Objective: To study cell cycle retardation, apoptosis and the expression of antioncogene p57kip2 by radioactive rays in nasopharyngeal carcinoma cells. Methods: Cell cycle retardation, apoptosis and cell survival rate...Objective: To study cell cycle retardation, apoptosis and the expression of antioncogene p57kip2 by radioactive rays in nasopharyngeal carcinoma cells. Methods: Cell cycle retardation, apoptosis and cell survival rate induced by radioac- tive rays were tested by the methods of flow cytometry and MTT method. The expression of antioncogene p57kip2 was detected by immunohistochemistry and Western blot. Results: After irradiation, G1 phase had no obvious retardation, S phase showed transient delay. There was a positive correlation between irradiation dosage and retardation strength in G2/M phase (P < 0.01). Peak value appeared at 24 h after 12 Gy irradiation, then decreased. There was a positive correlation between apop- tosis incidence and irradiation dosage or after-irradiation time extention (P < 0.01). There was a negative correlation between cell survival rate and irradiation dosage or apoptosis incidence (P < 0.01). The expression of p57kip2 protein was up-regulated along with the prolongation of time and dosage after irradiation (P < 0.01). Conclusion: G2/M phase arrest, apoptosis and the up-regulation of the expression of p57kip2 protein all can reflect predict the radiosensitivity of nasopharyngeal carcinoma cells.展开更多
Triple-negative breast cancer(TNBC)due to lack of clear target and notorious“cold”tumor microenvironment(TME)is one of the most intractable and lethal malignancies.Tuning“cold”TME into“hot”becomes an emerging th...Triple-negative breast cancer(TNBC)due to lack of clear target and notorious“cold”tumor microenvironment(TME)is one of the most intractable and lethal malignancies.Tuning“cold”TME into“hot”becomes an emerging therapeutic strategy to TNBC.Herewith,we report that integrin-targeting micellar gemcitabine and paclitaxel(ATN-mG/P,ATN sequence:Ac-PhScNK-NH2)cooperating with polymersomal CpG(NanoCpG)effectively“heated up”and treated TNBC.ATN-mG/P exhibited greatly boosted apoptotic activity in 4T1 cells,induced potent immunogenic cell death(ICD),and efficiently stimulated maturation of bone marrow-derived dendritic cells(BMDCs).Remarkably,in a postoperative TNBC model,ATN-mG/P combining with NanoCpG promoted strong anti-cancer immune responses,showing a greatly augmented proportion of mature DCs and CD8^(+)T cells while reduced immune-suppressive myeloid-derived suppressor cells(MDSCs)and regulatory T cells(T_(reg)),which led to complete inhibition of lung metastasis and 60%mice tumor-free.The co-delivery of gemcitabine and paclitaxel at desired ratio in combination with NanoCpG provides a unique platform for potent chemoimmunotherapy of“cold”tumors like TNBC.展开更多
文摘Objective: To study cell cycle retardation, apoptosis and the expression of antioncogene p57kip2 by radioactive rays in nasopharyngeal carcinoma cells. Methods: Cell cycle retardation, apoptosis and cell survival rate induced by radioac- tive rays were tested by the methods of flow cytometry and MTT method. The expression of antioncogene p57kip2 was detected by immunohistochemistry and Western blot. Results: After irradiation, G1 phase had no obvious retardation, S phase showed transient delay. There was a positive correlation between irradiation dosage and retardation strength in G2/M phase (P < 0.01). Peak value appeared at 24 h after 12 Gy irradiation, then decreased. There was a positive correlation between apop- tosis incidence and irradiation dosage or after-irradiation time extention (P < 0.01). There was a negative correlation between cell survival rate and irradiation dosage or apoptosis incidence (P < 0.01). The expression of p57kip2 protein was up-regulated along with the prolongation of time and dosage after irradiation (P < 0.01). Conclusion: G2/M phase arrest, apoptosis and the up-regulation of the expression of p57kip2 protein all can reflect predict the radiosensitivity of nasopharyngeal carcinoma cells.
基金This work is supported by research grants from the National Natural Science Foundation of China(NSFC 52033006).
文摘Triple-negative breast cancer(TNBC)due to lack of clear target and notorious“cold”tumor microenvironment(TME)is one of the most intractable and lethal malignancies.Tuning“cold”TME into“hot”becomes an emerging therapeutic strategy to TNBC.Herewith,we report that integrin-targeting micellar gemcitabine and paclitaxel(ATN-mG/P,ATN sequence:Ac-PhScNK-NH2)cooperating with polymersomal CpG(NanoCpG)effectively“heated up”and treated TNBC.ATN-mG/P exhibited greatly boosted apoptotic activity in 4T1 cells,induced potent immunogenic cell death(ICD),and efficiently stimulated maturation of bone marrow-derived dendritic cells(BMDCs).Remarkably,in a postoperative TNBC model,ATN-mG/P combining with NanoCpG promoted strong anti-cancer immune responses,showing a greatly augmented proportion of mature DCs and CD8^(+)T cells while reduced immune-suppressive myeloid-derived suppressor cells(MDSCs)and regulatory T cells(T_(reg)),which led to complete inhibition of lung metastasis and 60%mice tumor-free.The co-delivery of gemcitabine and paclitaxel at desired ratio in combination with NanoCpG provides a unique platform for potent chemoimmunotherapy of“cold”tumors like TNBC.
