Large Intestine Cancer

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Jiarui Han - One of the best experts on this subject based on the ideXlab platform.

  • LncRNA TTN-AS1/miR-134-5p/PAK3 axis regulates the radiosensitivity of human Large Intestine Cancer cells through the P21 pathway and AKT/GSK-3β/β-catenin pathway.
    Cell biology international, 2020
    Co-Authors: Zhenkui Zuo, Yage Zhang, Zining Peng, Jiarui Han
    Abstract:

    Radiotherapy is an important adjuvant treatment for Large Intestine Cancer even though it does not cause any response in many patients. The present study aimed to investigate the effects of the TTN antisense RNA 1 (TTN-AS1) long noncoding RNA (lncRNA) on radiotherapy dynamics of Large Intestine Cancer cells and to explore the underlying molecular mechanisms. TTN-AS1 expression was evaluated by reverse-transcription quantitative polymerase chain reaction, western blot, and cellular immunofluorescence, and flow cytometry analysis was used to measure apoptosis. Radiotherapy was simulated in vitro by exposing Cancer cells to X-ray. TTN-AS1 was highly expressed in Large Intestine Cancer cells after an X-ray exposition for 24 hr. TTN-AS1 knockdown improved the radiosensitivity of Large Intestine Cancer cells and promoted apoptosis by increasing Bax/Bcl2 protein expression and the active-caspase 3/caspase 3 ratios following X-ray treatment. In addition, TTN-AS1 negatively regulated miR-134-5p expression, and miR-134-5p-mimic transfection decreased PAK3 protein expression in Large Intestine Cancer cells. Importantly, TTN-AS1 promoted PAK3 and P21 protein expression in HT29 cells after X-ray treatment. Moreover, the knockdown of P21 protein expression improved radiosensitivity and promoted X-ray-induced apoptosis of HT29 cells. Finally, PAK3 knockdown expression decreased the p-AKT/AKT and p-GSK-3β/GSK-3β ratios and promoted the β-catenin transfer from the nucleus to the cytoplasm. These data suggest that the TTN-AS1 lncRNA promoted resistance to radiotherapy of Large Intestine Cancer cells by increasing PAK3 expression via miR-134-5p inhibition, and this may be related to the P21 and AKT/GSK-3β/β-catenin pathway.

  • lncrna ttn as1 mir 134 5p pak3 axis regulates the radiosensitivity of human Large Intestine Cancer cells through the p21 pathway and akt gsk 3β β catenin pathway
    Cell Biology International, 2020
    Co-Authors: Zhenkui Zuo, Yage Zhang, Zining Peng, Jiarui Han
    Abstract:

    Radiotherapy is an important adjuvant treatment for Large Intestine Cancer even though it does not cause any response in many patients. The present study aimed to investigate the effects of the TTN antisense RNA 1 (TTN-AS1) long noncoding RNA (lncRNA) on radiotherapy dynamics of Large Intestine Cancer cells and to explore the underlying molecular mechanisms. TTN-AS1 expression was evaluated by reverse-transcription quantitative polymerase chain reaction, western blot, and cellular immunofluorescence, and flow cytometry analysis was used to measure apoptosis. Radiotherapy was simulated in vitro by exposing Cancer cells to X-ray. TTN-AS1 was highly expressed in Large Intestine Cancer cells after an X-ray exposition for 24 hr. TTN-AS1 knockdown improved the radiosensitivity of Large Intestine Cancer cells and promoted apoptosis by increasing Bax/Bcl2 protein expression and the active-caspase 3/caspase 3 ratios following X-ray treatment. In addition, TTN-AS1 negatively regulated miR-134-5p expression, and miR-134-5p-mimic transfection decreased PAK3 protein expression in Large Intestine Cancer cells. Importantly, TTN-AS1 promoted PAK3 and P21 protein expression in HT29 cells after X-ray treatment. Moreover, the knockdown of P21 protein expression improved radiosensitivity and promoted X-ray-induced apoptosis of HT29 cells. Finally, PAK3 knockdown expression decreased the p-AKT/AKT and p-GSK-3β/GSK-3β ratios and promoted the β-catenin transfer from the nucleus to the cytoplasm. These data suggest that the TTN-AS1 lncRNA promoted resistance to radiotherapy of Large Intestine Cancer cells by increasing PAK3 expression via miR-134-5p inhibition, and this may be related to the P21 and AKT/GSK-3β/β-catenin pathway.

Zhenkui Zuo - One of the best experts on this subject based on the ideXlab platform.

