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发布于:2019-5-17 01:18:02  访问:8 次 回复:0 篇
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Sitivity to radiotherapy was also influenced by miR-99b. Our benefits
Our results not just offer some new clues for mTOR upregulation in radiation-treated pancreatic clinical PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28506461 samples and cell lines, but also demonstrated that miR-99b played important roles in pancreatic cancer radioresistance and perhaps a candidate therapeutic target for pancreatic cancer. Contemplating mTOR was up-regulated by radiation by way of miR-99b and mTOR signal pathway plays essential roles in regulating cancer cell survival, proliferation and apoptosis, we wonder regardless of whether mTOR inhibition have synergistic effects with radiotherapy. AZD8055, an mTORC1/C2 dual inhibitor, was employed to inhibit mTOR activity and block the feedback activation of AKT. Results demonstrated that AZD8055 therapy considerably potentiates the cytotoxic effects of ionizing radiation in human pancreatic cancer cell lines. In addition, we also confirmed that the growth inhibition was accompanied by a perturbation of cell cycle with all the marked Dacomitinib Cancer reduction of cells in S phase and an accumulation in G0/Gphase.Sitivity to radiotherapy was also influenced by miR-99b. Our results not only provide some new clues for mTOR upregulation in radiation-treated pancreatic clinical PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28506461 samples and cell lines, but in addition demonstrated that miR-99b played significant roles in pancreatic cancer radioresistance and possibly a candidate therapeutic target for pancreatic cancer. Thinking about mTOR was up-regulated by radiation by means of miR-99b and mTOR signal pathway plays essential roles in regulating cancer cell survival, proliferation and apoptosis, we wonder irrespective of whether mTOR inhibition have synergistic effects with radiotherapy. AZD8055, an mTORC1/C2 dual inhibitor, was employed to inhibit mTOR activity and block the feedback activation of AKT. Results demonstrated that AZD8055 treatment drastically potentiates the cytotoxic effects of ionizing radiation in human pancreatic cancer cell lines. Furthermore, we also confirmed that the development inhibition was accompanied by a perturbation of cell cycle with all the marked reduction of cells in S phase and an accumulation in G0/Gphase. Moreover, AZD8055 remedy enhanced radiation induced cell apoptosis. Intriguingly, these events have been paralleled by suppressing the expression and function of mTOR, but do not influence the anti-apoptotic members of the family which include Bcl-2, Bcl-XL and Mcl-1, suggesting that AZD8055 and radiation synergistically induced cell apoptosis through mTOR associated signaling pathways but not Bcl-2 household in pancreatic cancer cells.Sitivity to radiotherapy was also influenced by miR-99b. Our benefits not just give some new clues for mTOR upregulation in radiation-treated pancreatic clinical PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28506461 samples and cell lines, but in addition demonstrated that miR-99b played important roles in pancreatic cancer radioresistance and possibly a candidate therapeutic target for pancreatic cancer. Thinking about mTOR was up-regulated by radiation via miR-99b and mTOR signal pathway plays vital roles in regulating cancer cell survival, proliferation and apoptosis, we wonder regardless of whether mTOR inhibition have synergistic effects with radiotherapy. AZD8055, an mTORC1/C2 dual inhibitor, was employed to inhibit mTOR activity and block the feedback activation of AKT. Outcomes demonstrated that AZD8055 treatment considerably potentiates the cytotoxic effects of ionizing radiation in human pancreatic cancer cell lines. Furthermore, we also confirmed that the development inhibition was accompanied by a perturbation of cell cycle using the marked reduction of cells in S phase and an accumulation in G0/Gphase. Furthermore, AZD8055 therapy enhanced radiation induced cell apoptosis.
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