mithramycin A

01/01/2022 - "Mithramycin A (MIT) has reacquired extensive research attention due to its anti-solid tumor activity and improved pharmacological production. "
10/01/2018 - "In addition, we found that Mithramycin A, a XRCC1 expression inhibitor, efficiently kills cancer cells expressing low levels of ALDH2. "
01/01/2018 - "As a selective Sp1 inhibitor, Mithramycin A (MIT) has been reported to have anti-tumor activities in multiple cancers. "
01/01/2018 - "Mithramycin A Enhances Tumor Sensitivity to Mitotic Catastrophe Resulting From DNA Damage."
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. "

01/01/2021 - "Treatment of cervical cancer cells with the p53 activator Mithramycin A restored the levels of the endogenous ERBB2 inhibitor miR‑3184‑5p and may represent a novel treatment strategy for cervical cancer."
01/01/2021 - "The p53 activator Mithramycin A stimulated p53 and miR‑3184‑5p expression, thereby lowering the levels of ERBB2 and attenuating proliferation, migration and sphere‑formation of cervical cancer cells. "
11/24/2014 - "Modulation of specificity protein 1 by mithramycin A as a novel therapeutic strategy for cervical 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."
01/01/2017 - "Previous studies have shown that mithramycin A (MIT) is a promising candidate for the treatment of pancreatic carcinoma through inhibiting transcription factor Sp1. "
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."

10/23/2019 - "Mithramycin A Inhibits Colorectal Cancer Growth by Targeting Cancer Stem Cells."
10/23/2019 - "Herein, we show for the first time that mithramycin A (Mit-A) can successfully inhibit CSC proliferation, in addition to inhibiting bulk cancer cells in a model of colorectal cancer (CRC), the second leading cause of death among men and women in the United States. "
01/01/2021 - "Combination Therapy of Mithramycin A and Immune Checkpoint Inhibitor for the Treatment of Colorectal Cancer in an Orthotopic Murine Model."
09/24/2008 - "Mithramycin A and PFT-alpha also reduced H2O2-induced apoptosis synergistically and abrogated the expression of procaspase 3 and procaspase 9. Our findings suggest that PUMA plays a role in H2O2-induced apoptosis, and that Sp1 works together with p53 in the regulation of H2O2-induced PUMA expression and apoptosis in colorectal cancer cells. "
01/01/2019 - "Our experiments were designed toward clarifying three goals: (a) to determine the mRNA expression profile of transcription factors in colorectal cancer patients using a microarray-based analysis; (b) to determine the effects of baicalin on the sp1 transcription factor with western blotting and reporter cell assays; and (c) to contrast the effects of mithramycin-A (an sp1 transcription factor inhibitor) and baicalin using western blotting and reporter cell assays. "

01/01/2023 - "Cell cycle arrest and apoptosis are early events in radiosensitization of EWS::FLI1+ Ewing sarcoma cells by Mithramycin A."
01/01/2021 - "Mithramycin A Radiosensitizes EWS:Fli1+ Ewing Sarcoma Cells by Inhibiting Double Strand Break Repair."
11/25/2020 - "Mithramycin A (MTM) inhibits the oncogenic transcription factor EWS-FLI1 in Ewing sarcoma, but poor pharmacokinetics (PK) and toxicity limit its clinical use. "
01/01/2018 - "Mithramycin A (1) was identified as the top potential inhibitor of the aberrant ETS transcription factor EWS-FLI1, which causes Ewing sarcoma. "