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Elevated S100A6 (Calcyclin) enhances tumorigenesis and suppresses CXCL14-induced apoptosis in clear cell renal cell carcinoma.

Lyu XJ, Li HZ, Ma X, Li XT, Gao Y, Ni D, Shen DL, Gu LY, Wang BJ, Zhang Y, Zhang X - Oncotarget (2015)

Bottom Line: We found elevated S100A6 levels in ccRCC tissues, associated with higher grade pathological features and clinical stages in ccRCC patients.Knockdown of S100A6 inhibited cell proliferation in vitro and tumor growth in vivo.We suggest that the S100A6/CXCL14 signaling pathway is a potential therapeutic target in ccRCC.

View Article: PubMed Central - PubMed

Affiliation: Department of Urology/State Key Laboratory of Kidney Diseases, Chinese People's Liberation Army General Hospital/PLA Medical School, Beijing, People's Republic of China.

ABSTRACT
Clear cell renal cell carcinoma (ccRCC) is often resistant to existing therapy. We found elevated S100A6 levels in ccRCC tissues, associated with higher grade pathological features and clinical stages in ccRCC patients. Knockdown of S100A6 inhibited cell proliferation in vitro and tumor growth in vivo. Gene expression profiling suggests a novel function of S100A6 in suppressing apoptosis, as well as a relationship between S100A6 and CXCL14, a pro-inflammatory chemokine. We suggest that the S100A6/CXCL14 signaling pathway is a potential therapeutic target in ccRCC.

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Inhibition of S100A6 suppressed cell proliferation in vitro and vivo, and effected the G2/M phase(A) Western blot assayed to identify the transfection efficiency of the 786-O and Caki-1 S100A6 stable cells, using the 786-O and Caki-1 untreated cells as control. The efficiency was satisfactory. (B) The proliferation curve by MTS assays showed that overexpression of S100A6 did not promote the 786-O and Caki-1 cells growth, whereas knockdown of S100A6 suppressed the cells growth. The data were expressed as mean ± SD. (C) Tumor growth curve of shS100A6, shControl and 786-O Untreated cells in nude mice. Tumor sizes were determined as described in the Materials and Methods. The tumor weight derived from the shS100A6 group was lower than from the shControl and 786-O untreated groups when nude mice were sacrificed at 8 weeks after injection. The data show as the min to max of tumor weight. (D) Influence of S100A6 in 786-O and Caki-1 cells on cell cycle distribution. 786-O and Caki-1 cells were stable transfected by overexpression and knockdown of S100A6, compared to vector control respectively and untreated cells control. The overexpression of S100A6 in both cell lines showed no differences in cycling phase distribution comparing to the empty vector control. The shS100A6 groups in both cell lines showed a lower percentage in G0/G1 phase and a higher percentage in G2/M phase comparing to the shControl and untreated cells control. *p < 0.05; **p < 0.01; ***p < 0.001.
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Figure 2: Inhibition of S100A6 suppressed cell proliferation in vitro and vivo, and effected the G2/M phase(A) Western blot assayed to identify the transfection efficiency of the 786-O and Caki-1 S100A6 stable cells, using the 786-O and Caki-1 untreated cells as control. The efficiency was satisfactory. (B) The proliferation curve by MTS assays showed that overexpression of S100A6 did not promote the 786-O and Caki-1 cells growth, whereas knockdown of S100A6 suppressed the cells growth. The data were expressed as mean ± SD. (C) Tumor growth curve of shS100A6, shControl and 786-O Untreated cells in nude mice. Tumor sizes were determined as described in the Materials and Methods. The tumor weight derived from the shS100A6 group was lower than from the shControl and 786-O untreated groups when nude mice were sacrificed at 8 weeks after injection. The data show as the min to max of tumor weight. (D) Influence of S100A6 in 786-O and Caki-1 cells on cell cycle distribution. 786-O and Caki-1 cells were stable transfected by overexpression and knockdown of S100A6, compared to vector control respectively and untreated cells control. The overexpression of S100A6 in both cell lines showed no differences in cycling phase distribution comparing to the empty vector control. The shS100A6 groups in both cell lines showed a lower percentage in G0/G1 phase and a higher percentage in G2/M phase comparing to the shControl and untreated cells control. *p < 0.05; **p < 0.01; ***p < 0.001.

Mentions: To explore the biological mechanism of S100A6 elevated in ccRCC, we knocked down and overexpressed S100A6 in two ccRCC cell lines, 786-O and Caki-1. The efficiency of stable transfection S100A6 was detected in both cell lines by Western blotting analysis (Figure 2A). The vector maps were shown in Supplementary Figure 1A and 1B. The efficiency of transfection was shown in Supplementary Figure 1C and 1D. The cell growth of shS100A6, shControl, CMV-S100A6, CMV-eGFP and two untreated cell lines were measured by MTS assay at the time points of 0 h, 24 h, 48 h, 72 h, and 96 h. The results revealed that knockdown of S100A6 suppressed cell growth, while overexpression of S100A6 did not promote the 786-O, and Caki-1 cell growth (Figure 2B).


