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miR156a Mimic Represses the Epithelial-Mesenchymal Transition of Human Nasopharyngeal Cancer Cells by Targeting Junctional Adhesion Molecule A.

Tian Y, Cai L, Tian Y, Tu Y, Qiu H, Xie G, Huang D, Zheng R, Zhang W - PLoS ONE (2016)

Bottom Line: We demonstrated that a total of 84 conserved miRNAs and 184 putative novel miRNAs were found in broccoli by sequencing technology.Knockdown of JAMA was consistent with the effects of miR156a mimic on the EMT of NPC, and the up-regulation of JAMA could partially restore EMT repressed by miR156a mimic.In conclusion, these results indicate that the miR156a mimic inhibits the EMT of NPC cells by targeting the 3' UTR of JAMA.

View Article: PubMed Central - PubMed

Affiliation: Department of Radiation Oncology, Cancer Center of Guangzhou Medical University, Guangzhou, Guangdong Province, People's Republic of China.

ABSTRACT
MicroRNAs (miRNAs) have been documented as having an important role in the development of cancer. Broccoli is very popular in large groups of the population and has anticancer properties. Junctional adhesion molecule A (JAMA) is preferentially concentrated at tight junctions and influences cell morphology and migration. Epithelial-mesenchymal transition (EMT) is a developmental program associated with cancer progression and metastasis. In this study we aimed to investigate the role of miRNAs from broccoli in human nasopharyngeal cancer (NPC). We demonstrated that a total of 84 conserved miRNAs and 184 putative novel miRNAs were found in broccoli by sequencing technology. Among these, miR156a was expressed the most. In addition, synthetic miR156a mimic inhibited the EMT of NPC cells in vitro. Furthermore, it was confirmed that JAMA was the target of miR156a mimic as validated by 3' UTR luciferase reporter assays and western blotting. Knockdown of JAMA was consistent with the effects of miR156a mimic on the EMT of NPC, and the up-regulation of JAMA could partially restore EMT repressed by miR156a mimic. In conclusion, these results indicate that the miR156a mimic inhibits the EMT of NPC cells by targeting the 3' UTR of JAMA. These miRNA profiles of broccoli provide a fundamental basis for further research. Moreover, the discovery of miR156a may have clinical implications for the treatment of patients with NPC.

No MeSH data available.


Related in: MedlinePlus

JAMA is essential for miR156a mimic-induced EMT of NPC cells and is involved in the activation of p-Akt in vitro.(A and B) Analysis of protein expression by western blotting, JAMA and p-Akt protein is reduced by miR156a mimic. (C) JAMA, vimentin and p-Akt are reduced by small interfering RNA (JAMA-siRNA) in CNE2 (C) and HONE1 cells (D). (E) Western blotting assay analyzed CNE2 cells transfected with the JAMA plasmid or vector control, along with miR156a or negative controls.
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pone.0157686.g004: JAMA is essential for miR156a mimic-induced EMT of NPC cells and is involved in the activation of p-Akt in vitro.(A and B) Analysis of protein expression by western blotting, JAMA and p-Akt protein is reduced by miR156a mimic. (C) JAMA, vimentin and p-Akt are reduced by small interfering RNA (JAMA-siRNA) in CNE2 (C) and HONE1 cells (D). (E) Western blotting assay analyzed CNE2 cells transfected with the JAMA plasmid or vector control, along with miR156a or negative controls.

Mentions: Previous studies have confirmed that JAMA regulates epithelial cell proliferation through Akt/β-catenin signaling [16]. Our results consistently indicated that the epithelial marker E-cadherin was significantly increased in CNE2 and HONE1 cell lines, whereas the protein expression of JAMA and p-Akt was reduced after transfection with miR156a mimic. However, the ERK signaling pathway was not affected (Fig 4A and 4B). JAMA was shown to be an authentic target for miR156a, but further investigation was needed to determine whether miR156a mimic inhibited EMT through direct down regulation JAMA. First, we investigated whether reducing JAMA expression might exert a similar repression effect on miR156a mimic. The results indicated that after transfection of JAMA-siRNA into CNE2 and HONE1 cell lines the expression of E-cadherin was increased, whereas p-Akt and the mesenchymal cell marker vimentin were substantially knocked down (Fig 4C and 4D).


miR156a Mimic Represses the Epithelial-Mesenchymal Transition of Human Nasopharyngeal Cancer Cells by Targeting Junctional Adhesion Molecule A.

