p53-Induced miR-15a/16-1 and AP4 Form a Double-Negative Feedback Loop to Regulate Epithelial–Mesenchymal Transition and Metastasis in Colorectal Cancer

Shi, Lei; Jackstadt, René; Siemens, Helge; Li, Huihui; Kirchner, Thomas; Hermeking, Heiko

doi:10.1158/0008-5472.can-13-2203

Cited by 111 publications

(96 citation statements)

References 47 publications

(63 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Slug (Snail2) is one of transcription factors that play a central role in the activation of EMT. And epithelial-to-mesenchymal transition (EMT) is considerate to be involved in migration, tumor invasion and dissemination [25,26,27]. Decreased E-cadherin and elevated Vimentin and N-cadherin expression is one hallmark of EMT which is a key element in the cancer invasion [28].…”

Section: Discussionmentioning

confidence: 99%

Down-Regulation of miR-140 Induces EMT and Promotes Invasion by Targeting Slug in Esophageal Cancer

Jiang

Zhou

et al. 2014

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: MicroRNAs (miRNAs) are reported to regulate cell invasion and functions by interfering with the translation of target mRNAs, but the role of miRNAs in esophageal cancer (EC) remains unclear. Methods: RT-PCR and Western blot were used to detect the expression of miRNAs and candidate genes in EC samples (n=89). miR-140 mimics and inhibitor were tansfected in human TE-1 and Eca-109 cells. The transwell assay was used to examine the cell invasive ability. The regulation mechanism was confirmed by luciferase reporter assay. The markers of EMT were detected by using Western blot. Results: miR-140 expression was decreased in the EC tissues compared with the corresponding adjacent tumor tissues. Low expression of miR-140 promotes cell invasion by using transwell assay, while the effect of miR-140 high expression is reverse. Slug, a target gene of miR-140, was examined by luciferase assay and Western blot. Conclusions: miR-140 may regulate the cell invasion of EC via controlling Slug expression.

show abstract

Section: Discussionmentioning

confidence: 99%

Down-Regulation of miR-140 Induces EMT and Promotes Invasion by Targeting Slug in Esophageal Cancer

Jiang

Zhou

et al. 2014

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…The human transcription factor activating protein-4 (AP4) is a basic helix-loop-helix leucine-zipper (bHLH-LZ) transcription factor, which forms homodimers that bind to the Ebox motif CAGCTG [10][11][12][13][14][15]. AP4 has been found to be a direct transcriptional target of c-MYC.…”

Section: Introductionmentioning

confidence: 99%

Regulation of activating protein-4-associated metastases of non-small cell lung cancer cells by miR-144

et al. 2015

View full text Add to dashboard Cite

Activating protein-4 (AP4) has been recently shown to regulate the cancer metastases in some cancers including non-small cell lung cancer (NSCLC). Specifically, AP4 regulates mTor/p21 and transforming growth factor β (TGFβ) receptor signaling pathway to increase an epithelial-mesenchymal transition process to augment cell invasiveness. Nevertheless, how AP4 is regulated in NSCLC has not been studied. Here, we showed that in the specimens from the NSCLC patients, the levels of miR-144 were significantly decreased and the levels of AP4 were significantly increased, compared to the paired non-tumor lung tissue. The levels of miR-144 and AP4 inversely correlated in patients' specimens. Bioinformatics analyses revealed that miR-144 targeted the 3'-UTR of AP4 mRNA to inhibit its translation, confirmed by luciferase-reporter assay. Moreover, miR-144 overexpression inhibited AP4-mediated cell invasiveness, while miR-144 depletion increased AP4-mediated cell invasiveness in NSCLC cells. Together, our data suggest that miR-144 suppression may be the cause of the increased levels of AP4, as well as the augmented cancer metastases, in NSCLC.

show abstract

“…However, the potential mechanism of miR-491 in EC still remains unclear. EMT is considered to be involved in migration, tumor invasion and dissemination [32][33][34]. Decreased E-cadherin and elevated Vimentin and N-cadherin expression is one hallmark of EMT which is a key element in the cancer invasion [35].…”

Section: Discussionmentioning

confidence: 99%

Low Expression of miR-491 Promotes Esophageal Cancer Cell Invasion by Targeting TPX2

Niu

Gong

Tian

et al. 2015

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: MicroRNAs (miRNAs) have a key role in carcinogenesis and cancer development, but the role of miRNAs in the progression of esophageal cancer (EC) remains unclear. Methods: The TE-1 and Eca-109 EC cell lines were used. The expression of miR-491 and candidate gene TPX2 in EC samples (n=99) were detected by RT-PCR. The cells invasive ability was determined by transwell assay. The luciferase reporter assay was used to confirm the regulation mechanism. Results: A decreased expression of miR-491 was detected in the EC clinical samples compared with the corresponding adjacent tumor tissues. Aberrant expression of miR-491 regulated cells invasion and EMT markers. Furthermore, we verified that TPX2 was a target gene of miR-491. Conclusions: miR-491 may play a critical role in EC.

show abstract

p53-Induced miR-15a/16-1 and AP4 Form a Double-Negative Feedback Loop to Regulate Epithelial–Mesenchymal Transition and Metastasis in Colorectal Cancer

Cited by 111 publications

References 47 publications

Down-Regulation of miR-140 Induces EMT and Promotes Invasion by Targeting Slug in Esophageal Cancer

Down-Regulation of miR-140 Induces EMT and Promotes Invasion by Targeting Slug in Esophageal Cancer

Regulation of activating protein-4-associated metastases of non-small cell lung cancer cells by miR-144

Low Expression of miR-491 Promotes Esophageal Cancer Cell Invasion by Targeting TPX2

Contact Info

Product

Resources

About