The Lin28/let-7a/c-Myc pathway plays a role in non-muscle invasive bladder cancer

Li, Yunfei; Liu, Haitao; Lai, Caiyong; Du, Xinghua; Su, Zexuan; Gao, Shuangquan

doi:10.1007/s00441-013-1715-6

Cited by 25 publications

(19 citation statements)

References 39 publications

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“…c-Myc is a key basic helix-loop-helix leucine zipper transcription factor that acts as an important regulator of several cellular processes, including cell migration, growth and proliferation in various cell types [23]–[25]. Moreover, the c-Myc oncogene is overexpressed in many types of human cancers and contributes to cancer cell cycle progression, cell invasion, migration, metastasis, and angiogenesis [26]–[28].…”

Section: Discussionmentioning

confidence: 99%

The Tumor-Suppressive MicroRNA-135b Targets c-Myc in Osteoscarcoma

Liu

Zhang

et al. 2014

PLoS ONE

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Osteosarcoma is the most common primary tumor of the bone. It leads to many deaths because of its rapid proliferation and metastasis. Recent studies have shown that microRNAs are important gene regulators that are involved in various cancer-related processes. In this study, we found that miR-135b was down-regulated in both osteoscarcoma patient tumor tissues and osteoscarcoma cell lines in comparison to paired adjacent non-tumor bone tissue. We observed that a lower level of miR-135b was associated with metastasis. The ectopic expression of miR-135b markedly suppressed osteoscarcoma cell proliferation, migration, and invasion. Conversely, the inhibition of miR-135b expression dramatically accelerated cell proliferation, migration, and invasion. The forced expression of miR-135b in osteosarcoma cells resulted in a significant reduction in the protein level of c-Myc and repressed the activity of a luciferase reporter that contained the 3′-untranslated region of the c-Myc mRNA. These effects were abolished by the mutation of the predicted miR-135b-binding site, which indicates that c-Myc may be a miR-135b target gene. Moreover, the ectopic expression of c-Myc partially reversed the inhibition of cell proliferation and invasion that was caused by miR-135b. These data therefore suggest that miR-135b may function as a tumor suppressor to regulate osteosarcoma cell proliferation and invasion through a mechanism that targets the c-Myc oncogene. These findings indicate that miR-135b may play a role in the pathogenesis of osteosarcoma.

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Section: Discussionmentioning

confidence: 99%

The Tumor-Suppressive MicroRNA-135b Targets c-Myc in Osteoscarcoma

Liu

Zhang

et al. 2014

PLoS ONE

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“…In our present study, overexpression of let-7a upregulated the expression of c-Myc, which is known to sustain the stemness of stem cells targeted by the let-7 family 41. These findings imply that agmatine may reduce c-Myc via controlling let-7a , thereby influencing self-renewal and proliferation of NSCs.…”

Section: Discussionsupporting

confidence: 67%

Suppression of MicroRNAlet-7aExpression by Agmatine Regulates Neural Stem Cell Differentiation

Song

Kim

et al. 2016

Yonsei Med J

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PurposeNeural stem cells (NSCs) effectively reverse some severe central nervous system (CNS) disorders, due to their ability to differentiate into neurons. Agmatine, a biogenic amine, has cellular protective effects and contributes to cellular proliferation and differentiation in the CNS. Recent studies have elucidated the function of microRNA let-7a (let-7a) as a regulator of cell differentiation with roles in regulating genes associated with CNS neurogenesis.Materials and MethodsThis study aimed to investigate whether agmatine modulates the expression of crucial regulators of NSC differentiation including DCX, TLX, c-Myc, and ERK by controlling let-7a expression.ResultsOur data suggest that high levels of let-7a promoted the expression of TLX and c-Myc, as well as repressed DCX and ERK expression. In addition, agmatine attenuated expression of TLX and increased expression of ERK by negatively regulating let-7a.ConclusionOur study therefore enhances the present understanding of the therapeutic potential of NSCs in CNS disorders.

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“…When c-Myc was down-regulating, cellular proliferation was hindered. Recent report showed the relationship in bladder cancer that Let7a regulates cMyc by participating Lin28/Let7a/c-Myc pathway in the cancer progression [34]. Although the regulating loop was elucidated and delineated in activating or maintain the cell proliferation, most of studies are in endowing the immortality on cancer cell.…”

Section: Discussionmentioning

confidence: 98%

Let7a involves in neural stem cell differentiation relating with TLX level

Song

Cho

et al. 2015

Biochemical and Biophysical Research Communications

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Neural stem cells (NSCs) have the potential for differentiation into neurons known as a groundbreaking therapeutic solution for central nervous system (CNS) diseases. To resolve the therapeutic efficiency of NSCs, recent researchers have focused on the study on microRNA's role in CNS. Some micro RNAs have been reported significant functions in NSC self-renewal and differentiation through the post-transcriptional regulation of neurogenesis genes. MicroRNA-Let7a (Let7a) has known as the regulator of diverse cellular mechanisms including cell differentiation and proliferation. In present study, we investigated whether Let7a regulates NSC differentiation by targeting the nuclear receptor TLX, which is an essential regulator of NSC self-renewal, proliferation and differentiation. We performed the following experiments: western blot analysis, TaqMan assay, RT-PCR, and immunocytochemistry to confirm the alteration of NSCs. Our data showed that let7a play important roles in controlling NSC fate determination. Thus, manipulating Let-7A and TLX could be a novel strategy to enhance the efficiency of NSC's neuronal differentiation for CNS disorders.

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The Lin28/let-7a/c-Myc pathway plays a role in non-muscle invasive bladder cancer

Cited by 25 publications

References 39 publications

The Tumor-Suppressive MicroRNA-135b Targets c-Myc in Osteoscarcoma

The Tumor-Suppressive MicroRNA-135b Targets c-Myc in Osteoscarcoma

Suppression of MicroRNAlet-7aExpression by Agmatine Regulates Neural Stem Cell Differentiation

Let7a involves in neural stem cell differentiation relating with TLX level

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