Tian Y, Cai L, Tian Y, Tu Y, Qiu H, Xie G, Huang D, Zheng R, Zhang W - PLoS ONE (2016)

JAMA is essential for miR156a mimic-induced EMT of NPC cells and is involved in the activation of p-Akt in vitro.(A and B) Analysis of protein expression by western blotting, JAMA and p-Akt protein is reduced by miR156a mimic. (C) JAMA, vimentin and p-Akt are reduced by small interfering RNA (JAMA-siRNA) in CNE2 (C) and HONE1 cells (D). (E) Western blotting assay analyzed CNE2 cells transfected with the JAMA plasmid or vector control, along with miR156a or negative controls.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4920421&req=5

pone.0157686.g004: JAMA is essential for miR156a mimic-induced EMT of NPC cells and is involved in the activation of p-Akt in vitro.(A and B) Analysis of protein expression by western blotting, JAMA and p-Akt protein is reduced by miR156a mimic. (C) JAMA, vimentin and p-Akt are reduced by small interfering RNA (JAMA-siRNA) in CNE2 (C) and HONE1 cells (D). (E) Western blotting assay analyzed CNE2 cells transfected with the JAMA plasmid or vector control, along with miR156a or negative controls.
Mentions: Previous studies have confirmed that JAMA regulates epithelial cell proliferation through Akt/β-catenin signaling [16]. Our results consistently indicated that the epithelial marker E-cadherin was significantly increased in CNE2 and HONE1 cell lines, whereas the protein expression of JAMA and p-Akt was reduced after transfection with miR156a mimic. However, the ERK signaling pathway was not affected (Fig 4A and 4B). JAMA was shown to be an authentic target for miR156a, but further investigation was needed to determine whether miR156a mimic inhibited EMT through direct down regulation JAMA. First, we investigated whether reducing JAMA expression might exert a similar repression effect on miR156a mimic. The results indicated that after transfection of JAMA-siRNA into CNE2 and HONE1 cell lines the expression of E-cadherin was increased, whereas p-Akt and the mesenchymal cell marker vimentin were substantially knocked down (Fig 4C and 4D).

Bottom Line: We demonstrated that a total of 84 conserved miRNAs and 184 putative novel miRNAs were found in broccoli by sequencing technology.Knockdown of JAMA was consistent with the effects of miR156a mimic on the EMT of NPC, and the up-regulation of JAMA could partially restore EMT repressed by miR156a mimic.In conclusion, these results indicate that the miR156a mimic inhibits the EMT of NPC cells by targeting the 3' UTR of JAMA.

View Article: PubMed Central - PubMed

Affiliation: Department of Radiation Oncology, Cancer Center of Guangzhou Medical University, Guangzhou, Guangdong Province, People's Republic of China.

ABSTRACT
MicroRNAs (miRNAs) have been documented as having an important role in the development of cancer. Broccoli is very popular in large groups of the population and has anticancer properties. Junctional adhesion molecule A (JAMA) is preferentially concentrated at tight junctions and influences cell morphology and migration. Epithelial-mesenchymal transition (EMT) is a developmental program associated with cancer progression and metastasis. In this study we aimed to investigate the role of miRNAs from broccoli in human nasopharyngeal cancer (NPC). We demonstrated that a total of 84 conserved miRNAs and 184 putative novel miRNAs were found in broccoli by sequencing technology. Among these, miR156a was expressed the most. In addition, synthetic miR156a mimic inhibited the EMT of NPC cells in vitro. Furthermore, it was confirmed that JAMA was the target of miR156a mimic as validated by 3' UTR luciferase reporter assays and western blotting. Knockdown of JAMA was consistent with the effects of miR156a mimic on the EMT of NPC, and the up-regulation of JAMA could partially restore EMT repressed by miR156a mimic. In conclusion, these results indicate that the miR156a mimic inhibits the EMT of NPC cells by targeting the 3' UTR of JAMA. These miRNA profiles of broccoli provide a fundamental basis for further research. Moreover, the discovery of miR156a may have clinical implications for the treatment of patients with NPC.

No MeSH data available.


Related in: MedlinePlus