  • LncRNA TTN-AS1/miR-134-5p/PAK3 axis regulates the radiosensitivity of human Large Intestine Cancer cells through the P21 pathway and AKT/GSK-3β/β-catenin pathway.
    Cell biology international, 2020
    Co-Authors: Zhenkui Zuo, Yage Zhang, Zining Peng, Jiarui Han
    Abstract:

    Radiotherapy is an important adjuvant treatment for Large Intestine Cancer even though it does not cause any response in many patients. The present study aimed to investigate the effects of the TTN antisense RNA 1 (TTN-AS1) long noncoding RNA (lncRNA) on radiotherapy dynamics of Large Intestine Cancer cells and to explore the underlying molecular mechanisms. TTN-AS1 expression was evaluated by reverse-transcription quantitative polymerase chain reaction, western blot, and cellular immunofluorescence, and flow cytometry analysis was used to measure apoptosis. Radiotherapy was simulated in vitro by exposing Cancer cells to X-ray. TTN-AS1 was highly expressed in Large Intestine Cancer cells after an X-ray exposition for 24 hr. TTN-AS1 knockdown improved the radiosensitivity of Large Intestine Cancer cells and promoted apoptosis by increasing Bax/Bcl2 protein expression and the active-caspase 3/caspase 3 ratios following X-ray treatment. In addition, TTN-AS1 negatively regulated miR-134-5p expression, and miR-134-5p-mimic transfection decreased PAK3 protein expression in Large Intestine Cancer cells. Importantly, TTN-AS1 promoted PAK3 and P21 protein expression in HT29 cells after X-ray treatment. Moreover, the knockdown of P21 protein expression improved radiosensitivity and promoted X-ray-induced apoptosis of HT29 cells. Finally, PAK3 knockdown expression decreased the p-AKT/AKT and p-GSK-3β/GSK-3β ratios and promoted the β-catenin transfer from the nucleus to the cytoplasm. These data suggest that the TTN-AS1 lncRNA promoted resistance to radiotherapy of Large Intestine Cancer cells by increasing PAK3 expression via miR-134-5p inhibition, and this may be related to the P21 and AKT/GSK-3β/β-catenin pathway.

  • lncrna ttn as1 mir 134 5p pak3 axis regulates the radiosensitivity of human Large Intestine Cancer cells through the p21 pathway and akt gsk 3β β catenin pathway
    Cell Biology International, 2020
    Co-Authors: Zhenkui Zuo, Yage Zhang, Zining Peng, Jiarui Han
    Abstract:

    Radiotherapy is an important adjuvant treatment for Large Intestine Cancer even though it does not cause any response in many patients. The present study aimed to investigate the effects of the TTN antisense RNA 1 (TTN-AS1) long noncoding RNA (lncRNA) on radiotherapy dynamics of Large Intestine Cancer cells and to explore the underlying molecular mechanisms. TTN-AS1 expression was evaluated by reverse-transcription quantitative polymerase chain reaction, western blot, and cellular immunofluorescence, and flow cytometry analysis was used to measure apoptosis. Radiotherapy was simulated in vitro by exposing Cancer cells to X-ray. TTN-AS1 was highly expressed in Large Intestine Cancer cells after an X-ray exposition for 24 hr. TTN-AS1 knockdown improved the radiosensitivity of Large Intestine Cancer cells and promoted apoptosis by increasing Bax/Bcl2 protein expression and the active-caspase 3/caspase 3 ratios following X-ray treatment. In addition, TTN-AS1 negatively regulated miR-134-5p expression, and miR-134-5p-mimic transfection decreased PAK3 protein expression in Large Intestine Cancer cells. Importantly, TTN-AS1 promoted PAK3 and P21 protein expression in HT29 cells after X-ray treatment. Moreover, the knockdown of P21 protein expression improved radiosensitivity and promoted X-ray-induced apoptosis of HT29 cells. Finally, PAK3 knockdown expression decreased the p-AKT/AKT and p-GSK-3β/GSK-3β ratios and promoted the β-catenin transfer from the nucleus to the cytoplasm. These data suggest that the TTN-AS1 lncRNA promoted resistance to radiotherapy of Large Intestine Cancer cells by increasing PAK3 expression via miR-134-5p inhibition, and this may be related to the P21 and AKT/GSK-3β/β-catenin pathway.

