<scp>MICAL</scp>1 facilitates breast cancer cell proliferation via <scp>ROS</scp>‐sensitive <scp>ERK</scp>/cyclin D pathway

Deng, Wenjie; Wang, Yueyuan; Zhao, Shuo; Zhang, Yujie; Cao, Yan; Zhao, Xuyang; Liu, Lei; Sun, Shixiu; Zhang, Lin; Ye, Bixing; Du, Jie

doi:10.1111/jcmm.13588

Cited by 65 publications

(36 citation statements)

References 30 publications

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“…AKT and MAPK signaling pathways have been shown to play an important role in regulating the cell cycle and can inhibit cyclin D expression, leading to G1 phase arrest [ 21 , 22 ]. Our data showed that p-AKT and p-ERK levels were significantly decreased in CD73 knockdown cells compared with control cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

The distinct role of CD73 in the progression of pancreatic cancer

et al. 2019

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Recent studies have shown that the non-enzymatic function of CD73 plays a key role in tumor progression, but this function of CD73 in pancreatic cancer cells has not been studied. Furthermore, little is known about the mechanism involved in CD73 regulation in tumors. Here, we found that CD73 expression was upregulated in pancreatic ductal adenocarcinoma (PDAC) and that its expression correlated with poor prognosis. CD73 knockdown inhibited cell growth and induced G1 phase arrest via the AKT/ERK/cyclin D signaling pathway. We also found that tumor necrosis factor receptor (TNFR) 2 was involved in CD73-induced AKT and ERK signaling pathway activation in PDAC. Further, miR-30a-5p overexpression significantly increased the cytotoxic effect of gemcitabine in pancreatic cancer by directly targeting CD73 messenger RNA (mRNA), suggesting that regulation of the miR-30a-5p/CD73 axis may play an important role in the development of gemcitabine resistance in pancreatic cancer. In summary, this regulatory network of CD73 appears to represent a new molecular mechanism underlying PDAC progression, and the mechanistic interaction between miR-30a-5p, CD73, and TNFR2 may provide new insights into therapeutic strategies for pancreatic cancer. Key messages CD73 was upregulated in PDAC and correlated with poor prognosis. CD73 knockdown inhibited cell growth and induced G1 phase arrest. TNFR2 was involved in CD73-induced AKT and ERK signaling pathway. miR-30a-5p targeted CD73 and increased the sensitivity to gemcitabine. Electronic supplementary material The online version of this article (10.1007/s00109-018-01742-0) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 99%

The distinct role of CD73 in the progression of pancreatic cancer

et al. 2019

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“…Breast cancer is a one of the most common cancers in women worldwide [ 20 , 21 ]. Although treatment for breast cancer has improved, it still represents a high disease morbisity and mortality.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA LINC00511 contributes to breast cancer tumourigenesis and stemness by inducing the miR-185-3p/E2F1/Nanog axis

et al. 2018

J Exp Clin Cancer Res

234

199

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BackgroundEmerging evidence have illustrated the vital role of long noncoding RNAs (lncRNAs) long intergenic non-protein coding RNA 00511 (LINC00511) on the human cancer progression and tumorigenesis. However, the role of LINC00511 in breast cancer tumourigenesis is still unknown. This research puts emphasis on the function of LINC00511 on the breast cancer tumourigenesis and stemness, and investigates the in-depth mechanism.MethodsThe lncRNA and RNA expression were measured using RT-PCR. Protein levels were measured using western blotting analysis. CCK-8, colony formation assays and transwell assay were performed to evaluate the cell proliferation ability and invasion. Sphere-formation assay was also performed for the stemness. Bioinformatic analysis, chromatin immunoprecipitation (ChIP) and luciferase reporter assays were carried to confirm the molecular binding.ResultsLINC00511 was measured to be highly expressed in the breast cancer specimens and the high-expression was correlated with the poor prognosis. Functionally, the gain and loss-of-functional experiments revealed that LINC00511 promoted the proliferation, sphere-formation ability, stem factors (Oct4, Nanog, SOX2) expression and tumor growth in breast cancer cells. Mechanically, LINC00511 functioned as competing endogenous RNA (ceRNA) for miR-185-3p to positively recover E2F1 protein. Furthermore, transcription factor E2F1 bind with the promoter region of Nanog gene to promote it transcription.ConclusionIn conclusion, our data concludes that LINC00511/miR-185-3p/E2F1/Nanog axis facilitates the breast cancer stemness and tumorigenesis, providing a vital insight for them.Electronic supplementary materialThe online version of this article (10.1186/s13046-018-0945-6) contains supplementary material, which is available to authorized users.

