Clinical significance of serum miR-223, miR-25 and miR-375 in patients with esophageal squamous cell carcinoma

Wu, Chaohui; Li, Minjie; Hu, Chao; Duan, Hongbing

doi:10.1007/s11033-013-2970-z

Cited by 73 publications

(57 citation statements)

References 48 publications

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“…In many cancers, miR-25 acts as an oncogene, and exerts pro-growth, anti-apoptotic, cell cycle-promoting activity via regulation of its target genes, including Bim, p57 and death receptor 4 (DR4) [27–29]. Its role in osteoblasts/osteoblastic cells has not been extensively studied.…”

Section: Discussionmentioning

confidence: 99%

microRNA-25 targets PKCζ and protects osteoblastic cells from dexamethasone via activating AMPK signaling

et al. 2016

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AMP-activated protein kinase (AMPK) activation could protect osteoblasts from dexamethasone (Dex). This study aims to provoke AMPK activation via microRNA downregulation of its negative regulator protein kinase C ζ (PKCζ). Results show that microRNA-25-5p (miR-25-5p) targets PKCζ's 3’ untranslated regions (UTRs). Forced-expression of miR-25 downregulated PKCζ and activated AMPK in human osteoblastic cells (OB-6 and hFOB1.19 lines), which thereafter protected cells from Dex. Reversely, expression of antagomiR-25, the miR-25 inhibitor, upregulated PKCζ and inhibited AMPK activation, exacerbating Dex damages. Notably, PKCζ shRNA knockdown similarly activated AMPK and protected osteoblastic cells from Dex. AMPK activation was required for miR-25-induced osteoblastic cell protection. AMPKα shRNA or dominant negative mutation almost completely blocked miR-25-induced cytoprotection against Dex. Further studies showed that miR-25 expression increased NADPH activity and suppressed Dex-induced oxidative stress in osteoblastic cells. Such effects by miR-25 were abolished with AMPKα knockdown or mutation. Significantly, miR-25-5p level was increased in patients’ necrotic femoral head tissues, which was correlated with PKCζ downregulation and AMPK hyper-activation. These results suggest that miR-25-5p targets PKCζ and protects osteoblastic cells from Dex possibly via activating AMPK signaling.

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Section: Discussionmentioning

confidence: 99%

microRNA-25 targets PKCζ and protects osteoblastic cells from dexamethasone via activating AMPK signaling

et al. 2016

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“…Several lines of evidence has defined that miR-25 is dysregulated in human cancers [182-184]. For example, miR-25 was observed to be down-regulated in human colon cancer tissue.…”

Section: Introductionmentioning

confidence: 99%

Aberrant regulation of FBW7 in cancer

Wang

Ye²,

Liu³

et al. 2014

Oncotarget

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FBW7 (F-box and WD repeat domain-containing 7) or Fbxw7 is a tumor suppressor, which promotes the ubiquitination and subsequent degradation of numerous oncoproteins including Mcl-1, Cyclin E, Notch, c- Jun, and c-Myc. In turn, FBW7 is regulated by multiple upstream factors including p53, C/EBP-δ, EBP2, Pin1, Hes-5 and Numb4 as well as by microRNAs such as miR-223, miR-27a, miR-25, and miR-129-5p. Given that the Fbw7 tumor suppressor is frequently inactivated or deleted in various human cancers, targeting FBW7 regulators is a promising anti-cancer therapeutic strategy.

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“…Secretion of the above miRNAs has been associated with different malignancies: miR-451a and miR-223-3p have been reported as up-regulated in serum samples from esophageal cancer patients [60], and SEVs from monocytes containing miR-150-5p has been reported to promote angiogenesis [27]. These earlier findings, combined with the knowledge that cancer cell lines secrete larger amounts of SEVs than non-cancerous lines [9, 23], suggest that the SEV-mediated miRNA excretion plays a role in promoting the growth of the tumor cell itself, as well as the tumor stroma.…”

Section: Discussionmentioning

confidence: 99%

Selective extracellular vesicle exclusion of miR-142-3p by oral cancer cells promotes both internal and extracellular malignant phenotypes

Dickman¹,

Lawson²,

Jabalee³

et al. 2017

Oncotarget

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Packaging of small molecular factors, including miRNAs, into small extracellular vesicles (SEVs) may contribute to malignant phenotypes and facilitate communication between cancer cells and tumor stroma. The process by which some miRNAs are enclosed in SEVs is selective rather than indiscriminate, with selection in part governed by specific miRNA sequences. Herein, we describe the selective packaging and removal via SEVs of four miRNAs (miR-142-3p, miR-150-5p, miR-451a, and miR-223-3p) in a panel of oral dysplasia and oral squamous cell carcinoma cell lines. Inhibition of exosome export protein Rab27A increased intracellular concentration of these miRNA candidates and prevented their exclusion via SEVs. Increased intracellular miR-142-3p specifically was found to target TGFBR1, causing a decrease in TGFBR1 expression in donor cells and a reduction of malignant features such as growth and colony formation. Conversely, increased excretion of miR-142-3p via donor cell SEVs and uptake by recipient endothelial cells was found to reduce TGFBR1 activity and cause tumor-promoting changes in these cells in vitro and in vivo.

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Clinical significance of serum miR-223, miR-25 and miR-375 in patients with esophageal squamous cell carcinoma

Cited by 73 publications

References 48 publications

microRNA-25 targets PKCζ and protects osteoblastic cells from dexamethasone via activating AMPK signaling

microRNA-25 targets PKCζ and protects osteoblastic cells from dexamethasone via activating AMPK signaling

Aberrant regulation of FBW7 in cancer

Selective extracellular vesicle exclusion of miR-142-3p by oral cancer cells promotes both internal and extracellular malignant phenotypes

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