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

  • LncRNA TTN-AS1/miR-134-5p/PAK3 axis regulates the radiosensitivity of human Large Intestine Cancer cells through the P21 pathway and AKT/GSK-3β/β-catenin pathway.
    Cell biology international, 2020
    Co-Authors: Zhenkui Zuo, Yage Zhang, Zining Peng, Jiarui Han
    Abstract:

    Radiotherapy is an important adjuvant treatment for Large Intestine Cancer even though it does not cause any response in many patients. The present study aimed to investigate the effects of the TTN antisense RNA 1 (TTN-AS1) long noncoding RNA (lncRNA) on radiotherapy dynamics of Large Intestine Cancer cells and to explore the underlying molecular mechanisms. TTN-AS1 expression was evaluated by reverse-transcription quantitative polymerase chain reaction, western blot, and cellular immunofluorescence, and flow cytometry analysis was used to measure apoptosis. Radiotherapy was simulated in vitro by exposing Cancer cells to X-ray. TTN-AS1 was highly expressed in Large Intestine Cancer cells after an X-ray exposition for 24 hr. TTN-AS1 knockdown improved the radiosensitivity of Large Intestine Cancer cells and promoted apoptosis by increasing Bax/Bcl2 protein expression and the active-caspase 3/caspase 3 ratios following X-ray treatment. In addition, TTN-AS1 negatively regulated miR-134-5p expression, and miR-134-5p-mimic transfection decreased PAK3 protein expression in Large Intestine Cancer cells. Importantly, TTN-AS1 promoted PAK3 and P21 protein expression in HT29 cells after X-ray treatment. Moreover, the knockdown of P21 protein expression improved radiosensitivity and promoted X-ray-induced apoptosis of HT29 cells. Finally, PAK3 knockdown expression decreased the p-AKT/AKT and p-GSK-3β/GSK-3β ratios and promoted the β-catenin transfer from the nucleus to the cytoplasm. These data suggest that the TTN-AS1 lncRNA promoted resistance to radiotherapy of Large Intestine Cancer cells by increasing PAK3 expression via miR-134-5p inhibition, and this may be related to the P21 and AKT/GSK-3β/β-catenin pathway.

  • lncrna ttn as1 mir 134 5p pak3 axis regulates the radiosensitivity of human Large Intestine Cancer cells through the p21 pathway and akt gsk 3β β catenin pathway
    Cell Biology International, 2020
    Co-Authors: Zhenkui Zuo, Yage Zhang, Zining Peng, Jiarui Han
    Abstract:

    Radiotherapy is an important adjuvant treatment for Large Intestine Cancer even though it does not cause any response in many patients. The present study aimed to investigate the effects of the TTN antisense RNA 1 (TTN-AS1) long noncoding RNA (lncRNA) on radiotherapy dynamics of Large Intestine Cancer cells and to explore the underlying molecular mechanisms. TTN-AS1 expression was evaluated by reverse-transcription quantitative polymerase chain reaction, western blot, and cellular immunofluorescence, and flow cytometry analysis was used to measure apoptosis. Radiotherapy was simulated in vitro by exposing Cancer cells to X-ray. TTN-AS1 was highly expressed in Large Intestine Cancer cells after an X-ray exposition for 24 hr. TTN-AS1 knockdown improved the radiosensitivity of Large Intestine Cancer cells and promoted apoptosis by increasing Bax/Bcl2 protein expression and the active-caspase 3/caspase 3 ratios following X-ray treatment. In addition, TTN-AS1 negatively regulated miR-134-5p expression, and miR-134-5p-mimic transfection decreased PAK3 protein expression in Large Intestine Cancer cells. Importantly, TTN-AS1 promoted PAK3 and P21 protein expression in HT29 cells after X-ray treatment. Moreover, the knockdown of P21 protein expression improved radiosensitivity and promoted X-ray-induced apoptosis of HT29 cells. Finally, PAK3 knockdown expression decreased the p-AKT/AKT and p-GSK-3β/GSK-3β ratios and promoted the β-catenin transfer from the nucleus to the cytoplasm. These data suggest that the TTN-AS1 lncRNA promoted resistance to radiotherapy of Large Intestine Cancer cells by increasing PAK3 expression via miR-134-5p inhibition, and this may be related to the P21 and AKT/GSK-3β/β-catenin pathway.

Zining Peng - One of the best experts on this subject based on the ideXlab platform.

