MIER3 suppresses colorectal cancer progression by down-regulating Sp1, inhibiting epithelial-mesenchymal transition

Peng, Man; Hu, Yukun; Song, Wen; Duan, Shiyu; Xu, Qiong; Ding, Yan‐Qing; Geng, Jiao; Zhou, Jun

doi:10.1038/s41598-017-11374-y

Cited by 25 publications

(26 citation statements)

References 32 publications

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“…Sp1 participates in the process of eMT by regulating the expression of eMT markers (19,20,33). a previous study identified that in gastric cancer, Sp1 was a target of miR-335-5p (21).…”

Section: Discussionmentioning

confidence: 96%

“…The expression levels of n-cadherin and Snail exhibited no significant difference between JEG-3 cells transfected with mir-335-5p mimics for 24 and 48 h, whereas e-cadherin expression was significantly increased in the mir-335-5p mimics 48 h group compared with the 24 h group (P<0.001). (19,20). a previous study revealed that Sp1 was the target of mir-335-5p in gastric cancer (21).…”

Section: Mir-335-5p Significantly Suppresses the Migration Of Jeg-3 Cmentioning

confidence: 95%

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ROS/p53/miR‑335‑5p/Sp1 axis modulates the migration and epithelial to mesenchymal transition of JEG‑3 cells

Shao

et al. 2019

Mol Med Report

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differential expression of microrna (mir)-335-5p, a key tumor suppressor, has been detected in pre-eclampsia (Pe) placentas. However, the role of mir-335-5p in the pathogenesis of Pe and the factor modulating its aberrant expression remain unknown. The present study used JeG-3 cells in vitro to investigate these mechanisms. The role of mir-335-5p in proliferation, apoptosis and migration of JeG-3 cells was investigated using MTT, annexin V-FiTc/Pi, Transwell migration and wound healing assays, respectively. mir-335-5p expression levels were analyzed using reverse transcription-quantitative Pcr. The expression levels of e-cadherin, N-cadherin, Snail, specificity protein 1 (Sp1) and p53 were assessed using western blot analysis. cell viability analysis was performed using the cell counting Kit-8 assay. The intracellular reactive oxygen species (roS) levels were detected using a 2,7-dichlorodihydrofluorescein diacetate assay. The present results suggested that mir-335-5p did not affect the proliferation or apoptotic rate of JeG-3 cells. overexpression of miR-335-5p significantly inhibited the migration of JEG-3 cells, decreased the expression levels of Sp1, n-cadherin and Snail, and increased e-cadherin expression. Sp1 silencing produced similar results in JeG-3 cells. H 2 o 2 significantly increased the intracellular roS levels and mir-335-5p expression, whereas n-acetyl-cysteine pretreatment prior to H 2 o 2 treatment reversed the increases in mir-335-5p expression. Knockdown of p53 significantly decreased the expression levels of mir-335-5p in JeG-3 cells and in H 2 o 2-treated cells. The present results suggested that mir-335-5p expression levels in trophoblast cells could be increased by roS in a p53-dependent manner, leading to the downregulation of Sp1 and subsequent inhibition of epithelial to mesenchymal transition and cell migration. The present results may provide novel evidence on the etiology of Pe.

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“…Sp1 participates in the process of eMT by regulating the expression of eMT markers (19,20,33). a previous study identified that in gastric cancer, Sp1 was a target of miR-335-5p (21).…”

Section: Discussionmentioning

confidence: 96%

Section: Mir-335-5p Significantly Suppresses the Migration Of Jeg-3 Cmentioning

confidence: 95%

ROS/p53/miR‑335‑5p/Sp1 axis modulates the migration and epithelial to mesenchymal transition of JEG‑3 cells

Shao

et al. 2019

Mol Med Report

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“…Furthermore, it was widely reported that a single gene can inhibit CRC. For instance, MIER3 [ 14 ], LASP2 [ 15 ], SIRT1 [ 16 ], and LZTS1 [ 17 ] genes can inhibit the development of CRC. Because the neoplasm develops through a complex process, it cannot be completely elucidated by understanding the changes in a single gene; therefore, the aims of this study are as follows: to elucidate the molecular mechanism of the development of CRC in the midst of each stage generally, and to analyze the links among signal control network during each stage.…”

