|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | A CRISPR knockout negative screen reveals synergy between CDKs inhibitor and metformin in the treatment of human cancer in vitro and in vivo显示文摘Laboratory research and pharmacoepidemiology provide support for metformin as a potential antitumor agent.However,the lack of a clear understanding of the indications of metformin limits its efficacy.Here,we performed a genome-wide CRISPR knockout negative screen to identify potential targets that might synergize with metformin.Next-generation sequencing of pooled genomic DNAs isolated from surviving cells after 18 days of metformin treatment(T18)compared to those of the untreated cells at day 0(T0)yielded candidate genes.Knockdown of a group of cyclin-dependent kinases(CDKs),including CDK1,CDK4,and CDK6,confirmed the results of the screen.Combination treatment of the CDKs inhibitor abemaciclib with metformin profoundly inhibited tumor viability in vitro and in vivo.Although cell cycle parameters were not further altered under the combination treatment,investigation of the metabolome revealed significant changes in cell metabolism,especially with regard to fatty acid oxidation,the tricarboxylic acid cycle and aspartate metabolism.Such changes appeared to be mediated through inhibition of the mTOR pathway.Collectively,our study suggests that the combination of CDKs inhibitor with metformin could be recognized as a potential therapy in future clinical applications. | Yarui Ma Qing Zhu Junbo Liang Yifei Li Mo Li Ying Zhang Xiaobing Wang Yixin Zeng Yuchen Jiao | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 1 |
| 2 | AHR mediates the aflatoxin B1 toxicity associated with hepatocellular carcinoma显示文摘Aflatoxin exposure is a crucial factor in promoting the development of primary hepatocellular carcinoma(HCC)in individuals infected with the hepatitis virus.However,the molecular pathways leading to its bioactivation and subsequent toxicity in hepatocytes have not been well-defined.Here,we carried out a genome-wide CRISPR-Cas9 genetic screen to identify aflatoxin B1(AFB1)targets.Among the most significant hits was the aryl hydrocarbon receptor(AHR),a ligand-binding transcription factor regulating cell metabolism,differentiation,and immunity. | Qing Zhu Yarui Ma Junbo Liang Zhewen Wei Mo Li Ying Zhang Mei Liu Huan He Chunfeng Qu Jianqiang Cai Xiaobing Wang Yixin Zeng Yuchen Jiao | 2021 | Signal Transduction and Targeted Therapy2021，6，9： | 1 |
| 3 | Correction: AHR mediates the Aflatoxin B1 toxicity associated with hepatocellular carcinoma显示文摘Correction to:Signal Transduction and Targeted Therapy http://gffzzd3cc09b8251d45dfscbnvvvk9w5xc6qkc.ffgz.tsg.suse.edu.cn/10.1038/s41392-021-00713-1 z published online 9 August 2021 After online publication of the article^(1),the authors noticed one inadvertent mistake occurred during the production process in Fig.7 that needs to be corrected.The correct data are provided as follows.The key findings of the article are not affected by these corrections.The original article has been corrected. | Qing Zhu Yarui Ma Junbo Liang Zhewen Wei Mo Li Ying Zhang Mei Liu Huan He Chunfeng Qu Jianqiang Cai Xiaobing Wang Yixin Zeng Yuchen Jiao | 2022 | Signal Transduction and Targeted Therapy2022，7，1： | 0 |
| 4 | Knockdown Wiskott-Aldrich syndrome protein family member 3(WASF3)inhibits colorectal cancer metastasis and sensitizes to cisplatin through targeting ZNF471显示文摘:Colorectal cancer(CRC)is a heterogeneous cancer,and many risk factors for colorectal cancer have been established.For CRC metastasis,tumor cell migration,adhesion as well as invasion are important processes.Wiskott-Aldrich syndrome protein family member 3(WASF3)is necessary for metastasis of various types of cancers.However,its role in CRC progression has not been fully elucidated.This study examined the in vitro functional roles of WASF3 in the CRC and explored the underlying molecular mechanisms.We used siRNA-WASF3 to gene silence WASF3 in colon cancer cell(HCT116)in vitro.The effects of WASF3 silencing on HCT116 cell apoptosis,proliferation,migration,as well as invasion were assessed by flow cytometry,CCK-8,and transwell assays.ZNF471 protein expressions were detected by immunofluorescence staining and RT-PCR.Moreover,the effects of ZNF471 were studied on a series of in vitro antitumor-promoting assays using HCT116.WASF3 knockdown expression using small interfering RNA(siRNA)ameliorated CRC cell proliferation,anchorage-independent growth,invasion,and metastasis.Furthermore,we observed that WASF3 contributed to upregulating the metastasis signaling pathway through inhibiting the expression of ZNF471.Our study suggests that targeting WASF3 signaling might be a novel therapeutic strategy for treating CRC. | ZHIYONG ZHANG YAN PAN YAN ZHAO MUDAN REN YARUI LI YUN FENG GUIFANG LU SHUIXIANG HE | 2022 | BIOCELL2022，46，8： | 0 |
