Inhibition of c-Myc by let-7b mimic reverses mutidrug resistance in gastric cancer cells

Yang, Xiaojun; Cai, Hui; Liang, Yu-He; Chen, Lin; Wang, Xiangdong; Si, Ruohuang; Qu, Kunpeng; Jiang, Zongyuan; Ma, Bingqiang; Miao, Changfeng; Li, Jing; Wang, Bin; Gao, Peng

doi:10.3892/or.2015.3757

Cited by 47 publications

(36 citation statements)

References 48 publications

(51 reference statements)

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“…In addition, various studies found miRNAs may be upstream regulators of c-Myc by targeting its mRNA, then inhibiting its translation (34,35). In addition, miRNA has been proved to be able to regulate chemoresistance of cancer cells by inhibiting c-Myc (36,37). The present study confirmed that c-Myc was directly targeted by miR-451 in bladder cancer.…”

Section: Discussionsupporting

confidence: 80%

miR-451 suppresses bladder cancer cell migration and invasion via directly targeting c-Myc

et al. 2016

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MicroRNA (miRNA) expression is shown dysregulated in tumors. It has been reported that miR-451 alters gene expression and regulates tumorigenesis in various cancer tissues. However, its underlying biological significance in bladder cancer remains to be clarified. In the present study, we investigated the function and molecular mechanism of miR-451 involved in bladder cancer cell migration and invasion. Our results showed that miR-451 was downregulated in clinical bladder carcinoma tissues compared with adjacent bladder tissues. Overexpression of miR-451 significantly retarded the proliferation, migration and invasion of bladder cancer T24 and 5637 cells in vitro. Moreover, the attenuated cell migration and invasion by miR-451 was correlated with increased apoptosis. However, our dual-luciferase reporter assay validated that c-Myc, an oncogene in many tumors, was a direct target gene of miR-451 in bladder cancer. The expression of c-Myc was repressed by miR-451 in bladder cancer cells, and knockdown of c-Myc mimicked the effects of miR-451 overexpression. This discovery suggested that miR-451 is a tumor suppressor modulating bladder cancer cell migration and invasion by directly targeting c-Myc. In addition, apoptosis promoted by miR-451 may participates in this biological behavior. Therefore, target miR-451 may be a novel therapeutic intervention for bladder cancer.

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Section: Discussionsupporting

confidence: 80%

miR-451 suppresses bladder cancer cell migration and invasion via directly targeting c-Myc

et al. 2016

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“…Insulin like growth factor 2 mRNA binding proteins (IGF2BP1, IGF2BP2, IGF2BP3), high mobility group AT-hook 1 (HMGA1), ARID3B, and MYC protooncogene (c-MYC) are all let-7 miRNA targets with known roles in cell proliferation [18,[35][36][37][38][39][40][41]. IGF2BPs are highly conserved RNA binding oncofetal proteins with three paralogs, IGF2BP1, IGF2BP2, and IGF2BP3 [42].…”

Section: Introductionmentioning

confidence: 99%

Trophectoderm-Specific Knockdown of LIN28 Decreases Expression of Genes Necessary for Cell Proliferation and Reduces Elongation of Sheep Conceptus

Ali

Stenglein

Spencer

et al. 2020

IJMS

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LIN28 inhibits let-7 miRNA maturation which prevents cell differentiation and promotes proliferation. We hypothesized that the LIN28-let-7 axis regulates proliferation-associated genes in sheep trophectoderm in vivo. Day 9-hatched sheep blastocysts were incubated with lentiviral particles to deliver shRNA targeting LIN28 specifically to trophectoderm cells. At day 16, conceptus elongation was significantly reduced in LIN28A and LIN28B knockdowns. Let-7 miRNAs were significantly increased and IGF2BP1-3, HMGA1, ARID3B, and c-MYC were decreased in trophectoderm from knockdown conceptuses. Ovine trophoblast (OTR) cells derived from day 16 trophectoderm are a useful tool for in vitro experiments. Surprisingly, LIN28 was significantly reduced and let-7 miRNAs increased after only a few passages of OTR cells, suggesting these passaged cells represent a more differentiated phenotype. To create an OTR cell line more similar to day 16 trophectoderm we overexpressed LIN28A and LIN28B, which significantly decreased let-7 miRNAs and increased IGF2BP1-3, HMGA1, ARID3B, and c-MYC compared to control. This is the first study showing the role of the LIN28-let-7 axis in trophoblast proliferation and conceptus elongation in vivo. These results suggest that reduced LIN28 during early placental development can lead to reduced trophoblast proliferation and sheep conceptus elongation at a critical period for successful establishment of pregnancy.

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“…Combinatorial treatment for NSCLC with let-7b and miR-34a resulted in the strongest synergistic enhancement of the efficacy of erlotinib. In addition, transfection with let-7b is known to reverse drug sensitivity in chemotherapy-resistant SGC7901/DDP and SGC7901/ VCR gastric cancer cells by targeting the downregulation of c-Myc [57]. These results indicate that let-7 miRNAs can effectively reverse drug resistance and can be used as adjuvant therapeutics for the treatment of human cancers to modulate chemotherapy and radiation resistance [58,59].…”

Section: Restoration Of Let-7 Expression Shows Therapeutic Effects Inmentioning

confidence: 90%

Let-7 Family miRNAs Represent Potential Broad-Spectrum Therapeutic Molecules for Human Cancer

Guan¹,

Guo²,

M³

2015

J Genet Syndr Gene Ther

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miRNAs are a class of small non-coding RNAs that modulate gene expression. Let-7 was first discovered in Caenorhabditis elegans and is one of the most extensively studied miRNAs. The human let-7 family contains 13 miRNAs. The expression of these miRNAs is decreased in most human cancers and contributes to carcinogenesis and progression. Thus, the let-7 family of miRNAs has attracted the attention of researchers in various fields. Exogenous let-7 restoration has been confirmed to show antitumor efficacy in many human cancers. Let-7 functions as a tumor suppressor by acting upon several multi-signaling pathways and multiple downstream target oncogenes that are involved in most human cancers. Let-7 shows potential for modulation of chemoresistance and radiation sensitivity in human cancers. miRNAs in the let-7 family represent potential broad-spectrum antitumor molecules for human cancer therapy, and miRNAs in this family have been studied intensively for their therapeutic potential. However, most previous studies have been limited to a single functional aspect or focused on a single effect in a particular type of cancer. Here, we review the latest research on let-7 and discuss its potential value as a broadspectrum antitumor molecule.

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Inhibition of c-Myc by let-7b mimic reverses mutidrug resistance in gastric cancer cells

Cited by 47 publications

References 48 publications

miR-451 suppresses bladder cancer cell migration and invasion via directly targeting c-Myc

miR-451 suppresses bladder cancer cell migration and invasion via directly targeting c-Myc

Trophectoderm-Specific Knockdown of LIN28 Decreases Expression of Genes Necessary for Cell Proliferation and Reduces Elongation of Sheep Conceptus

Let-7 Family miRNAs Represent Potential Broad-Spectrum Therapeutic Molecules for Human Cancer

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