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Restored expression levels of TET1 decrease the proliferation and migration of renal carcinoma cells.

Fan M, He X, Xu X - Mol Med Rep (2015)

Bottom Line: Ten‑eleven translocation methylcytosine dioxygenase 1 (TET1) is a member of the TET family of enzymes, and is expressed at low levels in multiple malignancies.As a result, TET1 was observed to exhibit markedly low expression levels in 54 tumor tissue samples from 54 patients with renal carcinoma.In conclusion, the results demonstrated that TET1 is involved in tumor inhibition in renal carcinoma by promoting cell apoptosis and inhibiting cell proliferation and invasion, which may be exploited as a novel therapeutic target in the treatment of renal carcinoma.

View Article: PubMed Central - PubMed

Affiliation: Department of Urology, The First People's Hospital of Changzhou, Changzhou, Jiangsu 213003, P.R. China.

ABSTRACT
Renal carcinoma is the most common type of kidney cancer in adults and is responsible for ~90‑95% of the cases of kidney cancer. Ten‑eleven translocation methylcytosine dioxygenase 1 (TET1) is a member of the TET family of enzymes, and is expressed at low levels in multiple malignancies. In the present study, a series of experiments were designed and performed to investigate whether the expression of TET1 is clinically correlated with clinical outcomes in renal carcinoma, and to examine the associations between TET1 expression level and the proliferation and migration in renal carcinoma cells. As a result, TET1 was observed to exhibit markedly low expression levels in 54 tumor tissue samples from 54 patients with renal carcinoma. Furthermore, statistical analysis revealed a clinical correlation between low expression levels of TET1 and the prognosis of patients with renal carcinoma. When TET1 was overexpressed in renal carcinoma cells, the viability and invasive abilities of the cells were decreased, and the rate of apoptosis was increased. In conclusion, the results demonstrated that TET1 is involved in tumor inhibition in renal carcinoma by promoting cell apoptosis and inhibiting cell proliferation and invasion, which may be exploited as a novel therapeutic target in the treatment of renal carcinoma.

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Overexpressed TET1 inhibits ACHN cell proliferation and metastasis, and improves apoptosis. (A) TET1 was overexpressed in the ACHN renal carcinoma cell line. The ACHN cells were transfected with pCMV6-XL5-TET1 and screened using puromycin to generate a stable cell line. The protein levels in the whole cell extracts were analyzed using western blot analysis. (B) Proliferation rate of the TET1-overexpressed ACHN cells was determined using flow cytometric analysis. The PI was calculated as follows: PI= (S + G2/M) / (S + G2/M + G0/G1). (C) Metastatic ability of the TET1-overexpressed ACHN cells was determined using a Transwell assay. (D) Apoptotic rate of the TET1 overexpressed ACHN cells was analyzed using flow cytometry subsequent to labeling with PI and annexin V. (*P<0.05, compared with the vector group). TET1, ten-eleven translocation methylcytosine dioxygenase 1; FITC, fluorescein isothiocyanate.
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f4-mmr-12-04-4837: Overexpressed TET1 inhibits ACHN cell proliferation and metastasis, and improves apoptosis. (A) TET1 was overexpressed in the ACHN renal carcinoma cell line. The ACHN cells were transfected with pCMV6-XL5-TET1 and screened using puromycin to generate a stable cell line. The protein levels in the whole cell extracts were analyzed using western blot analysis. (B) Proliferation rate of the TET1-overexpressed ACHN cells was determined using flow cytometric analysis. The PI was calculated as follows: PI= (S + G2/M) / (S + G2/M + G0/G1). (C) Metastatic ability of the TET1-overexpressed ACHN cells was determined using a Transwell assay. (D) Apoptotic rate of the TET1 overexpressed ACHN cells was analyzed using flow cytometry subsequent to labeling with PI and annexin V. (*P<0.05, compared with the vector group). TET1, ten-eleven translocation methylcytosine dioxygenase 1; FITC, fluorescein isothiocyanate.

Mentions: The present study also investigated the role of TET1 in renal carcinoma cells. Exogenous TET1 was expressed at high levels in the ACHN renal carcinoma cell line and was 217.34% of the level observed in the control cells (Fig. 4A). The proliferation index of the ACHN cells overexpressing TET1 was markedly decreased (P<0.05) compared with ACHN expressing background levels of TET1 (Fig. 4B). Additionally, the metastatic ability was also reduced when TET1 was overexpressed in the ACHN cells (Fig. 4C). The results of the flow cytometric analysis demonstrated that 12.5% of the ACHN cells containing exogenous TET1 were at the early stage of apoptosis, whereas only 1.28% of ACHN cells expressing background levels of TET1 were at the early stage (Fig. 4D). Taken together, these results suggested that the overexpression of TET1 inhibited renal carcinoma.


