Radioresistance

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Xiaohong Hong - One of the best experts on this subject based on the ideXlab platform.

  • trim21 serpinb5 aids gmps repression to protect nasopharyngeal carcinoma cells from radiation induced apoptosis
    Journal of Biomedical Science, 2020
    Co-Authors: Panpan Zhang, Keqing Song, Qingmei He, Qiuping He, Xiao Jing Yang, Yaqin Wang, Xiaomin Li, Lu Lu Zhang, Xiaohong Hong
    Abstract:

    The main strategy against nasopharyngeal carcinoma (NPC) is radiotherapy. However, Radioresistance mediated recurrence is a leading clinical bottleneck in NPC. Revealing the mechanism of NPC Radioresistance will help improve the therapeutic effect. In this study, the role of TRIM21 (tripartite motif–containing 21) in NPC receiving ionizing radiation was firstly examined both in vivo and in vitro. Mass spectrometry analysis was performed to identify the downstream targets of TRIM21. NPC cells with TRIM21 or SERPINB5 (serpin family B member 5) overexpression or knockout were used to determine the epistatic relationship among SERPINB5, GMPS (guanine monophosphate synthase) and TRIM21. Flow cytometry, co-immunoprecipitation, western blot and immunofluorescence were employed to strengthen the results. Finally, immunohistochemistry using 4 radiosensitive and 8 radioresistent NPC patient samples was perform to examine the association between SERPINB5 or GMPS expression and patient radio-sensitivity. As an E3 ligase, TRIM21 was highly expressed in NPC. After ionizing radiation, TRIM21 repressed TP53 expression by mediating GMPS ubiquitination and degradation. Overexpression of TRIM21 protected NPC cells from radiation mediated cell apoptosis in vitro and in vivo. Further analysis revealed that TRIM21 mediated GMPS repression was dependent on SERPINB5, and SERPINB5 served as an adaptor which prevented GMPS from entering into the nucleus and introduced TRIM21 for GMPS ubiquitination. Moreover, the in vitro and in vivo results validated the finding that SERPINB5 promoted NPC cell Radioresistance, and the radioresistant patients had higher SERPINB5 expression. Overall, our data showed that TRIM21–SERPINB5-mediated GMPS degradation facilitated TP53 repression, which promoted the Radioresistance of NPC cells. This novel working model related to TP53 suppression provided new insight into NPC radioresistence clinically.

  • trim21 serpinb5 aids gmps repression to protect nasopharyngeal carcinoma cells from radiation induced apoptosis
    bioRxiv, 2019
    Co-Authors: Panpan Zhang, Keqing Song, Qingmei He, Qiuping He, Xiao Jing Yang, Yaqin Wang, Xiaomin Li, Lu Lu Zhang, Xiaohong Hong
    Abstract:

    Nasopharyngeal carcinoma (NPC) is the most prevalent head and neck malignancy in South China and Southeast Asia. The main NPC treatment strategy is radiotherapy. However, recurrence resulting from Radioresistance is a leading clinical bottleneck. Revealing the mechanism of NPC Radioresistance would help improve the therapeutic effect. Here, our work reveals that TRIM21 (tripartite motif-containing 21) functions as an oncogene in NPC progression, and its ablation increases NPC cell radiosensitivity. Further analysis indicated that TRIM21 represses TP53 expression by mediating GMPS (guanine monophosphate synthase) ubiquitination and degradation after ionizing radiation. Mass spectrometry and co-immunoprecipitation showed that SERPINB5 (serpin family B member 5) interacts with both TRIM21 and GMPS. Epistatic analysis showed that SERPINB5 acts as an adaptor to recruit GMPS and introduce TRIM21 for ubiquitination. The in vitro and in vivo results validated the finding that SERPINB5 promotes NPC cell Radioresistance. Furthermore, immunohistochemistry indicated that radioresistant patients have higher SERPINB5 expression. Overall, our data show that TRIM21-SERPINB5-mediated GMPS degradation facilitates TP53 repression, which promotes the Radioresistance of NPC cells.

