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Figure 3. Continued. PLCε regulates DNA damage repair by altering the AR/DNA‑PKcs pathway. (C) mRNA and (D) protein expression levels of PLCε, AR, DNA‑PKcs and <t>H2AX</t> in PCa cells. ‘#’ indicates irradiated cells. *P<0.05, **P<0.01 and ***P<0.001. PCa, prostate cancer; PLCε, phospholipase Cε; AR, androgen receptor.
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Figure 3. Continued. PLCε regulates DNA damage repair by altering the AR/DNA‑PKcs pathway. (C) mRNA and (D) protein expression levels of PLCε, AR, DNA‑PKcs and <t>H2AX</t> in PCa cells. ‘#’ indicates irradiated cells. *P<0.05, **P<0.01 and ***P<0.001. PCa, prostate cancer; PLCε, phospholipase Cε; AR, androgen receptor.
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Figure 3. Continued. PLCε regulates DNA damage repair by altering the AR/DNA‑PKcs pathway. (C) mRNA and (D) protein expression levels of PLCε, AR, DNA‑PKcs and <t>H2AX</t> in PCa cells. ‘#’ indicates irradiated cells. *P<0.05, **P<0.01 and ***P<0.001. PCa, prostate cancer; PLCε, phospholipase Cε; AR, androgen receptor.
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Figure 3. Continued. PLCε regulates DNA damage repair by altering the AR/DNA‑PKcs pathway. (C) mRNA and (D) protein expression levels of PLCε, AR, DNA‑PKcs and <t>H2AX</t> in PCa cells. ‘#’ indicates irradiated cells. *P<0.05, **P<0.01 and ***P<0.001. PCa, prostate cancer; PLCε, phospholipase Cε; AR, androgen receptor.
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Figure 3. Continued. PLCε regulates DNA damage repair by altering the AR/DNA‑PKcs pathway. (C) mRNA and (D) protein expression levels of PLCε, AR, DNA‑PKcs and <t>H2AX</t> in PCa cells. ‘#’ indicates irradiated cells. *P<0.05, **P<0.01 and ***P<0.001. PCa, prostate cancer; PLCε, phospholipase Cε; AR, androgen receptor.
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Figure 3. Continued. PLCε regulates DNA damage repair by altering the AR/DNA‑PKcs pathway. (C) mRNA and (D) protein expression levels of PLCε, AR, DNA‑PKcs and <t>H2AX</t> in PCa cells. ‘#’ indicates irradiated cells. *P<0.05, **P<0.01 and ***P<0.001. PCa, prostate cancer; PLCε, phospholipase Cε; AR, androgen receptor.
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Figure 3. Continued. PLCε regulates DNA damage repair by altering the AR/DNA‑PKcs pathway. (C) mRNA and (D) protein expression levels of PLCε, AR, DNA‑PKcs and <t>H2AX</t> in PCa cells. ‘#’ indicates irradiated cells. *P<0.05, **P<0.01 and ***P<0.001. PCa, prostate cancer; PLCε, phospholipase Cε; AR, androgen receptor.
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Figure 3. Continued. PLCε regulates DNA damage repair by altering the AR/DNA‑PKcs pathway. (C) mRNA and (D) protein expression levels of PLCε, AR, DNA‑PKcs and <t>H2AX</t> in PCa cells. ‘#’ indicates irradiated cells. *P<0.05, **P<0.01 and ***P<0.001. PCa, prostate cancer; PLCε, phospholipase Cε; AR, androgen receptor.
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Spectrogon US narrow bandpass filter spectrogon filter n13-1270-010-8
Figure 3. Continued. PLCε regulates DNA damage repair by altering the AR/DNA‑PKcs pathway. (C) mRNA and (D) protein expression levels of PLCε, AR, DNA‑PKcs and <t>H2AX</t> in PCa cells. ‘#’ indicates irradiated cells. *P<0.05, **P<0.01 and ***P<0.001. PCa, prostate cancer; PLCε, phospholipase Cε; AR, androgen receptor.
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Thorlabs optical bandwidth filter thorlabs fl05532-10
Figure 3. Continued. PLCε regulates DNA damage repair by altering the AR/DNA‑PKcs pathway. (C) mRNA and (D) protein expression levels of PLCε, AR, DNA‑PKcs and <t>H2AX</t> in PCa cells. ‘#’ indicates irradiated cells. *P<0.05, **P<0.01 and ***P<0.001. PCa, prostate cancer; PLCε, phospholipase Cε; AR, androgen receptor.
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OptiGrate Corp ultra-narrow bandpass filter
Figure 3. Continued. PLCε regulates DNA damage repair by altering the AR/DNA‑PKcs pathway. (C) mRNA and (D) protein expression levels of PLCε, AR, DNA‑PKcs and <t>H2AX</t> in PCa cells. ‘#’ indicates irradiated cells. *P<0.05, **P<0.01 and ***P<0.001. PCa, prostate cancer; PLCε, phospholipase Cε; AR, androgen receptor.
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Image Search Results


Figure 3. Continued. PLCε regulates DNA damage repair by altering the AR/DNA‑PKcs pathway. (C) mRNA and (D) protein expression levels of PLCε, AR, DNA‑PKcs and H2AX in PCa cells. ‘#’ indicates irradiated cells. *P<0.05, **P<0.01 and ***P<0.001. PCa, prostate cancer; PLCε, phospholipase Cε; AR, androgen receptor.