Section: Introductionmentioning

confidence: 99%

Construction of key signal regulatory network in metastatic colorectal cancer

Lü

Ding

2017

Oncotarget

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There are many stages in the development and metastasis of colorectal cancer (CRC). In this study, we compared the differential expression genes in different stages of metastatic CRC. Then, we screened the continuously up-regulated genes and the continuously down-regulated genes that were associated with the development and metastasis of CRC. After analyzing the intersection of differential expression genes in each stage, we screened the continuously up-regulated genes and deviated genes in the extracellular matrix and the continuously down-regulated genes and deviated genes in the mitochrondia of CRC. Then, we performed gene ontology enrichment analysis of the deviated genes in different phases, and we found that key molecular events occurred in the period extending from stage II to III (early stage of metastasis) of CRC. Furthermore, in this period we found that the chemotaxis of inflammatory cells had decreased in the extracellular matrix. On the other hand, the aerobic respiration had increased in the mitochondrion. Then, we constructed protein-protein interaction network of deviated genes in the extracellular matrix and mitochondrion. We used the network module and hub network to analyze the protein-protein interaction network. The network module analysis showed that the protein complex of VEGFA and CCL7-CCR3 is the key node in the extracellular matrix, while MAPK1 is the key node in the mitochondrion. The hub network analysis showed that the signal transmission chain FN1→SPARC→COL1A1→MMP2 is the key regulatory pathway for extracellular signal transmission. Furthermore, it also showed that CAV1→MAPK3→RAF1→NR3C1→MAPK1→ESR1 is the key regulatory pathway for signal transmission in mitochondrion.

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“…Sp1 is ubiquitously expressed and dysregulated in various cancers. About 12,000 Sp1 sites are estimated existing in human genome; among them, Sp1 regulation on protein coding genes has been extensively investigated, 4 , 29 , 30 whereas its regulation on non-protein coding genes was less studied. Recently, few studies explored Sp1 regulation on miRNAs.…”

Section: Discussionmentioning

confidence: 99%

Sp1 Suppresses miR-3178 to Promote the Metastasis Invasion Cascade via Upregulation of TRIOBP

Wang

et al. 2018

Molecular Therapy - Nucleic Acids

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Specificity protein (Sp1) plays an important role in invasion-metastasis cascade. Sp1 regulation on protein coding genes has been extensively investigated; however, little is known about its regulation on protein non-coding genes. In this study, miR-3178 is reported as a novel target of Sp1 in multiple cancer cell models. Sp1 functions as its transcriptional suppressor as evidenced by luciferase reporter and chromatin immunoprecipitation (ChIP) assays. In line with the pro-metastatic role of Sp1, miR-3178 exerts anti-metastasis function. Overexpression of miR-3178 inhibits both migration and invasion of highly metastatic prostate, lung, and breast cancer cells whereas antagonizing miR-3178 promotes those events in their lowly metastatic counterparts. The in vivo study demonstrates that miR-3178 suppresses the tail vein inoculated prostate cancer cells to form colonies in lung, lymph node, and liver of BALB/c nude mice. miR-3178 directly targets the 3′ UTR of TRIOBP-1 and TRIOBP-5, two isoforms of TRIOBP expressed in prostate, lung, and breast cancer cells. Overexpression of TRIOBP-1 could rescue miR-3178 inhibition on cell migration and invasion. Collectively, our findings reveal the regulatory axis of Sp1/miR-3178/TRIOBP in metastasis cascade. Our results suggest miR-3178 as a promising application to suppress metastasis in Sp1-overexpressed cancers.

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MIER3 suppresses colorectal cancer progression by down-regulating Sp1, inhibiting epithelial-mesenchymal transition

Cited by 25 publications

References 32 publications

ROS/p53/miR‑335‑5p/Sp1 axis modulates the migration and epithelial to mesenchymal transition of JEG‑3 cells

ROS/p53/miR‑335‑5p/Sp1 axis modulates the migration and epithelial to mesenchymal transition of JEG‑3 cells

Construction of key signal regulatory network in metastatic colorectal cancer

Sp1 Suppresses miR-3178 to Promote the Metastasis Invasion Cascade via Upregulation of TRIOBP

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