Panpan Zhang - One of the best experts on this subject based on the ideXlab platform.

  • trim21 serpinb5 aids gmps repression to protect nasopharyngeal carcinoma cells from radiation induced apoptosis
    Journal of Biomedical Science, 2020
    Co-Authors: Panpan Zhang, Keqing Song, Qingmei He, Qiuping He, Xiao Jing Yang, Yaqin Wang, Xiaomin Li, Lu Lu Zhang, Xiaohong Hong
    Abstract:

    The main strategy against nasopharyngeal carcinoma (NPC) is radiotherapy. However, Radioresistance mediated recurrence is a leading clinical bottleneck in NPC. Revealing the mechanism of NPC Radioresistance will help improve the therapeutic effect. In this study, the role of TRIM21 (tripartite motif–containing 21) in NPC receiving ionizing radiation was firstly examined both in vivo and in vitro. Mass spectrometry analysis was performed to identify the downstream targets of TRIM21. NPC cells with TRIM21 or SERPINB5 (serpin family B member 5) overexpression or knockout were used to determine the epistatic relationship among SERPINB5, GMPS (guanine monophosphate synthase) and TRIM21. Flow cytometry, co-immunoprecipitation, western blot and immunofluorescence were employed to strengthen the results. Finally, immunohistochemistry using 4 radiosensitive and 8 radioresistent NPC patient samples was perform to examine the association between SERPINB5 or GMPS expression and patient radio-sensitivity. As an E3 ligase, TRIM21 was highly expressed in NPC. After ionizing radiation, TRIM21 repressed TP53 expression by mediating GMPS ubiquitination and degradation. Overexpression of TRIM21 protected NPC cells from radiation mediated cell apoptosis in vitro and in vivo. Further analysis revealed that TRIM21 mediated GMPS repression was dependent on SERPINB5, and SERPINB5 served as an adaptor which prevented GMPS from entering into the nucleus and introduced TRIM21 for GMPS ubiquitination. Moreover, the in vitro and in vivo results validated the finding that SERPINB5 promoted NPC cell Radioresistance, and the radioresistant patients had higher SERPINB5 expression. Overall, our data showed that TRIM21–SERPINB5-mediated GMPS degradation facilitated TP53 repression, which promoted the Radioresistance of NPC cells. This novel working model related to TP53 suppression provided new insight into NPC radioresistence clinically.

  • trim21 serpinb5 aids gmps repression to protect nasopharyngeal carcinoma cells from radiation induced apoptosis
    bioRxiv, 2019
    Co-Authors: Panpan Zhang, Keqing Song, Qingmei He, Qiuping He, Xiao Jing Yang, Yaqin Wang, Xiaomin Li, Lu Lu Zhang, Xiaohong Hong
    Abstract:

    Nasopharyngeal carcinoma (NPC) is the most prevalent head and neck malignancy in South China and Southeast Asia. The main NPC treatment strategy is radiotherapy. However, recurrence resulting from Radioresistance is a leading clinical bottleneck. Revealing the mechanism of NPC Radioresistance would help improve the therapeutic effect. Here, our work reveals that TRIM21 (tripartite motif-containing 21) functions as an oncogene in NPC progression, and its ablation increases NPC cell radiosensitivity. Further analysis indicated that TRIM21 represses TP53 expression by mediating GMPS (guanine monophosphate synthase) ubiquitination and degradation after ionizing radiation. Mass spectrometry and co-immunoprecipitation showed that SERPINB5 (serpin family B member 5) interacts with both TRIM21 and GMPS. Epistatic analysis showed that SERPINB5 acts as an adaptor to recruit GMPS and introduce TRIM21 for ubiquitination. The in vitro and in vivo results validated the finding that SERPINB5 promotes NPC cell Radioresistance. Furthermore, immunohistochemistry indicated that radioresistant patients have higher SERPINB5 expression. Overall, our data show that TRIM21-SERPINB5-mediated GMPS degradation facilitates TP53 repression, which promotes the Radioresistance of NPC cells.

