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miR-502 medaited histone methyltransferase SET8 expression is associated with outcome of esophageal squamous cell carcinoma

View Article: PubMed Central - PubMed

ABSTRACT

The histone methyltransferase SET8, whose expression is regulated by miR-502 though the binding site in the 3′ UTR of SET8, implicated in cancer development. Single nucleotide polymorphism (SNP) of rs16917496 located in the miR-502 and SET8 binding site was analyzed in esophageal squamous cell carcinoma (ESCC) patients, the SET8 C/C genotype was independently associated with longer post-operative survival by multivariate analysis (relative risk, 2.250; 95% CI, 1.041–4.857; p = 0.039). Moreover, the reduced SET8 expression mediated by SET8 C/C genotype was associated with longer ESCC survival. Functional assay indicated that the SET8 knock down could inhibit proliferation and promote apoptosis of ESCC cells. The subsequent assay also showed the markedly inhibition of ESCC cell migration and invasion by SET8 knock down. Our data suggested that the altering SET8 expression, which is mediated at least partly by miR-502 through changing the binding affinity between miR-502 and SET8 3′ UTR, could modify the ESCC outcome by inhibiting the proliferation and invasion as well as promoting the apoptosis of ECSS cell. Our data indicated that SET8 was a new target for ESCC therapy.

No MeSH data available.


Related in: MedlinePlus

SET8 knockdown inhibits proliferation, induces apoptosis, suppresses migration and invasion of ESCC cells.(A) Western blot analysis with anti-SET8 and anti-β-actin antibodies to selection of SET8siRNA in Eca109 cells; (B) SET8 knockdown inhibits ESCC cell proliferation by MTT assay; (C) Quantification of results of B; (D) SET8 knockdown suppresses migration of ESCC cells by wound healing assay; (E) Quantification of results of D; (F) SET8 knockdown suppresses invasion of ESCC cells by transwell assay; (G) SET8 knockdown induces apoptosis of ESCC cells by flow cytometry analysis; (H) Quantification of results of G. **p ≤ 0.01; *p ≤ 0.05.
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f2: SET8 knockdown inhibits proliferation, induces apoptosis, suppresses migration and invasion of ESCC cells.(A) Western blot analysis with anti-SET8 and anti-β-actin antibodies to selection of SET8siRNA in Eca109 cells; (B) SET8 knockdown inhibits ESCC cell proliferation by MTT assay; (C) Quantification of results of B; (D) SET8 knockdown suppresses migration of ESCC cells by wound healing assay; (E) Quantification of results of D; (F) SET8 knockdown suppresses invasion of ESCC cells by transwell assay; (G) SET8 knockdown induces apoptosis of ESCC cells by flow cytometry analysis; (H) Quantification of results of G. **p ≤ 0.01; *p ≤ 0.05.

Mentions: Eca109 cells were successfully transfected four psi-H1-SET8siRNAs, as shown in Fig. 2A, the SET8siRNA2 ligated in psi-H1 plasmid could reduce the protein levels of SET8 dramatically in comparing with other SET8siRNAs, so we use SET8siRNA2 for further analysis.


miR-502 medaited histone methyltransferase SET8 expression is associated with outcome of esophageal squamous cell carcinoma
SET8 knockdown inhibits proliferation, induces apoptosis, suppresses migration and invasion of ESCC cells.(A) Western blot analysis with anti-SET8 and anti-β-actin antibodies to selection of SET8siRNA in Eca109 cells; (B) SET8 knockdown inhibits ESCC cell proliferation by MTT assay; (C) Quantification of results of B; (D) SET8 knockdown suppresses migration of ESCC cells by wound healing assay; (E) Quantification of results of D; (F) SET8 knockdown suppresses invasion of ESCC cells by transwell assay; (G) SET8 knockdown induces apoptosis of ESCC cells by flow cytometry analysis; (H) Quantification of results of G. **p ≤ 0.01; *p ≤ 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5015112&req=5

f2: SET8 knockdown inhibits proliferation, induces apoptosis, suppresses migration and invasion of ESCC cells.(A) Western blot analysis with anti-SET8 and anti-β-actin antibodies to selection of SET8siRNA in Eca109 cells; (B) SET8 knockdown inhibits ESCC cell proliferation by MTT assay; (C) Quantification of results of B; (D) SET8 knockdown suppresses migration of ESCC cells by wound healing assay; (E) Quantification of results of D; (F) SET8 knockdown suppresses invasion of ESCC cells by transwell assay; (G) SET8 knockdown induces apoptosis of ESCC cells by flow cytometry analysis; (H) Quantification of results of G. **p ≤ 0.01; *p ≤ 0.05.
Mentions: Eca109 cells were successfully transfected four psi-H1-SET8siRNAs, as shown in Fig. 2A, the SET8siRNA2 ligated in psi-H1 plasmid could reduce the protein levels of SET8 dramatically in comparing with other SET8siRNAs, so we use SET8siRNA2 for further analysis.

View Article: PubMed Central - PubMed

ABSTRACT

The histone methyltransferase SET8, whose expression is regulated by miR-502 though the binding site in the 3′ UTR of SET8, implicated in cancer development. Single nucleotide polymorphism (SNP) of rs16917496 located in the miR-502 and SET8 binding site was analyzed in esophageal squamous cell carcinoma (ESCC) patients, the SET8 C/C genotype was independently associated with longer post-operative survival by multivariate analysis (relative risk, 2.250; 95% CI, 1.041–4.857; p = 0.039). Moreover, the reduced SET8 expression mediated by SET8 C/C genotype was associated with longer ESCC survival. Functional assay indicated that the SET8 knock down could inhibit proliferation and promote apoptosis of ESCC cells. The subsequent assay also showed the markedly inhibition of ESCC cell migration and invasion by SET8 knock down. Our data suggested that the altering SET8 expression, which is mediated at least partly by miR-502 through changing the binding affinity between miR-502 and SET8 3′ UTR, could modify the ESCC outcome by inhibiting the proliferation and invasion as well as promoting the apoptosis of ECSS cell. Our data indicated that SET8 was a new target for ESCC therapy.

No MeSH data available.


Related in: MedlinePlus