|1.||Cho, Sung-Dae: 5 articles (01/2014 - 04/2011)|
|2.||Li, Qiang: 5 articles (08/2011 - 05/2007)|
|3.||Wang, Liwei: 5 articles (08/2011 - 05/2007)|
|4.||Wei, Daoyan: 5 articles (08/2011 - 05/2007)|
|5.||Jia, Zhiliang: 5 articles (08/2011 - 05/2007)|
|6.||Xie, Keping: 5 articles (08/2011 - 05/2007)|
|7.||Jung, Ji-Youn: 4 articles (01/2014 - 04/2011)|
|8.||Choi, Eun-Sun: 4 articles (01/2014 - 04/2011)|
|9.||Cho, Nam-Pyo: 4 articles (01/2014 - 04/2011)|
|10.||Le, Xiangdong: 4 articles (08/2011 - 05/2007)|
01/01/2014 - "Previous studies suggested that mithramycin A (Mith) inhibits the growth of various cancers by decreasing Sp1 protein. "
01/01/2014 - "Modulation of specificity protein 1 by mithramycin A as a novel therapeutic strategy for cervical cancer."
01/01/2013 - "Mithramycin A (Mith) is a natural polyketide that has been used in multiple areas of research including apoptosis of various cancer cells. "
02/01/2011 - "Mithramycin A (MitA) is a chemotherapeutic compound which has been used in the therapy of several types of cancer. "
05/15/2007 - "Treatment with mithramycin A, an Sp1 inhibitor, suppressed the expression of Sp1 and its downstream target genes in both cell culture and tumors growing in nude mice. "
|2.||Pancreatic Neoplasms (Pancreatic Cancer)
12/15/2007 - "Therapeutic inhibition of Sp1 expression in growing tumors by mithramycin a correlates directly with potent antiangiogenic effects on human pancreatic cancer."
08/01/2011 - "Combining betulinic acid and mithramycin a effectively suppresses pancreatic cancer by inhibiting proliferation, invasion, and angiogenesis."
04/01/2011 - "Combined treatment of pancreatic cancer with mithramycin a and tolfenamic Acid promotes sp1 degradation and synergistic antitumor activity--letter."
02/01/2010 - "Combined treatment of pancreatic cancer with mithramycin A and tolfenamic acid promotes Sp1 degradation and synergistic antitumor activity."
12/15/2007 - "Archived human pancreatic cancer specimens were used to assess gene expression and microvessel density (MVD) status by immunohistochemistry: Small-interfering RNA (siRNA) was used to determine the impact of altered Sp1 expression on tumor growth and angiogenesis, and mithramycin A (MIT) was used to evaluate Sp1-targeted antiangiogenic treatment of human pancreatic cancer in animal models. "
|3.||Lung Neoplasms (Lung Cancer)
04/01/2010 - "Transcriptional activity of the MDM2 promoter containing the SNP309 GG genotype was significantly lower than that containing the TT genotype in p53-null lung cancer cells cotransfected with wild-type p53 expression plasmid under mithramycin A treatment. "
12/01/2012 - "In addition, both BA treatment and mithramycin A (MMA) treatment inhibited lung tumor growth and down-regulated Sp1 protein expression in Kras(G12D)-induced lung cancers of bitransgenic mice. "
11/01/2007 - "Mithramycin A inhibits DNA methyltransferase and metastasis potential of lung cancer cells."
10/01/2015 - "DIG-MSK (demycarosil-3D-β-D-digitoxosyl mithramycin SK; EC-8042), a novel analogue of mithramycin A, induced autophagy in HCT116 human colon carcinoma and, to a lesser extent, in A2780 human ovarian carcinoma cell lines, which was followed by apoptosis and/or necrotic cell death in a time-dependent way. "
11/01/2012 - "The effects of mithramycin SK (MSK) and demycarosyl-3D-β-D-digitoxosyl-mithramycin SK (DIG-MSK; EC-8042), two novel analogs of the antitumor antibiotic mithramycin A, on gene transcription were examined in human HCT116 colon carcinoma cells by quantitative real-time PCR of 89 genes mainly involved in cell cycle control. "
06/01/2010 - "HCT116 (p21(-/-)) human colon carcinoma cells treated with mithramycin SK (MSK), a novel analog of the antitumor antibiotic mithramycin A (MTA), were transiently arrested in G2/M, with some cells entering a faulty mitotic cycle without cytokinesis that resulted in G1-like cell arrest, which consisted of post-mitotic aneuploid G1 cells. "
|5.||Prostatic Neoplasms (Prostate Cancer)
09/01/2013 - "Mithramycin A induces apoptosis by regulating the mTOR/Mcl-1/tBid pathway in androgen-independent prostate cancer cells."
01/01/2013 - "Myeloid cell leukemia-1 is a key molecular target for mithramycin A-induced apoptosis in androgen-independent prostate cancer cells and a tumor xenograft animal model."
|1.||Tumor Necrosis Factor-alpha (Tumor Necrosis Factor)
|3.||Small Interfering RNA (siRNA)
|4.||Transcription Factors (Transcription Factor)
|6.||DNA (Deoxyribonucleic Acid)
|9.||Caspase 3 (Caspase-3)
|10.||X-Linked Inhibitor of Apoptosis Protein
|1.||Heterologous Transplantation (Xenotransplantation)