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“…These genes have important roles in different biological and molecular processes including actin-mediated cell contraction, cardiac muscle contraction, oxidoreductase activity, and demethylase activity among others [21][22][23][24]. The top downregulated genes including Ptprf (-1.01-fold), Fgf10 (-1.03-fold), Prl2c3 (-1.034), Tgfb3 (-1.04-fold), Mical1 (-1.05-fold), Ndrg2 (-1.05-fold), Ptgs1 (-1.0487-fold), Aplp1 (-1.08-fold), and Steap3 (-1.08-fold) have important roles in processes including cell proliferation, apoptosis, regulation of DNA replication, and metabolic processes among others [25][26][27]. DEG (585 total) were subjected to Gene Ontology to establish a connection with the biological processes and molecular functions that these genes contribute to (Fig 2).…”

Section: Plos Onementioning

confidence: 99%

Retinal astrocytes transcriptome reveals Cyp1b1 regulates the expression of genes involved in cell adhesion and migration

Falero-Perez¹,

Sorenson²

2020

PLoS ONE

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Astrocytes (AC) are the most abundant cells in the central nervous system. In the retina, astrocytes play important roles in the development and integrity of the retinal neurovasculature. Astrocytes dysfunction contributes to pathogenesis of a variety of neurovascular diseases including diabetic retinopathy. Recent studies have demonstrated the expression of Cyp1b1 in the neurovascular cells of the central nervous system including AC. We recently showed retinal AC constitutively express Cyp1b1, and global Cyp1b1-deficiency (Cyp1b1-/-) attenuates retinal ischemia-mediated neovascularization in vivo and the pro-angiogenic activity of retinal vascular cells in vitro. We also demonstrated that Cyp1b1 expression is a key regulator of retinal AC function. However, the underlying mechanisms involved need further investigation. Here we determined changes in the transcriptome profiles of Cyp1b1+/+ and Cyp1b1-/retinal AC by RNA sequencing. We identified 585 differentially expressed genes, whose pathway enrichment analysis revealed the most significant pathways impacted in Cyp1b1-/-AC. These genes included those of axon guidance, extracellular matrix proteins and their receptors, cancer, cell adhesion molecules, TGF-β signaling, and the focal adhesion modulation. The expression of a selected set of differentially expressed genes was confirmed by RT-qPCR analysis. To our knowledge, this is the first report of RNAseq investigation of the retinal AC transcriptome and the molecular pathways impacted by Cyp1b1 expression. These results demonstrated an important role for Cyp1b1 expression in the regulation of various retinal AC functions, which are important in neurovascular development and integrity.

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MICAL1 facilitates breast cancer cell proliferation via ROS‐sensitive ERK/cyclin D pathway

Cited by 65 publications

References 30 publications

The distinct role of CD73 in the progression of pancreatic cancer

The distinct role of CD73 in the progression of pancreatic cancer

Long noncoding RNA LINC00511 contributes to breast cancer tumourigenesis and stemness by inducing the miR-185-3p/E2F1/Nanog axis

Retinal astrocytes transcriptome reveals Cyp1b1 regulates the expression of genes involved in cell adhesion and migration

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