Lu Lu Zhang - One of the best experts on this subject based on the ideXlab platform.

  • trim21 serpinb5 aids gmps repression to protect nasopharyngeal carcinoma cells from radiation induced apoptosis
    Journal of Biomedical Science, 2020
    Co-Authors: Panpan Zhang, Keqing Song, Qingmei He, Qiuping He, Xiao Jing Yang, Yaqin Wang, Xiaomin Li, Lu Lu Zhang, Xiaohong Hong
    Abstract:

    The main strategy against nasopharyngeal carcinoma (NPC) is radiotherapy. However, Radioresistance mediated recurrence is a leading clinical bottleneck in NPC. Revealing the mechanism of NPC Radioresistance will help improve the therapeutic effect. In this study, the role of TRIM21 (tripartite motif–containing 21) in NPC receiving ionizing radiation was firstly examined both in vivo and in vitro. Mass spectrometry analysis was performed to identify the downstream targets of TRIM21. NPC cells with TRIM21 or SERPINB5 (serpin family B member 5) overexpression or knockout were used to determine the epistatic relationship among SERPINB5, GMPS (guanine monophosphate synthase) and TRIM21. Flow cytometry, co-immunoprecipitation, western blot and immunofluorescence were employed to strengthen the results. Finally, immunohistochemistry using 4 radiosensitive and 8 radioresistent NPC patient samples was perform to examine the association between SERPINB5 or GMPS expression and patient radio-sensitivity. As an E3 ligase, TRIM21 was highly expressed in NPC. After ionizing radiation, TRIM21 repressed TP53 expression by mediating GMPS ubiquitination and degradation. Overexpression of TRIM21 protected NPC cells from radiation mediated cell apoptosis in vitro and in vivo. Further analysis revealed that TRIM21 mediated GMPS repression was dependent on SERPINB5, and SERPINB5 served as an adaptor which prevented GMPS from entering into the nucleus and introduced TRIM21 for GMPS ubiquitination. Moreover, the in vitro and in vivo results validated the finding that SERPINB5 promoted NPC cell Radioresistance, and the radioresistant patients had higher SERPINB5 expression. Overall, our data showed that TRIM21–SERPINB5-mediated GMPS degradation facilitated TP53 repression, which promoted the Radioresistance of NPC cells. This novel working model related to TP53 suppression provided new insight into NPC radioresistence clinically.

  • trim21 serpinb5 aids gmps repression to protect nasopharyngeal carcinoma cells from radiation induced apoptosis
    bioRxiv, 2019
    Co-Authors: Panpan Zhang, Keqing Song, Qingmei He, Qiuping He, Xiao Jing Yang, Yaqin Wang, Xiaomin Li, Lu Lu Zhang, Xiaohong Hong
    Abstract:

    Nasopharyngeal carcinoma (NPC) is the most prevalent head and neck malignancy in South China and Southeast Asia. The main NPC treatment strategy is radiotherapy. However, recurrence resulting from Radioresistance is a leading clinical bottleneck. Revealing the mechanism of NPC Radioresistance would help improve the therapeutic effect. Here, our work reveals that TRIM21 (tripartite motif-containing 21) functions as an oncogene in NPC progression, and its ablation increases NPC cell radiosensitivity. Further analysis indicated that TRIM21 represses TP53 expression by mediating GMPS (guanine monophosphate synthase) ubiquitination and degradation after ionizing radiation. Mass spectrometry and co-immunoprecipitation showed that SERPINB5 (serpin family B member 5) interacts with both TRIM21 and GMPS. Epistatic analysis showed that SERPINB5 acts as an adaptor to recruit GMPS and introduce TRIM21 for ubiquitination. The in vitro and in vivo results validated the finding that SERPINB5 promotes NPC cell Radioresistance. Furthermore, immunohistochemistry indicated that radioresistant patients have higher SERPINB5 expression. Overall, our data show that TRIM21-SERPINB5-mediated GMPS degradation facilitates TP53 repression, which promotes the Radioresistance of NPC cells.

