MicroRNA-22 suppresses the growth, migration and invasion of colorectal cancer cells through a Sp1 negative feedback loop

Xia, Shu-Sen; Zhang, Guangjun; Liu, Zuo-Liang; Tian, Hongpeng; He, Yi; Meng, Chunyan; Li, Lifa; Wang, Ziwei; Zhou, Tong

doi:10.18632/oncotarget.16742

Cited by 43 publications

(58 citation statements)

References 47 publications

(46 reference statements)

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“…Recent studies have shown that miR‐22 is involved in various biologic processes, including cell proliferation, apoptosis, viability, EMT, and cell cycle. Evidence has shown that miR‐22 suppresses colon cancer cell migration and invasion by inhibiting the expression of TIAM1 (41) and SP1 (42). In our current study, overexpression of miR‐22 in HCT116 and RKO cells inhibited proliferation and migration in vitro , which is consistent with findings from previous studies (41–43).…”

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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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: 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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“…MiR-181a 31–33 , miR-16 34–36 and miR-133b 37–39 were individually investigated in three studies. MiR-126 8, 40 , miR-133a 41, 42 , miR-182 43, 44 , miR-183 45, 46 , miR-199b 47, 48 , miR-22 49, 50 , miR-224 51, 52 , miR-24-3p 53, 54 , miR-7 55, 56 , were separately analyzed in two studies. Seven researches studied two miRs concomitantly 30, 34, 38, 39, 57–59 , while the others analyzed a single miR.…”

Section: Resultsmentioning

confidence: 99%

“…Some of the selected studies investigated the target genes of the miRs associated with the prognostic aspects of CRC. In total, 65 target genes were analyzed in which the most frequent ones were: PTEN, investigated in six studies 29, 32, 33, 50, 60, 61 , SMAD4, investigated in three studies 62–64 , and TP53 65, 66 investigated in two studies.…”

Section: Resultsmentioning

confidence: 99%

“…Twenty-four studies demonstrated the downregulation of twenty-five miRs associated with advanced TNM stage: miR-302c 67 , miR-466 68 , miR-340 69 , miR-196b-5p 70 , miR-944 71 , miR-30d 72 , miR-22 50 , miR-296 73 , miR-384 74 , miR-199b 48 , miR-128 75 , miR-33b 76 , miR-155-5p 77 , miR-154 78 , miR-149 79 , miR-194 80 , miR-133b 37 , miR-15a 34 , miR-100 81 , miR-133a 41 , miR-335 82 , miR-378a-3p 58 , miR-378a-5p 58 , miR-218 83 and miR-16 34 . Two studies demonstrated the upregulation of miR-182 43, 44 associated with advanced TNM stage and others 22 studies pointed 23 different upregulated miRs associated with advanced TNM stage.…”

Section: Resultsmentioning

confidence: 99%

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Tissue micro-RNAs associated with colorectal cancer prognosis: a systematic review

Santos

Penna

Carneiro

et al. 2019

Preprint

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Colorectal cancer (CRC) is a multifactorial disease commonly diagnosed worldwide, with high mortality rates. Several studies demonstrate important associations between differential expression of micro-RNAs (miRs) and the prognosis of CRC. However, only a few systematic reviews emphasize the most relevant miRs able to contribute to the establishment of new prognostic biomarkers in CRC patients. The present study aimed to identify differentially expressed tissue miRs associated with prognostic factors in CRC patients, through a systematic review of the Literature. Using the PubMed database, Cochrane Library and Web of Science, studies published in English evaluating miRs differentially expressed in tumor tissue and significantly associated with the prognostic aspects of CRC were selected. All the included studies used RT-PCR (Taqman or SYBR Green) for miR expression analysis and the period of publication was from 2009 to 2018. A total of 115 articles accomplished the inclusion criteria and were included in the review. The studies investigated the expression of 102 different miRs associated with prognostic aspects in colorectal cancer patients. The most frequent oncogenic miRs investigated were miR-21, miR-181a, miR-182, miR-183, miR-210 and miR-224 and the hyperexpression of these miRs was associated with distant metastasis, lymph node metastasis and worse survival in patients with CRC. The most frequent tumor suppressor miRs were miR-126, miR-199b and miR-22 and the hypoexpression of these miRs was associated with distant metastasis, worse prognosis and a higher risk of disease relapse (worse disease-free survival). Specific tissue miRs are shown to be promising prognostic biomarkers in patients with CRC, given their strong association with the prognostic aspects of these tumors, however, new studies are necessary to establish the sensibility and specificity of the miRs in order to use them in clinical practice.

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“…To our knowledge, lncRNAs can regulate gene expression by sponging miRNAs ( present study, we found 23 potential targets of miR-525-5p by using two bioinformatics prediction tools (PITA and RNA22; Figure 5a). Among which, SP1 has been reported both in CH and miRNA-mRNA axis (Domínguez, 2013;Ji et al, 2017;Sack, Disch, Rockman, & Kelly, 1997;Xia et al, 2017). Therefore, we chose SP1 to do further study.…”

Section: Syne1-as1 Enhanced the Expression Of Sp1 By Sponging Mir-5mentioning

confidence: 99%

SP1‐SYNE1‐AS1‐miR‐525‐5p feedback loop regulates Ang‐II‐induced cardiac hypertrophy

Wang

Cao

Yang

et al. 2019

Journal Cellular Physiology

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Cardiac hypertrophy (CH) has become a huge threat to human health. Recent years, long noncoding RNAs (lncRNAs) have been studied in human diseases, including CH. According to bioinformatics analysis, 10 lncRNAs possibly involved in the progression of CH were screened out. Among which, lncRNA SYNE1 antisense RNA 1 (SYNE1‐AS1) could be upregulated by Angiotensin II (Ang‐II) in cardiomyocytes. Thus, we chose SYNE1‐AS1 to do further study. To identify the biological function of SYNE1‐AS1 in CH, SYNE1‐AS1 was silenced in Ang‐II‐induced cardiomyocytes. Results of immunofluorescence staining demonstrated that increased cell surface area in Ang‐II‐induced cardiomyocytes was reduced by SYNE1‐AS1 knockdown. Moreover, the hypertrophic responses were attenuated by SYNE1‐AS1 knockdown. Mechanically, SYNE1‐AS1 positively regulated Sp1 transcription factor (SP1) by sponging microRNA‐525‐5p (miR‐525‐5p). On the basis of previous reports, SP1 can transcriptionally activate lncRNAs. Therefore, we investigated the interaction between SP1 and SYNE1‐AS1 promoter. Intriguingly, SYNE1‐AS1 was activated by SP1. At last, rescue assays demonstrated the function of SP1‐SYNE1‐AS1 axis in CH. In conclusion, SP1‐induced upregulation of lncRNA SYNE1‐AS1 promoted CH via miR‐525‐5p/SP1 axis.

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MicroRNA-22 suppresses the growth, migration and invasion of colorectal cancer cells through a Sp1 negative feedback loop

Cited by 43 publications

References 47 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

Tissue micro-RNAs associated with colorectal cancer prognosis: a systematic review

SP1‐SYNE1‐AS1‐miR‐525‐5p feedback loop regulates Ang‐II‐induced cardiac hypertrophy

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