MiR-182-5p Knockdown Targeting PTEN Inhibits Cell Proliferation and Invasion of Breast Cancer Cells

Zhao, Yue; Yang, Wei; Xin, Hong Wei; Han, Ji Xia; Su, Gang

doi:10.3349/ymj.2019.60.2.148

Cited by 42 publications

(28 citation statements)

References 30 publications

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“…The reason that miRNAs have been widely studied is that circRNA can function as "miRNA sponges" to regulate downstream gene expression, thus participating in the regulation of cancer progression [17,18]. MiR-182-5p is a widely highly expressed miRNA in many cancers and can promote proliferation and metastasis in cancer cells, such as breast cancer and hepatocellular carcinoma [19,20]. Studies have shown that miR-182-5p is upregulated in OSCC and is related to OSCC metastasis [21,22].…”

Section: Introductionmentioning

confidence: 99%

Circ_0000140 restrains the proliferation, metastasis and glycolysis metabolism of oral squamous cell carcinoma through upregulating CDC73 via sponging miR-182-5p

Guo

Zhang

2020

Cancer Cell Int

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Background: Oral squamous cell carcinoma (OSCC) is a more common cancer in the world. Emerging evidence suggests that circular RNAs (circRNAs) participate in the progression of OSCC. However, the role of circ_0000140 in OSCC is still unknown. Methods: The expression of circ_0000140 and microRNA-182-5p (miR-182-5p) were assessed by quantitative realtime polymerase chain reaction (qRT-PCR). Also, cell proliferation, migration and invasion were measured by colony formation and transwell assays, respectively. Western blot (WB) analysis was used to test the levels of proliferation, metastasis and glycolysis metabolism-related proteins as well as cell division cycle 73 (CDC73) protein. Further, the extracellular acidification rate (ECAR) of cells was detected by the Seahorse XF Extracellular Flux Analyzer. The lactate acid level of cells was tested by Lactate Assay Kit. Moreover, dual-luciferase reporter was used to verify the interaction between miR-182-3p and circ_0000140 or CDC73, and RNA immunoprecipitation (RIP) assay was employed to further confirm the relationship between miR-182-3p and circ_0000140. In addition, mice xenograft models were built to measure the effect of circ_0000140 on OSCC tumor growth in vivo. Results: Circ_0000140 was lowly expressed in OSCC, and its overexpression hindered proliferation, migration, invasion and glycolysis metabolism in OSCC cells. MiR-182-5p could be sponged by circ_0000140, and its mimic could invert the suppression of circ_0000140 overexpression on OSCC progression. CDC73 could be targeted by miR-182-3p, and its silencing could reverse the inhibition of miR-182-3p inhibitor on OSCC progression. Further, overexpressed circ_0000140 reduced the OSCC tumor growth in vivo. Conclusions: Circ_0000140 might play an anti-cancer role in OSCC, which provided a novel target for clinical therapy of OSCC.

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Section: Introductionmentioning

confidence: 99%

Circ_0000140 restrains the proliferation, metastasis and glycolysis metabolism of oral squamous cell carcinoma through upregulating CDC73 via sponging miR-182-5p

Guo

Zhang

2020

Cancer Cell Int

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“…miR-548 promoted NSCLC cell invasion by regulating PTEN ( 23 ). Moreover, miR-182 promoted breast cancer cell viability and invasion via targeting PTEN ( 24 ). A previous study has shown that miR-494-3p can promote the progression of endometrial cancer by regulating the PTEN/PI3K/AKT pathway ( 25 ).…”

Section: Introductionmentioning

confidence: 99%

miR‑494 promotes progression of retinoblastoma via PTEN through PI3K/AKT signaling pathway

Liu

Wang

et al. 2020

Oncol Lett

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Increasing evidence has indicated that the dysregulation of microRNA (miRNA) occur in the pathogenesis of retinoblastoma (RB). Aim of the present study was to investigate the possible role of miR-494 (miR-494-3p) in RB. It was demonstrated that miR-494 expression was increased in RB tissue samples and cell lines. Also, it was prominently associated with clinicopathological features. Functional assays showed that RB cell proliferation, invasion and migration can be promoted by miR-494 overexpression. Besides, phosphatase and tensin homolog (PTEN) was verified as a possible target of miR-494 by a luciferase assay, western blot and qRT-PCR assay in RB. miR-494 and PTEN expression was negatively related in a correlation analysis on tumor tissues of 66 patients. In addition, PTEN was proved to reverse miR-494 effect on RB cell progression. Moreover, PI3K/AKT signaling pathway was validated to take part in RB progression. Taken together, the current study proposes that miR-494 might function as a tumor promoter and regulates RB progression through targeting PTEN.

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“…These results indicated that glioma-secreted exosomes can be effectively absorbed by endothelial cells. miR-182-5p has been reported to be involved in tumor proliferation (47)(48)(49)(50)(51)(52)(53), invasion (47,49,51), and metastasis (48,(54)(55)(56)(57). However, the role of miR-182-5p in vascular endothelial cells remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Hypoxic Cancer-Secreted Exosomal miR-182-5p Promotes Glioblastoma Angiogenesis by Targeting Kruppel-like Factor 2 and 4

Yuan

et al. 2020

Molecular Cancer Research

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Glioblastoma (GBM) is the most lethal primary brain tumor and has a complex molecular profile. Hypoxia plays a critical role during tumor progression and in the tumor microenvironment (TME). Exosomes released by tumor cells contain informative nucleic acids, proteins, and lipids involved in the interaction between cancer and stromal cells, thus leading to TME remodeling. Accumulating evidence indicates that exosomes play a pivotal role in cell-to-cell communication. However, the mechanism by which hypoxia affects tumor angiogenesis via exosomes derived from tumor cells remains largely unknown. In our study, we found that, compared with the parental cells under normoxic conditions, the GBM cells produced more exosomes, and miR-182-5p was significantly upregulated in the exosomes from GBM cells under hypoxic conditions. Exosomal miR-182-5p directly suppressed its targets Kruppel-like factor 2 and 4, leading to the accumulation of VEGFR, thus promoting tumor angiogenesis. Furthermore, exosome-mediated miR-182-5p also inhibited tight junction-related proteins (such as ZO-1, occludin, and claudin-5), thus enhancing vascular permeability and tumor transendothelial migration. Knockdown of miR-182-5p reduced angiogenesis and tumor proliferation. Interestingly, we found elevated levels circulating miR-182-5p in patient blood serum and cerebrospinal fluid samples, and its expression level was inversely related to the prognosis. Implications: Overall, our data clarify the diagnostic and prognostic value of tumor-derived exosome-mediated miR-182-5p and reveal the distinctive cross-talk between tumor cells and human umbilical vein endothelial cells mediated by tumorderived exosomes that modulate tumor vasculature.

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MiR-182-5p Knockdown Targeting PTEN Inhibits Cell Proliferation and Invasion of Breast Cancer Cells

Cited by 42 publications

References 30 publications

Circ_0000140 restrains the proliferation, metastasis and glycolysis metabolism of oral squamous cell carcinoma through upregulating CDC73 via sponging miR-182-5p

Circ_0000140 restrains the proliferation, metastasis and glycolysis metabolism of oral squamous cell carcinoma through upregulating CDC73 via sponging miR-182-5p

miR‑494 promotes progression of retinoblastoma via PTEN through PI3K/AKT signaling pathway

Hypoxic Cancer-Secreted Exosomal miR-182-5p Promotes Glioblastoma Angiogenesis by Targeting Kruppel-like Factor 2 and 4

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