microRNA-214 functions as a tumor suppressor in human colon cancer via the suppression of ADP-ribosylation factor-like protein 2

Long, Ling; He, Benfu; Huang, Guoqing; Guo, Ying; Liu, You‐Shuo; Huo, Jirong

doi:10.3892/ol.2014.2746

Cited by 41 publications

(37 citation statements)

References 26 publications

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“…Ectopic overexpression of miR‐214 inhibits cell proliferation and migration of human colon cancer cells. These results are similar to other findings in colon cancer (19, 44, 45). The underlying mechanism of miR‐214 in the progression of colon cancer remains to be clarified.…”

Section: Discussionsupporting

confidence: 93%

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miR‐22 and miR‐214 targeting BCL9L inhibit proliferation, metastasis, and epithelial‐mesenchymal transition by down‐regulating Wnt signaling in colon cancer

Sun

Liu²,

Lin

et al. 2019

FASEB j.

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The epithelial‐mesenchymal transition (EMT) is crucial for cancer progression. Evidence has shown that miR‐22 and miR‐214 play a key role in colon cancer progression; however, the underlying mechanism remains to be known. The effects of miR‐22 and miR‐214 on EMT are contradictory in different cancers, and whether miR‐22 and miR‐214 are involved in the colon cancer EMT process needs to be elucidated. In this study, we evaluated the exact role and the regulation mechanism of miR‐22 and miR‐214 in colon cancer. After transfection with miR‐22 expression vector, the cell proliferation and migration capacity of HCT116 and RKO cells were significantly suppressed. Also, E‐cadherin was increased and vimentin was decreased by miR‐22 overexpression. Similar effects were also observed after miR‐214 expression vector transfection. Dual‐lucif erase reporter confirmed that BCL9L is the target gene of both miR‐22 and miR‐214. Silencing of BCL9L inhibits cell proliferation and migration, and the expression of E‐cadherin and vimentin was also altered by BCL9L knockdown, which was consistent with miR‐22 or miR‐214 transfection. Furthermore, miR‐22 and miR‐214 inhibited tumor growth in nude mice. Moreover, although the association between BCL9L's lower expression and longer survival time was statistically nonsignificant, a trend existed; further studies in a larger cohort are needed. Collectively, these data suggest that miR‐22 and miR‐214 inhibit cell proliferation, migration, and EMT of colon cancer, most likely by targeting BCL9L.—Sun, R., Liu, Z., Han, L., Yang, Y., Wu, F., Jiang, Q., Zhang, H., Ma, R., Miao, J., He, K., Wang, X., Zhou, D., Huang, C. miR‐22 and miR‐214 targeting BCL9L inhibit proliferation, metastasis, and epithelial‐mesenchymal transition by down‐regulating Wnt signliang in colon cancer. FASEB J. 33, 5411–5424 (2019). http://www.fasebj.org

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Section: Discussionsupporting

confidence: 93%

“…Previously, miR‐214 was reported to function as a tumor suppressor in colon cancer (11, 44, 45). miR‐214 inhibits colon cancer proliferation and migration via the suppression of ARL2 (44) and HMGA1 (45). miR‐214/ MED19 axis suppresses tumor growth and metastasis in human CRC (11).…”

Section: Discussionmentioning

confidence: 99%

miR‐22 and miR‐214 targeting BCL9L inhibit proliferation, metastasis, and epithelial‐mesenchymal transition by down‐regulating Wnt signaling in colon cancer

Sun

Liu²,

Lin

et al. 2019

FASEB j.

