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MKK7 mediates miR-493-dependent suppression of liver metastasis of colon cancer cells.

Sakai H, Sato A, Aihara Y, Ikarashi Y, Midorikawa Y, Kracht M, Nakagama H, Okamoto K - Cancer Sci. (2014)

Bottom Line: However, major functional targets that mediate the antimetastatic activity of miR-493 remain elusive.Here, we extended our search for target genes and identified MKK7, a mitogen-activated protein kinase kinase, as a novel target of miR-493. miR-493 inhibits MKK7 expression by targeting the binding site at the 3'-UTR of the mkk7 gene.Immunohistochemical examination in human primary colon tumors revealed that the occurrence of liver metastasis is associated with elevated levels of MKK7.

View Article: PubMed Central - PubMed

Affiliation: Division of Cancer Development System, National Cancer Center Research Institute, Tokyo, Japan.

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MKK7 is expressed in colon cancer cells and involved in activating phosphorylation of JNK. (a) Western blots of MKK7 for the indicated colon cells. (b) Inhibition of JNK phosphorylation by MKK7 siRNA. HCT116 cells were transfected with control or MKK7 siRNA. Two days after transfection, the cells were treated with 0.5 M sorbitol or buffer for 30 min, and used for Western blot analyses with the indicated antibodies.
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fig02: MKK7 is expressed in colon cancer cells and involved in activating phosphorylation of JNK. (a) Western blots of MKK7 for the indicated colon cells. (b) Inhibition of JNK phosphorylation by MKK7 siRNA. HCT116 cells were transfected with control or MKK7 siRNA. Two days after transfection, the cells were treated with 0.5 M sorbitol or buffer for 30 min, and used for Western blot analyses with the indicated antibodies.

Mentions: Next, we examined MKK7 expression in colon cancer cell lines. Western blot analyses showed that MKK7 was expressed in six out of seven colon cancer cell lines examined (DLD-1, HCT116, HT29, RKO, SW480, and SW620), whereas the level of expression in non-transformed FHC colon epithelial cells was much lower than those in the cancer cells (Fig. 2a).


MKK7 mediates miR-493-dependent suppression of liver metastasis of colon cancer cells.

Sakai H, Sato A, Aihara Y, Ikarashi Y, Midorikawa Y, Kracht M, Nakagama H, Okamoto K - Cancer Sci. (2014)

MKK7 is expressed in colon cancer cells and involved in activating phosphorylation of JNK. (a) Western blots of MKK7 for the indicated colon cells. (b) Inhibition of JNK phosphorylation by MKK7 siRNA. HCT116 cells were transfected with control or MKK7 siRNA. Two days after transfection, the cells were treated with 0.5 M sorbitol or buffer for 30 min, and used for Western blot analyses with the indicated antibodies.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317799&req=5

fig02: MKK7 is expressed in colon cancer cells and involved in activating phosphorylation of JNK. (a) Western blots of MKK7 for the indicated colon cells. (b) Inhibition of JNK phosphorylation by MKK7 siRNA. HCT116 cells were transfected with control or MKK7 siRNA. Two days after transfection, the cells were treated with 0.5 M sorbitol or buffer for 30 min, and used for Western blot analyses with the indicated antibodies.
Mentions: Next, we examined MKK7 expression in colon cancer cell lines. Western blot analyses showed that MKK7 was expressed in six out of seven colon cancer cell lines examined (DLD-1, HCT116, HT29, RKO, SW480, and SW620), whereas the level of expression in non-transformed FHC colon epithelial cells was much lower than those in the cancer cells (Fig. 2a).

Bottom Line: However, major functional targets that mediate the antimetastatic activity of miR-493 remain elusive.Here, we extended our search for target genes and identified MKK7, a mitogen-activated protein kinase kinase, as a novel target of miR-493. miR-493 inhibits MKK7 expression by targeting the binding site at the 3'-UTR of the mkk7 gene.Immunohistochemical examination in human primary colon tumors revealed that the occurrence of liver metastasis is associated with elevated levels of MKK7.

View Article: PubMed Central - PubMed

Affiliation: Division of Cancer Development System, National Cancer Center Research Institute, Tokyo, Japan.

Show MeSH
Related in: MedlinePlus