  • LncRNA TTN-AS1/miR-134-5p/PAK3 axis regulates the radiosensitivity of human Large Intestine Cancer cells through the P21 pathway and AKT/GSK-3β/β-catenin pathway.
    Cell biology international, 2020
    Co-Authors: Zhenkui Zuo, Yage Zhang, Zining Peng, Jiarui Han
    Abstract:

    Radiotherapy is an important adjuvant treatment for Large Intestine Cancer even though it does not cause any response in many patients. The present study aimed to investigate the effects of the TTN antisense RNA 1 (TTN-AS1) long noncoding RNA (lncRNA) on radiotherapy dynamics of Large Intestine Cancer cells and to explore the underlying molecular mechanisms. TTN-AS1 expression was evaluated by reverse-transcription quantitative polymerase chain reaction, western blot, and cellular immunofluorescence, and flow cytometry analysis was used to measure apoptosis. Radiotherapy was simulated in vitro by exposing Cancer cells to X-ray. TTN-AS1 was highly expressed in Large Intestine Cancer cells after an X-ray exposition for 24 hr. TTN-AS1 knockdown improved the radiosensitivity of Large Intestine Cancer cells and promoted apoptosis by increasing Bax/Bcl2 protein expression and the active-caspase 3/caspase 3 ratios following X-ray treatment. In addition, TTN-AS1 negatively regulated miR-134-5p expression, and miR-134-5p-mimic transfection decreased PAK3 protein expression in Large Intestine Cancer cells. Importantly, TTN-AS1 promoted PAK3 and P21 protein expression in HT29 cells after X-ray treatment. Moreover, the knockdown of P21 protein expression improved radiosensitivity and promoted X-ray-induced apoptosis of HT29 cells. Finally, PAK3 knockdown expression decreased the p-AKT/AKT and p-GSK-3β/GSK-3β ratios and promoted the β-catenin transfer from the nucleus to the cytoplasm. These data suggest that the TTN-AS1 lncRNA promoted resistance to radiotherapy of Large Intestine Cancer cells by increasing PAK3 expression via miR-134-5p inhibition, and this may be related to the P21 and AKT/GSK-3β/β-catenin pathway.

  • lncrna ttn as1 mir 134 5p pak3 axis regulates the radiosensitivity of human Large Intestine Cancer cells through the p21 pathway and akt gsk 3β β catenin pathway
    Cell Biology International, 2020
    Co-Authors: Zhenkui Zuo, Yage Zhang, Zining Peng, Jiarui Han
    Abstract:

    Radiotherapy is an important adjuvant treatment for Large Intestine Cancer even though it does not cause any response in many patients. The present study aimed to investigate the effects of the TTN antisense RNA 1 (TTN-AS1) long noncoding RNA (lncRNA) on radiotherapy dynamics of Large Intestine Cancer cells and to explore the underlying molecular mechanisms. TTN-AS1 expression was evaluated by reverse-transcription quantitative polymerase chain reaction, western blot, and cellular immunofluorescence, and flow cytometry analysis was used to measure apoptosis. Radiotherapy was simulated in vitro by exposing Cancer cells to X-ray. TTN-AS1 was highly expressed in Large Intestine Cancer cells after an X-ray exposition for 24 hr. TTN-AS1 knockdown improved the radiosensitivity of Large Intestine Cancer cells and promoted apoptosis by increasing Bax/Bcl2 protein expression and the active-caspase 3/caspase 3 ratios following X-ray treatment. In addition, TTN-AS1 negatively regulated miR-134-5p expression, and miR-134-5p-mimic transfection decreased PAK3 protein expression in Large Intestine Cancer cells. Importantly, TTN-AS1 promoted PAK3 and P21 protein expression in HT29 cells after X-ray treatment. Moreover, the knockdown of P21 protein expression improved radiosensitivity and promoted X-ray-induced apoptosis of HT29 cells. Finally, PAK3 knockdown expression decreased the p-AKT/AKT and p-GSK-3β/GSK-3β ratios and promoted the β-catenin transfer from the nucleus to the cytoplasm. These data suggest that the TTN-AS1 lncRNA promoted resistance to radiotherapy of Large Intestine Cancer cells by increasing PAK3 expression via miR-134-5p inhibition, and this may be related to the P21 and AKT/GSK-3β/β-catenin pathway.

Cai Hai-qing - One of the best experts on this subject based on the ideXlab platform.

  • Clinical Feature and Treatment for Early State Intestine Obstruction after Large Intestine Cancer Operation
    Hainan Medical Journal, 2006
    Co-Authors: Cai Hai-qing
    Abstract:

    Objective To explore the diagnosis and treatment for the early stage Intestine obstruction after Large Intestine Cancer operation. Methods Recalling analyzing clinical data for 32 cases of early stage Intestine obstruction after 424 cases of Large Intestine Cancer operation. Results 22 cases of patients are operated to be found the most of patients(22/22) for obstruction, 20 cases of patients for operation curing; 2 cases of patients. are death with reason of delaying operation; 10 cases of patients for non-operation. Conclusions The early stage of Intestine obstruction has obstruction symptom after Large Intestine Cancer operation, but most of patients are deficiency in Intestine obstruction situation in clinic. The treatment should be made for non-operation at suitable time. The patients who have no relief should be operated again.