a direct target of miR-448. Notably, activation of SIRT1 by resveratrol treatment partially reversed the cell growth inhibition induced by miR-448 mimics. These findings suggested that the progression of NSCLC may be controlled by miR-448, which appears to hold promise as a therapeutic target for patients with NSCLC.

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Section: Discussionsupporting

confidence: 62%

Section: Introductionmentioning

confidence: 99%

miR‑448 promotes progression of non‑small‑cell lung cancer via targeting SIRT1

Qi¹,

Wang

Pang³

2019

Exp Ther Med

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“…Low miR-448 expression was significantly associated with differentiation, tumour-node-metastasis (TNM) stage and prognosis. Moreover, miR-448 is a poor independent prognostic factor for patients with lung squamous cell carcinoma (23). In colorectal cancer, the miR-448 level is decreased and negatively correlated with advanced TNM stage and lymph node metastasis (24).…”

Section: Discussionmentioning

confidence: 99%

“…For instance, Yu et al demonstrated that ectopic miR-448 expression inhibited pancreatic ductal adenocarcinoma cell migration and invasion in vitro and suppressed liver metastasis in vivo (22). Shan et al showed that restoration of miR-448 expression decreased the cell growth and metastasis of lung squamous cell carcinoma (23). Li et al also found that restoration of miR-448 expression prohibited cell proliferation, colony formation and motility in colorectal cancer (24).…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA‑448 inhibits the progression of retinoblastoma by directly targeting ROCK1 and regulating PI3K/AKT signalling pathway

Liu

et al. 2018

Oncol Rep

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Retinoblastoma (RB) is the most common primary intraocular malignancy during infancy and childhood worldwide. Numerous microRNAs (miRNAs) contribute to RB initiation and progression through the regulation of cell proliferation, cycle, apoptosis, migration, invasion and metastasis. Therefore, further investigation concerning the expression, roles and associated mechanisms of RB‑related miRNAs may be beneficial to develop novel strategies for patients with this malignancy. Recently, miRNA‑448 (miR‑448) has been reported to be aberrantly expressed and to play an important role in several types of human cancer. However, the expression patterns and biological roles of miR‑448 in RB have not been studied. The aim of the present study was to detect the expression levels of miR‑448 and investigate its functions in RB and its associated molecular mechanisms. In the present study, miR‑448 was significantly downregulated in RB tissues and cell lines. Upregulation of miR‑448 decreased cell proliferation and invasion and increased apoptosis in RB cells. Additionally, ρ‑associated coiled‑coil containing protein kinase 1 (ROCK1) was validated as a novel direct target gene of miR‑448 in RB. ROCK1 was overexpressed in RB tissues and inversely correlated with miR‑448 expression. Furthermore, ROCK1 silencing induced effects on the proliferation, invasion and apoptosis of RB cells similar to those observed following miR‑448 overexpression. Moreover, restoration of miR‑448 expression markedly reversed the effects of miR‑448 overexpression on RB cells, further supporting the hypothesis that ROCK1 is a direct functional target of miR‑448 in RB. Importantly, miR‑448 targeted ROCK1 to inhibit the activation of the PI3K/AKT signalling pathway in RB. These results demonstrated that miR‑448 may serve as a tumour suppressor in RB by directly targeting ROCK1 and regulating the PI3K/AKT signalling pathway, thereby suggesting that miR‑448 may be an effective therapeutic target for treating this aggressive cancer.

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Dysregulation of the Sirt5/IDH2 axis contributes to sunitinib resistance in human renal cancer cells

et al. 2021

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Sunitinib (Sun), a tyrosine kinase inhibitor of vascular endothelial growth factor receptor, is the standard first‐line treatment against advanced clear cell renal cell carcinoma (RCC), but resistance to therapy is inevitable. Reactive oxygen species production is associated with sensitivity to chemotherapy, but the underlying mechanisms are not completely understood. Here, we investigated the mechanisms contributing to Sun resistance using the RCC cell lines ACHN and 786‐O. We report that Sun‐resistant cells exhibited reduced apoptosis, increased cell viability, increased reactive oxygen species production and disrupted mitochondrial function. Furthermore, chronic Sun treatment resulted in an up‐regulation of Sirt5/isocitrate dehydrogenase 2 (IDH2) expression levels. Knockdown of Sirt5/IDH2 impaired mitochondrial function and partially attenuated Sun resistance. Finally, up‐regulation of Sirt5 enhanced the expression of IDH2 via modulation of succinylation at K413 and promoted protein stability. In conclusion, dysregulation of Sirt5/IDH2 partially contributes to Sun resistance in RCC cells by affecting antioxidant capacity.

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miR-448 is a novel prognostic factor of lung squamous cell carcinoma and regulates cells growth and metastasis by targeting DCLK1

Cited by 30 publications

References 27 publications

miR‑448 promotes progression of non‑small‑cell lung cancer via targeting SIRT1

miR‑448 promotes progression of non‑small‑cell lung cancer via targeting SIRT1

MicroRNA‑448 inhibits the progression of retinoblastoma by directly targeting ROCK1 and regulating PI3K/AKT signalling pathway

Dysregulation of the Sirt5/IDH2 axis contributes to sunitinib resistance in human renal cancer cells

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