Elevated S100A6 (Calcyclin) enhances tumorigenesis and suppresses CXCL14-induced apoptosis in clear cell renal cell carcinoma.

Lyu XJ, Li HZ, Ma X, Li XT, Gao Y, Ni D, Shen DL, Gu LY, Wang BJ, Zhang Y, Zhang X - Oncotarget (2015)

Inhibition of S100A6 suppressed cell proliferation in vitro and vivo, and effected the G2/M phase(A) Western blot assayed to identify the transfection efficiency of the 786-O and Caki-1 S100A6 stable cells, using the 786-O and Caki-1 untreated cells as control. The efficiency was satisfactory. (B) The proliferation curve by MTS assays showed that overexpression of S100A6 did not promote the 786-O and Caki-1 cells growth, whereas knockdown of S100A6 suppressed the cells growth. The data were expressed as mean ± SD. (C) Tumor growth curve of shS100A6, shControl and 786-O Untreated cells in nude mice. Tumor sizes were determined as described in the Materials and Methods. The tumor weight derived from the shS100A6 group was lower than from the shControl and 786-O untreated groups when nude mice were sacrificed at 8 weeks after injection. The data show as the min to max of tumor weight. (D) Influence of S100A6 in 786-O and Caki-1 cells on cell cycle distribution. 786-O and Caki-1 cells were stable transfected by overexpression and knockdown of S100A6, compared to vector control respectively and untreated cells control. The overexpression of S100A6 in both cell lines showed no differences in cycling phase distribution comparing to the empty vector control. The shS100A6 groups in both cell lines showed a lower percentage in G0/G1 phase and a higher percentage in G2/M phase comparing to the shControl and untreated cells control. *p < 0.05; **p < 0.01; ***p < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
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Figure 2: Inhibition of S100A6 suppressed cell proliferation in vitro and vivo, and effected the G2/M phase(A) Western blot assayed to identify the transfection efficiency of the 786-O and Caki-1 S100A6 stable cells, using the 786-O and Caki-1 untreated cells as control. The efficiency was satisfactory. (B) The proliferation curve by MTS assays showed that overexpression of S100A6 did not promote the 786-O and Caki-1 cells growth, whereas knockdown of S100A6 suppressed the cells growth. The data were expressed as mean ± SD. (C) Tumor growth curve of shS100A6, shControl and 786-O Untreated cells in nude mice. Tumor sizes were determined as described in the Materials and Methods. The tumor weight derived from the shS100A6 group was lower than from the shControl and 786-O untreated groups when nude mice were sacrificed at 8 weeks after injection. The data show as the min to max of tumor weight. (D) Influence of S100A6 in 786-O and Caki-1 cells on cell cycle distribution. 786-O and Caki-1 cells were stable transfected by overexpression and knockdown of S100A6, compared to vector control respectively and untreated cells control. The overexpression of S100A6 in both cell lines showed no differences in cycling phase distribution comparing to the empty vector control. The shS100A6 groups in both cell lines showed a lower percentage in G0/G1 phase and a higher percentage in G2/M phase comparing to the shControl and untreated cells control. *p < 0.05; **p < 0.01; ***p < 0.001.
Mentions: To explore the biological mechanism of S100A6 elevated in ccRCC, we knocked down and overexpressed S100A6 in two ccRCC cell lines, 786-O and Caki-1. The efficiency of stable transfection S100A6 was detected in both cell lines by Western blotting analysis (Figure 2A). The vector maps were shown in Supplementary Figure 1A and 1B. The efficiency of transfection was shown in Supplementary Figure 1C and 1D. The cell growth of shS100A6, shControl, CMV-S100A6, CMV-eGFP and two untreated cell lines were measured by MTS assay at the time points of 0 h, 24 h, 48 h, 72 h, and 96 h. The results revealed that knockdown of S100A6 suppressed cell growth, while overexpression of S100A6 did not promote the 786-O, and Caki-1 cell growth (Figure 2B).

Bottom Line: We found elevated S100A6 levels in ccRCC tissues, associated with higher grade pathological features and clinical stages in ccRCC patients.Knockdown of S100A6 inhibited cell proliferation in vitro and tumor growth in vivo.We suggest that the S100A6/CXCL14 signaling pathway is a potential therapeutic target in ccRCC.

View Article: PubMed Central - PubMed

Affiliation: Department of Urology/State Key Laboratory of Kidney Diseases, Chinese People's Liberation Army General Hospital/PLA Medical School, Beijing, People's Republic of China.

ABSTRACT
Clear cell renal cell carcinoma (ccRCC) is often resistant to existing therapy. We found elevated S100A6 levels in ccRCC tissues, associated with higher grade pathological features and clinical stages in ccRCC patients. Knockdown of S100A6 inhibited cell proliferation in vitro and tumor growth in vivo. Gene expression profiling suggests a novel function of S100A6 in suppressing apoptosis, as well as a relationship between S100A6 and CXCL14, a pro-inflammatory chemokine. We suggest that the S100A6/CXCL14 signaling pathway is a potential therapeutic target in ccRCC.

Show MeSH
Related in: MedlinePlus