Restored expression levels of TET1 decrease the proliferation and migration of renal carcinoma cells.

Fan M, He X, Xu X - Mol Med Rep (2015)

Overexpressed TET1 inhibits ACHN cell proliferation and metastasis, and improves apoptosis. (A) TET1 was overexpressed in the ACHN renal carcinoma cell line. The ACHN cells were transfected with pCMV6-XL5-TET1 and screened using puromycin to generate a stable cell line. The protein levels in the whole cell extracts were analyzed using western blot analysis. (B) Proliferation rate of the TET1-overexpressed ACHN cells was determined using flow cytometric analysis. The PI was calculated as follows: PI= (S + G2/M) / (S + G2/M + G0/G1). (C) Metastatic ability of the TET1-overexpressed ACHN cells was determined using a Transwell assay. (D) Apoptotic rate of the TET1 overexpressed ACHN cells was analyzed using flow cytometry subsequent to labeling with PI and annexin V. (*P<0.05, compared with the vector group). TET1, ten-eleven translocation methylcytosine dioxygenase 1; FITC, fluorescein isothiocyanate.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4581741&req=5

f4-mmr-12-04-4837: Overexpressed TET1 inhibits ACHN cell proliferation and metastasis, and improves apoptosis. (A) TET1 was overexpressed in the ACHN renal carcinoma cell line. The ACHN cells were transfected with pCMV6-XL5-TET1 and screened using puromycin to generate a stable cell line. The protein levels in the whole cell extracts were analyzed using western blot analysis. (B) Proliferation rate of the TET1-overexpressed ACHN cells was determined using flow cytometric analysis. The PI was calculated as follows: PI= (S + G2/M) / (S + G2/M + G0/G1). (C) Metastatic ability of the TET1-overexpressed ACHN cells was determined using a Transwell assay. (D) Apoptotic rate of the TET1 overexpressed ACHN cells was analyzed using flow cytometry subsequent to labeling with PI and annexin V. (*P<0.05, compared with the vector group). TET1, ten-eleven translocation methylcytosine dioxygenase 1; FITC, fluorescein isothiocyanate.
Mentions: The present study also investigated the role of TET1 in renal carcinoma cells. Exogenous TET1 was expressed at high levels in the ACHN renal carcinoma cell line and was 217.34% of the level observed in the control cells (Fig. 4A). The proliferation index of the ACHN cells overexpressing TET1 was markedly decreased (P<0.05) compared with ACHN expressing background levels of TET1 (Fig. 4B). Additionally, the metastatic ability was also reduced when TET1 was overexpressed in the ACHN cells (Fig. 4C). The results of the flow cytometric analysis demonstrated that 12.5% of the ACHN cells containing exogenous TET1 were at the early stage of apoptosis, whereas only 1.28% of ACHN cells expressing background levels of TET1 were at the early stage (Fig. 4D). Taken together, these results suggested that the overexpression of TET1 inhibited renal carcinoma.

Bottom Line: Ten‑eleven translocation methylcytosine dioxygenase 1 (TET1) is a member of the TET family of enzymes, and is expressed at low levels in multiple malignancies.As a result, TET1 was observed to exhibit markedly low expression levels in 54 tumor tissue samples from 54 patients with renal carcinoma.In conclusion, the results demonstrated that TET1 is involved in tumor inhibition in renal carcinoma by promoting cell apoptosis and inhibiting cell proliferation and invasion, which may be exploited as a novel therapeutic target in the treatment of renal carcinoma.

View Article: PubMed Central - PubMed

Affiliation: Department of Urology, The First People's Hospital of Changzhou, Changzhou, Jiangsu 213003, P.R. China.

ABSTRACT
Renal carcinoma is the most common type of kidney cancer in adults and is responsible for ~90‑95% of the cases of kidney cancer. Ten‑eleven translocation methylcytosine dioxygenase 1 (TET1) is a member of the TET family of enzymes, and is expressed at low levels in multiple malignancies. In the present study, a series of experiments were designed and performed to investigate whether the expression of TET1 is clinically correlated with clinical outcomes in renal carcinoma, and to examine the associations between TET1 expression level and the proliferation and migration in renal carcinoma cells. As a result, TET1 was observed to exhibit markedly low expression levels in 54 tumor tissue samples from 54 patients with renal carcinoma. Furthermore, statistical analysis revealed a clinical correlation between low expression levels of TET1 and the prognosis of patients with renal carcinoma. When TET1 was overexpressed in renal carcinoma cells, the viability and invasive abilities of the cells were decreased, and the rate of apoptosis was increased. In conclusion, the results demonstrated that TET1 is involved in tumor inhibition in renal carcinoma by promoting cell apoptosis and inhibiting cell proliferation and invasion, which may be exploited as a novel therapeutic target in the treatment of renal carcinoma.

Show MeSH
Related in: MedlinePlus