Xiao Jing Yang - One of the best experts on this subject based on the ideXlab platform.

  • trim21 serpinb5 aids gmps repression to protect nasopharyngeal carcinoma cells from radiation induced apoptosis
    Journal of Biomedical Science, 2020
    Co-Authors: Panpan Zhang, Keqing Song, Qingmei He, Qiuping He, Xiao Jing Yang, Yaqin Wang, Xiaomin Li, Lu Lu Zhang, Xiaohong Hong
    Abstract:

    The main strategy against nasopharyngeal carcinoma (NPC) is radiotherapy. However, Radioresistance mediated recurrence is a leading clinical bottleneck in NPC. Revealing the mechanism of NPC Radioresistance will help improve the therapeutic effect. In this study, the role of TRIM21 (tripartite motif–containing 21) in NPC receiving ionizing radiation was firstly examined both in vivo and in vitro. Mass spectrometry analysis was performed to identify the downstream targets of TRIM21. NPC cells with TRIM21 or SERPINB5 (serpin family B member 5) overexpression or knockout were used to determine the epistatic relationship among SERPINB5, GMPS (guanine monophosphate synthase) and TRIM21. Flow cytometry, co-immunoprecipitation, western blot and immunofluorescence were employed to strengthen the results. Finally, immunohistochemistry using 4 radiosensitive and 8 radioresistent NPC patient samples was perform to examine the association between SERPINB5 or GMPS expression and patient radio-sensitivity. As an E3 ligase, TRIM21 was highly expressed in NPC. After ionizing radiation, TRIM21 repressed TP53 expression by mediating GMPS ubiquitination and degradation. Overexpression of TRIM21 protected NPC cells from radiation mediated cell apoptosis in vitro and in vivo. Further analysis revealed that TRIM21 mediated GMPS repression was dependent on SERPINB5, and SERPINB5 served as an adaptor which prevented GMPS from entering into the nucleus and introduced TRIM21 for GMPS ubiquitination. Moreover, the in vitro and in vivo results validated the finding that SERPINB5 promoted NPC cell Radioresistance, and the radioresistant patients had higher SERPINB5 expression. Overall, our data showed that TRIM21–SERPINB5-mediated GMPS degradation facilitated TP53 repression, which promoted the Radioresistance of NPC cells. This novel working model related to TP53 suppression provided new insight into NPC radioresistence clinically.

  • trim21 serpinb5 aids gmps repression to protect nasopharyngeal carcinoma cells from radiation induced apoptosis
    bioRxiv, 2019
    Co-Authors: Panpan Zhang, Keqing Song, Qingmei He, Qiuping He, Xiao Jing Yang, Yaqin Wang, Xiaomin Li, Lu Lu Zhang, Xiaohong Hong
    Abstract:

    Nasopharyngeal carcinoma (NPC) is the most prevalent head and neck malignancy in South China and Southeast Asia. The main NPC treatment strategy is radiotherapy. However, recurrence resulting from Radioresistance is a leading clinical bottleneck. Revealing the mechanism of NPC Radioresistance would help improve the therapeutic effect. Here, our work reveals that TRIM21 (tripartite motif-containing 21) functions as an oncogene in NPC progression, and its ablation increases NPC cell radiosensitivity. Further analysis indicated that TRIM21 represses TP53 expression by mediating GMPS (guanine monophosphate synthase) ubiquitination and degradation after ionizing radiation. Mass spectrometry and co-immunoprecipitation showed that SERPINB5 (serpin family B member 5) interacts with both TRIM21 and GMPS. Epistatic analysis showed that SERPINB5 acts as an adaptor to recruit GMPS and introduce TRIM21 for ubiquitination. The in vitro and in vivo results validated the finding that SERPINB5 promotes NPC cell Radioresistance. Furthermore, immunohistochemistry indicated that radioresistant patients have higher SERPINB5 expression. Overall, our data show that TRIM21-SERPINB5-mediated GMPS degradation facilitates TP53 repression, which promotes the Radioresistance of NPC cells.

