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| 1 | SET8 Inhibition Potentiates Radiotherapy by Suppressing DNA Damage Repair in Carcinomas显示文摘Objective SET8 is a member of the SET domain-containing family and the only known lysine methyltransferase(KMT)that monomethylates lysine 20 of histone H4(H4 K20 me1).SET8 has been implicated in many essential cellular processes,including cell cycle regulation,DNA replication,DNA damage response,and carcinogenesis.There is no conclusive evidence,however,regarding the effect of SET8 on radiotherapy.In the current study we determined the efficacy of SET8 inhibition on radiotherapy of tumors and the underlying mechanism.Methods First,we explored the radiotherapy benefit of the SET8 expression signature by analyzing clinical data.Then,we measured a series of biological endpoints,including the xenograft tumor growth in mice and apoptosis,frequency of micronuclei,and foci of 53 BP1 andγ-H2 AX in cells to detect the SET8 effects on radiosensitivity.RNA sequencing and subsequent experiments were exploited to verify the mechanism underlying the SET8 effects on radiotherapy.Results Low expression of SET8 predicted a better benefit to radiotherapy in lung adenocarcinoma(LUAD)and invasive breast carcinoma(BRCA)patients.Furthermore,genetic deletion of SET8 significantly enhanced radiation treatment efficacy in a murine tumor model,and A549 and MCF7 cells;SET8 overexpression decreased the radiosensitivity.SET8 inhibition induced more apoptosis,the frequency of micronuclei,and blocked the kinetics process of DNA damage repair as 53 BP1 andγ-H2 AX foci remained in cells.Moreover,RNF8 was positively correlated with the SET8 impact on DNA damage repair.Conclusion Our results demonstrated that SET8 inhibition enhanced radiosensitivity by suppressing DNA damage repair,thus suggesting that SET8 potentiated radiotherapy of carcinomas.As new inhibitors of SET8 are synthesized and tested in preclinical and clinical settings,combining SET8 inhibitors with radiation warrants consideration for precise radiotherapy. | PAN Dong DU Ya Rong LI Rong SHEN Ai Hua LIU Xiao Dong LI Chuan Yuan HU Bu Rong | 2022 | Biomedical and Environmental Sciences2022，35，3： | 1 |
| 2 | 基于PI3K/Akt信号通路探讨温下方乙酸乙酯部位对A549细胞移植瘤裸鼠肿瘤生长的抑制作用显示文摘目的探讨温下方乙酸乙酯部位经调控PI3K/Akt信号通路抑制A549细胞移植瘤生长的作用及机制。方法建立人肺腺癌A549细胞移植瘤裸鼠模型,随机分为模型组、阳性对照组(顺铂注射液,2.0 mg/kg)和温下方高、中、低剂量组(400、200、100 mg/kg),每组5只,药物干预5周后,取裸鼠肿瘤,称定质量并计算抑瘤率,HE染色观察裸鼠肿瘤病理形态学变化,TUNEL染色检测裸鼠肿瘤凋亡情况,Western blot法检测裸鼠肿瘤组织Akt、p-Akt、PI3K、p-PI3K、MMP-3、caspase-3、Bcl-2蛋白表达。结果与模型组比较,顺铂组和温下方各剂量组肿瘤质量和瘤组织p-Akt、p-PI3K、MMP-3、Bcl-2蛋白表达降低(P<0.05),凋亡阳性细胞面积比例和瘤组织caspase-3蛋白表达升高(P<0.05),肿瘤细胞出现不同程度的坏死。结论温下方乙酸乙酯部位可抑制裸鼠A549细胞移植瘤的生长,其机制可能与调控PI3K/Akt信号通路有关。 | 王盟 李慧 吕传峰 郑斌 | 2023 | 中成药2023，45，10： | 0 |
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