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“…Wang et al reported that miR-499 could inhibit the dephosphorylation of calcineurin-induced Drp1 protein, reduce the accumulation of Drp1 in the mitochondria and inhibit the activation of Drp1-induced mitochondrial fission, in order to keep the cardiomyocytes from apoptosis [29] . According to Targetscan bioinformatic websites [30,31] , it's predicted that miR-208a could be complementarily paired with 3 0 UTR region of calcineurin mRNA, which indicated that miR-208a might also inhibit the calcineurin, inhibit the activation of mitochondrial apoptosis pathway, and thus inhibit the apoptosis. The focus of our further study would be seeking the target gene of miR-208a and the determination whether miR-208a actually inhibits the apoptosis by acting on such target gene.…”

Section: Discussionmentioning

confidence: 99%

Effect of microRNA-208a on mitochondrial apoptosis of cardiomyocytes of neonatal rats

Meng

Zhu³

et al. 2015

Asian Pacific Journal of Tropical Medicine

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“…It has been consistently reported to be deregulated in human cervical (CaCx) and colorectal cancers (CRC) and is associated with suppression of tumour growth and metastasis. A few oncogenic targets like GALNT7 , Bcl2l2 , and TFAM in CaCx and FGF‐1 and ARL2 in CRC have been identified. Many of these targets are suggested to be crucial to promotion of growth, epithelial‐to‐mesenchymal transition (EMT), and metastasis, but the identification of a target that could equally be a hub of deregulated signalling as miR‐214 would open up avenues to contemplate a novel, multidirectional approach to designing therapeutic interventions.…”

Section: Introductionmentioning

confidence: 99%

miR‐214 activates TP53 but suppresses the expression of RELA, CTNNB1, and STAT3 in human cervical and colorectal cancer cells

Chandrasekaran

Sathyanarayanan

Karunagaran

2017

Cell Biochemistry & Function

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High Mobility Group AT-hook 1 (HMGA1) was identified as a target of miR-214 in human cervical and colorectal cancers (CaCx and CRC) in a previous study. While the expression of miR-214 remains suppressed, HMGA1 behaves as a potent oncogene and plays crucial roles in several aberrant signalling pathways by interacting with intermediates like RELA, CTNNB1, STAT3, and TP53 in CaCx and CRC. Hypothetically, miR-214 should be able to regulate the stabilization of some of these intermediates through the regulation of HMGA1. This was assessed by ectopically expressing miR-214 or complementarily, by inhibiting the expression of HMGA1. In promoter luciferase assays, miR-214 inhibited NF-κB and Wnt activities but elevated TP53 activity in cancer cells. Further, miR-214 suppressed the expression of HMGA1, RELA, CTNNB1, and STAT3 while elevating TP53 levels, similar to when small interfering RNA (siRNA) against HMGA1 was used, as revealed by Western blotting. It is suggested that poor expression of miR-214, commonly reported in CaCx and CRC tissues, may not only result in the sustained expression of HMGA1 but also that of RELA, CTNNB1, and STAT3, and a congruent suppression of TP53 during cancer initiation/progression. These several states are, however, reversed when miR-214 is reintroduced and could explain the tumour suppressive functions observed in earlier studies. Further studies are, however, required to reveal how microRNA-mediated regulation of HMGA1 expression may affect individual signalling pathways in CaCx and CRC. Current results reveal that miR-214 is not only able to regulate the expression of its direct target, HMGA1, but also that of a few signalling intermediates like TP53, RELA, CTNNB1, and STAT3, with which HMGA1 interacts. These intermediates play crucial roles in signalling pathways commonly deregulated in human CaCx and CRC. Hence, it is proposed that miR-214 might act as a tumour suppressor by regulating several aberrant signalling pathways through HMGA1. This knowledge has the potential to help design novel therapeutic strategies in CaCx and CRC.

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microRNA-214 functions as a tumor suppressor in human colon cancer via the suppression of ADP-ribosylation factor-like protein 2

Cited by 41 publications

References 26 publications

miR‐22 and miR‐214 targeting BCL9L inhibit proliferation, metastasis, and epithelial‐mesenchymal transition by down‐regulating Wnt signaling in colon cancer

miR‐22 and miR‐214 targeting BCL9L inhibit proliferation, metastasis, and epithelial‐mesenchymal transition by down‐regulating Wnt signaling in colon cancer

Effect of microRNA-208a on mitochondrial apoptosis of cardiomyocytes of neonatal rats

miR‐214 activates TP53 but suppresses the expression of RELA, CTNNB1, and STAT3 in human cervical and colorectal cancer cells

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