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Silencing of STRN4 suppresses the malignant characteristics of cancer cells.

Wong M, Hyodo T, Asano E, Funasaka K, Miyahara R, Hirooka Y, Goto H, Hamaguchi M, Senga T - Cancer Sci. (2014)

Bottom Line: We previously reported that STRN4 directly associated with protein kinases, such as MINK1, TNIK and MAP4K4, which are associated with tumor suppression or tumor progression.However, it remains unclear whether STRN4 is associated with tumor progression.Our results demonstrate a possible role of STRN4 in tumor progression.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology and Hepatology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

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Depletion of STRN4 sensitizes KP4 cells to gemcitabine. (a) Expression of STRN4 was examined via immunoblot. (b) The cells were cultured in the presence of various concentrations of gemcitabine, and the proliferation ratio was evaluated. Data are presented as percent growth of cells treated without gemcitabine. (c) The cells were cultured in the presence of 1 μM of gemcitabine for 72 h and then subjected to TUNEL assay. The graph shows the percentage of apoptotic cells from three independent experiments. The data are shown as the mean ± SD (*P < 0.05).
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fig04: Depletion of STRN4 sensitizes KP4 cells to gemcitabine. (a) Expression of STRN4 was examined via immunoblot. (b) The cells were cultured in the presence of various concentrations of gemcitabine, and the proliferation ratio was evaluated. Data are presented as percent growth of cells treated without gemcitabine. (c) The cells were cultured in the presence of 1 μM of gemcitabine for 72 h and then subjected to TUNEL assay. The graph shows the percentage of apoptotic cells from three independent experiments. The data are shown as the mean ± SD (*P < 0.05).

Mentions: To determine whether STRN4 suppression can sensitize cancer cells to anticancer drugs, we tested gemcitabine, a nucleoside analog used for pancreatic cancer treatment, in KP4 pancreatic cancer cells. To avoid the toxicity of the transfection reagent, we established KP4 cells that constitutively expressed two different shRNA targeting STRN4 (shSTRN4-1 and shSTRN4-2) as well as control shRNA-expressing cells (shCtrl). The expression of STRN4 was reduced in both the shSTRN4-1 and shSTRN4-2 cells (Fig. 4a). These cells were cultured in the presence of various concentrations of gemcitabine, and cell growth was assessed. As shown in Figure 4(b), the STRN4-depleted KP4 cells were more sensitive to gemcitabine treatment than the control KP4 cells. To further confirm the increased sensitivity to gemcitabine, we performed a TUNEL assay. shCtrl and shSTRN4-1 cells were incubated with or without gemcitabine for 72 h and then analyzed. We observed a significant increase in apoptotic cells depleted of STRN4 (Fig. 4c). These results indicate that knockdown of STRN4 can sensitize cells to gemcitabine treatment.


Silencing of STRN4 suppresses the malignant characteristics of cancer cells.

Wong M, Hyodo T, Asano E, Funasaka K, Miyahara R, Hirooka Y, Goto H, Hamaguchi M, Senga T - Cancer Sci. (2014)

Depletion of STRN4 sensitizes KP4 cells to gemcitabine. (a) Expression of STRN4 was examined via immunoblot. (b) The cells were cultured in the presence of various concentrations of gemcitabine, and the proliferation ratio was evaluated. Data are presented as percent growth of cells treated without gemcitabine. (c) The cells were cultured in the presence of 1 μM of gemcitabine for 72 h and then subjected to TUNEL assay. The graph shows the percentage of apoptotic cells from three independent experiments. The data are shown as the mean ± SD (*P < 0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317966&req=5

fig04: Depletion of STRN4 sensitizes KP4 cells to gemcitabine. (a) Expression of STRN4 was examined via immunoblot. (b) The cells were cultured in the presence of various concentrations of gemcitabine, and the proliferation ratio was evaluated. Data are presented as percent growth of cells treated without gemcitabine. (c) The cells were cultured in the presence of 1 μM of gemcitabine for 72 h and then subjected to TUNEL assay. The graph shows the percentage of apoptotic cells from three independent experiments. The data are shown as the mean ± SD (*P < 0.05).
Mentions: To determine whether STRN4 suppression can sensitize cancer cells to anticancer drugs, we tested gemcitabine, a nucleoside analog used for pancreatic cancer treatment, in KP4 pancreatic cancer cells. To avoid the toxicity of the transfection reagent, we established KP4 cells that constitutively expressed two different shRNA targeting STRN4 (shSTRN4-1 and shSTRN4-2) as well as control shRNA-expressing cells (shCtrl). The expression of STRN4 was reduced in both the shSTRN4-1 and shSTRN4-2 cells (Fig. 4a). These cells were cultured in the presence of various concentrations of gemcitabine, and cell growth was assessed. As shown in Figure 4(b), the STRN4-depleted KP4 cells were more sensitive to gemcitabine treatment than the control KP4 cells. To further confirm the increased sensitivity to gemcitabine, we performed a TUNEL assay. shCtrl and shSTRN4-1 cells were incubated with or without gemcitabine for 72 h and then analyzed. We observed a significant increase in apoptotic cells depleted of STRN4 (Fig. 4c). These results indicate that knockdown of STRN4 can sensitize cells to gemcitabine treatment.

Bottom Line: We previously reported that STRN4 directly associated with protein kinases, such as MINK1, TNIK and MAP4K4, which are associated with tumor suppression or tumor progression.However, it remains unclear whether STRN4 is associated with tumor progression.Our results demonstrate a possible role of STRN4 in tumor progression.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology and Hepatology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Show MeSH
Related in: MedlinePlus