Journal: Oncology reports

Article Title: PLCε knockdown enhances the radiosensitivity of castration‑resistant prostate cancer via the AR/PARP1/DNA‑PKcs axis.

doi: 10.3892/or.2020.7520

Figure Lengend Snippet: Figure 3. Continued. PLCε regulates DNA damage repair by altering the AR/DNA‑PKcs pathway. (C) mRNA and (D) protein expression levels of PLCε, AR, DNA‑PKcs and H2AX in PCa cells. ‘#’ indicates irradiated cells. *P<0.05, **P<0.01 and ***P<0.001. PCa, prostate cancer; PLCε, phospholipase Cε; AR, androgen receptor.

Article Snippet: Following blocking with 5% skimmed milk for 2 h at room temperature, the membranes were incubated with primary antibodies targeting PLCε (1:500; cat. no. sc-28402; Santa Cruz Biotechnology, Inc.), AR (1:1,000; cat. no. 5153; CST Biological Reagents Co., Ltd.), PARP1 (1:1,000; cat. no. ab32138; Abcam), DNA-dependent protein kinase catalytic subunit (DNA-PKcs; 1:1,000; cat. no. ab168854; Abcam), H2AX (1:1,000; cat. no. 7631; CST Biological Reagents Co., Ltd.), γ-H2AX (1:1,000; cat. no. 7631; CST Biological Reagents Co., Ltd.) and GAPDH (1:1,000; cat. no. 5174; Cell Signaling Technology) overnight at 4 ̊C, washed with TBS + 0.05% Tween‐20 (Beijing Solarbio Science & Technology Co., Ltd.), and subsequently incubated with a horseradish peroxidase-conjugated goat anti-rabbit immunoglobulin G secondary antibody (1:2,000; cat. no. TA130015; OriGene Technologies, Inc.) for 1 h at room temperature.

Techniques: Expressing, Irradiation

Figure 7. PLCε knockdown inhibits the growth of CRPC in vivo. (A and B) Immunocompromised mice were subcutaneously injected with PLCε‑knockdown or control Bica‑R cells, and the tumor sizes and weights of the two groups are presented. (C) Comparison of positive rate of IHC in each group. (D) Expression of PLCε, AR, PARP1, DNA‑PKcs and γ‑H2AX in each group. Magnification, x200. *P<0.05 and ***P<0.001. PLCε, phospholipase Cε; CRPC, castration‑resistant prostate cancer; Bica‑R, Bicalutamide‑resistant; AR, Androgen receptor; PARP1, poly (ADP‑ribose) polymerase 1; H2AX, H2A histone family member X.

Journal: Oncology reports

Article Title: PLCε knockdown enhances the radiosensitivity of castration‑resistant prostate cancer via the AR/PARP1/DNA‑PKcs axis.

doi: 10.3892/or.2020.7520

Figure Lengend Snippet: Figure 7. PLCε knockdown inhibits the growth of CRPC in vivo. (A and B) Immunocompromised mice were subcutaneously injected with PLCε‑knockdown or control Bica‑R cells, and the tumor sizes and weights of the two groups are presented. (C) Comparison of positive rate of IHC in each group. (D) Expression of PLCε, AR, PARP1, DNA‑PKcs and γ‑H2AX in each group. Magnification, x200. *P<0.05 and ***P<0.001. PLCε, phospholipase Cε; CRPC, castration‑resistant prostate cancer; Bica‑R, Bicalutamide‑resistant; AR, Androgen receptor; PARP1, poly (ADP‑ribose) polymerase 1; H2AX, H2A histone family member X.

Article Snippet: Following blocking with 5% skimmed milk for 2 h at room temperature, the membranes were incubated with primary antibodies targeting PLCε (1:500; cat. no. sc-28402; Santa Cruz Biotechnology, Inc.), AR (1:1,000; cat. no. 5153; CST Biological Reagents Co., Ltd.), PARP1 (1:1,000; cat. no. ab32138; Abcam), DNA-dependent protein kinase catalytic subunit (DNA-PKcs; 1:1,000; cat. no. ab168854; Abcam), H2AX (1:1,000; cat. no. 7631; CST Biological Reagents Co., Ltd.), γ-H2AX (1:1,000; cat. no. 7631; CST Biological Reagents Co., Ltd.) and GAPDH (1:1,000; cat. no. 5174; Cell Signaling Technology) overnight at 4 ̊C, washed with TBS + 0.05% Tween‐20 (Beijing Solarbio Science & Technology Co., Ltd.), and subsequently incubated with a horseradish peroxidase-conjugated goat anti-rabbit immunoglobulin G secondary antibody (1:2,000; cat. no. TA130015; OriGene Technologies, Inc.) for 1 h at room temperature.

Techniques: Knockdown, In Vivo, Injection, Control, Comparison, Expressing