| 5 | GDF15 negatively regulates chemosensitivity via TGFBR2-AKT pathway-dependent metabolism in esophageal squamous cell carcinoma显示文摘Treating patients with esophageal squamous cell carcinoma(ESCC)is challenging due to the high chemoresistance.Growth differentiation factor 15(GDF15)is crucial in the development of various types of tumors and negatively related to the prognosis of ESCC patients according to our previous research.In this study,the link between GDF15 and chemotherapy resistance in ESCC was further explored.The relationship between GDF15 and the chemotherapy response was investigated through in vitro and in vivo studies.ESCC patients with high levels of GDF15 expression showed an inferior chemotherapeutic response.GDF15 improved the tolerance of ESCC cell lines to low-dose cisplatin by regulating AKT phosphorylation via TGFBR2.Through an in vivo study,we further validated that the anti-GDF15 antibody improved the tumor inhibition effect of cisplatin.Metabolomics showed that GDF15 could alter cellular metabolism and enhance the expression of UGT1A.AKT and TGFBR2 inhibition resulted in the reversal of the GDF15-induced expression of UGT1A,indicating that TGFBR2-AKT pathway-dependent metabolic pathways were involved in the resistance of ESCC cells to cisplatin.The present investigation suggests that a high level of GDF15 expression leads to ESCC chemoresistance and that GDF15 can be targeted during chemotherapy,resulting in beneficial therapeutic outcomes. | Yingxi Du Yarui Ma Qing Zhu Yong Fu Yutong Li Ying Zhang Mo Li Feiyue Feng Peng Yuan Xiaobing Wang | 2023 | Frontiers of Medicine2023，17，1： | 0 |
| 6 | Role of H2 receptor blocker famotidine over the clinical recovery of COVID-19 patients: A randomized controlled trial显示文摘BACKGROUND Coronavirus disease 2019(COVID-19)is a global pandemic putting the population at a high risk of infection-related health hazards,mortality and a potential failure of proper medical therapies.Therefore,it is necessary to evaluate the potential use of the existing drugs that could be used as options for the medical management of COVID-19 patients.AIM To evaluate the role of the H_(2) receptor blocker“famotidine”in COVID-19 illness.METHODS This study was done on seriously ill COVID-19 patients admitted to the intensive care unit(ICU)from different institutes in Bangladesh.Patients were divided into famotidine treatment group“A”(famotidine 40 mg to 60 mg oral formulation every 8 h with other treatment as given),and control group“B”(treatment as given).National early warning score(NEWS)-2,and sequential organ failure assessment day-1 score was calculated to evaluate the outcome.Outcomes were evaluated by the time required for clinical improvement,characterized as duration required from enrollment to the achievement of NEWS-2 of≤2 maintained for 24 h;time to symptomatic recovery,defined as the duration in days(from randomization)required for the recovery of the COVID-19 symptoms;mortality rate;duration of ICU and hospital stay;total period of hospitalization;the rate of supplementary oxygen requirement;the computed tomography(CT)chest recovery(%),the time required for the viral clearance and“NEWS-2”on discharge.RESULTS A total of 208 patients were enrolled in this study with 104 patients in each group.The famotidine treatment group had comparatively better recovery of 75%and a low mortality of 25%than the control with a recovery of 70%and a mortality of 30%.Duration of clinical improvement(group A 9.53 d,group B 14.21 d);hospitalization period among the recovered patients(group A 13.04 d,group B 16.31 d),pulmonary improvement in chest CT(group A 21.7%,group B 13.2%),and the time for viral clearance(group A 20.7 d,group B 23.8 d)were found to be statistically significant P≤0.05.However,the Kaplan Meier survival test was not significant among the two study groups,P=0.989.CONCLUSION According to our study,treatment with famotidine achieved a better clinical outcome compared to the control group in severe COVID-19 illness,although no significant survival benefit was found. | Abu Taiub Mohammed Mohiuddin Chowdhury Aktar Kamal Md Kafil Uddin Abbas Md Rezaul Karim Md Ahsan Ali Shubhashis Talukder H M Hamidullah Mehedi Hamid Hassan Abul Hossain Shahin Yarui Li Shuixiang He | 2022 | World Journal of Clinical Cases2022，10，23： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员