Xiaomin Li - One of the best experts on this subject based on the ideXlab platform.

  • trim21 serpinb5 aids gmps repression to protect nasopharyngeal carcinoma cells from radiation induced apoptosis
    Journal of Biomedical Science, 2020
    Co-Authors: Panpan Zhang, Keqing Song, Qingmei He, Qiuping He, Xiao Jing Yang, Yaqin Wang, Xiaomin Li, Lu Lu Zhang, Xiaohong Hong
    Abstract:

    The main strategy against nasopharyngeal carcinoma (NPC) is radiotherapy. However, Radioresistance mediated recurrence is a leading clinical bottleneck in NPC. Revealing the mechanism of NPC Radioresistance will help improve the therapeutic effect. In this study, the role of TRIM21 (tripartite motif–containing 21) in NPC receiving ionizing radiation was firstly examined both in vivo and in vitro. Mass spectrometry analysis was performed to identify the downstream targets of TRIM21. NPC cells with TRIM21 or SERPINB5 (serpin family B member 5) overexpression or knockout were used to determine the epistatic relationship among SERPINB5, GMPS (guanine monophosphate synthase) and TRIM21. Flow cytometry, co-immunoprecipitation, western blot and immunofluorescence were employed to strengthen the results. Finally, immunohistochemistry using 4 radiosensitive and 8 radioresistent NPC patient samples was perform to examine the association between SERPINB5 or GMPS expression and patient radio-sensitivity. As an E3 ligase, TRIM21 was highly expressed in NPC. After ionizing radiation, TRIM21 repressed TP53 expression by mediating GMPS ubiquitination and degradation. Overexpression of TRIM21 protected NPC cells from radiation mediated cell apoptosis in vitro and in vivo. Further analysis revealed that TRIM21 mediated GMPS repression was dependent on SERPINB5, and SERPINB5 served as an adaptor which prevented GMPS from entering into the nucleus and introduced TRIM21 for GMPS ubiquitination. Moreover, the in vitro and in vivo results validated the finding that SERPINB5 promoted NPC cell Radioresistance, and the radioresistant patients had higher SERPINB5 expression. Overall, our data showed that TRIM21–SERPINB5-mediated GMPS degradation facilitated TP53 repression, which promoted the Radioresistance of NPC cells. This novel working model related to TP53 suppression provided new insight into NPC radioresistence clinically.

  • trim21 serpinb5 aids gmps repression to protect nasopharyngeal carcinoma cells from radiation induced apoptosis
    bioRxiv, 2019
    Co-Authors: Panpan Zhang, Keqing Song, Qingmei He, Qiuping He, Xiao Jing Yang, Yaqin Wang, Xiaomin Li, Lu Lu Zhang, Xiaohong Hong
    Abstract:

    Nasopharyngeal carcinoma (NPC) is the most prevalent head and neck malignancy in South China and Southeast Asia. The main NPC treatment strategy is radiotherapy. However, recurrence resulting from Radioresistance is a leading clinical bottleneck. Revealing the mechanism of NPC Radioresistance would help improve the therapeutic effect. Here, our work reveals that TRIM21 (tripartite motif-containing 21) functions as an oncogene in NPC progression, and its ablation increases NPC cell radiosensitivity. Further analysis indicated that TRIM21 represses TP53 expression by mediating GMPS (guanine monophosphate synthase) ubiquitination and degradation after ionizing radiation. Mass spectrometry and co-immunoprecipitation showed that SERPINB5 (serpin family B member 5) interacts with both TRIM21 and GMPS. Epistatic analysis showed that SERPINB5 acts as an adaptor to recruit GMPS and introduce TRIM21 for ubiquitination. The in vitro and in vivo results validated the finding that SERPINB5 promotes NPC cell Radioresistance. Furthermore, immunohistochemistry indicated that radioresistant patients have higher SERPINB5 expression. Overall, our data show that TRIM21-SERPINB5-mediated GMPS degradation facilitates TP53 repression, which promotes the Radioresistance of NPC cells.