Overexpression of<i>E2F3</i>promotes proliferation of functional human β cells without induction of apoptosis

Rady, Brian; Chen, Yanmei; Vaca, Pilar; Wang, Qian; Wang, Yong; Salmon, Patrick; Oberholzer, José

doi:10.4161/cc.25834

Cited by 31 publications

(26 citation statements)

References 56 publications

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“…E2F3 is a member of E2F transcription factor family which is widely involved in the regulation of cell proliferation [17]. The expression of E2F3 is aberrantly altered in many cancers, and E2F3 plays an important role in the development of cancers [18,19].…”

Section: Discussionmentioning

confidence: 99%

miR-141 suppresses the growth and metastasis of HCC cells by targeting E2F3

et al. 2014

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MicroRNAs (miRNAs) function as essential post-transcriptional modulators of gene expression involved in a wide range of physiologic and pathologic states, including cancer. Numerous miRNAs have been deregulated in hepatocellular carcinoma (HCC). Here, we investigated the role of miR-141 in HCC. Decreased expression of miR-141 was observed in both HCC tissues and cell lines. Ectopic overexpression of miR-141 reduced proliferation, migration, and invasion of HCC cells. E2F transcription factor 3 (E2F3) was confirmed to be a target of miR-141 in HCC cells. Moreover, restoration of E2F3 significantly reversed the tumor suppressive effects of miR-141. Our results suggest a critical role of miR-141 in suppressing metastasis of HCC cells by targeting E2F3.

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Section: Discussionmentioning

confidence: 99%

miR-141 suppresses the growth and metastasis of HCC cells by targeting E2F3

et al. 2014

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“…But among all of the predicted target genes of miR-377-3p, we discovered E2F3 acted as a crucial effector of miR-377-3p. Recent research demonstrated the G1/S transition of the cell cycle was partly controled by E2F transcription factors [77, 78]. E2F family control genes expression which participated in numerous of cellular process, such as differentiation, mitosis, and apoptosis [78–80].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA NEAT1 promotes non-small cell lung cancer progression through regulation of miR-377-3p-E2F3 pathway

et al. 2016

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Recently, the long non-coding RNA (lncRNA) NEAT1 has been identified as an oncogenic gene in multiple cancer types and elevated expression of NEAT1 was tightly linked to tumorigenesis and cancer progression. However, the molecular basis for this observation has not been characterized in progression of non-small cell lung cancer (NSCLC). In our studies, we identified NEAT1 was highly expressed in patients with NSCLC and was a novel regulator of NSCLC progression. Patients whose tumors had high NEAT1 expression had a shorter overall survival than patients whose tumors had low NEAT1 expression. Further, NEAT1 significantly accelerates NSCLC cell growth and metastasis in vitro and tumor growth in vivo. Additionally, by using bioinformatics study and RNA pull down combined with luciferase reporter assays, we demonstrated that NEAT1 functioned as a competing endogenous RNA (ceRNA) for hsa-miR-377-3p, antagonized its functions and led to the de-repression of its endogenous targets E2F3, which was a core oncogene in promoting NSCLC progression. Taken together, these observations imply that the NEAT1 modulated the expression of E2F3 gene by acting as a ceRNA, which may build up the missing link between the regulatory miRNA network and NSCLC progression.

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“…21 Importantly, E2F3 can promote myogenic differentiation. 22 PI3-kinase is one of the primary signaling pathways leading to skeletal muscle differentiation; inhibition of PI3K blocks the differentiation program of rat and mouse skeletal muscle cell lines.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-432 targeting E2F3 and P55PIK inhibits myogenesis through PI3K/AKT/mTOR signaling pathway

Wang

Chen

et al. 2017

RNA Biology

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Skeletal muscle is the dominant executant in locomotion and regulator in energy metabolism. Embryonic myogenesis and postnatal muscle growth are controlled by a cascade of transcription factors and epigenetic regulatory mechanisms. MicroRNAs (miRNAs), a family of non-coding RNA of 22 nucleotides in length, post-transcriptionally regulates expression of mRNA by pairing the seed sequence to 3 0 UTR of target mRNA. Increasing evidence has demonstrated that miRNAs are important regulators in diverse myogenic processes. The profiling of miRNA expression revealed that miR-432 is more enriched in the longissimus dorsi of 35-day-old piglets than that of adult pigs. Our gain of function study showed that miR-432 can negatively regulate both myoblast proliferation and differentiation. Mechanically, we found that miR-432 is able to down-regulate E2F transcription factor 3 (E2F3) to inactivate the expression of cell cycle and myogenic genes. We also identified that phosphatidylinositol 3-kinase regulatory subunit (P55PIK) is another target gene of miR-432 in muscle cells. downregulation of P55PIK by miR-432 leads to inhibition of P55PIK-mediated PI3K/AKT/mTOR signaling pathway during differentiation. The blocking effect of miR-432 on this pathway can be rescued by insulin treatment. Taken together, our findings identified microRNA-432 as a potent inhibitor of myogenesis which functions by targeting E2F3 and P55PIK in muscle cells.

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Overexpression ofE2F3promotes proliferation of functional human β cells without induction of apoptosis

Cited by 31 publications

References 56 publications

miR-141 suppresses the growth and metastasis of HCC cells by targeting E2F3

miR-141 suppresses the growth and metastasis of HCC cells by targeting E2F3

Long non-coding RNA NEAT1 promotes non-small cell lung cancer progression through regulation of miR-377-3p-E2F3 pathway

MicroRNA-432 targeting E2F3 and P55PIK inhibits myogenesis through PI3K/AKT/mTOR signaling pathway

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