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Squalene epoxidase/SQLE is a candidate target for treatment of colorectal cancers with mutation and elevated c- expression.
Int J Biol Sci
September 2023
Experimental and Molecular Pathology, Institute of Pathology, Medical Faculty, Ludwig-Maximilians-Universität München, D-80337 Munich, Germany.
Elevated expression of c-MYC and inactivation of represent two of the most common alterations in colorectal cancer (CRC). However, c-MYC and defective p53 are difficult to target therapeutically. Therefore, effectors downstream of both c-MYC and p53 may represent attractive, alternative targets for cancer treatment.
View Article and Find Full Text PDFEffects of MYC Inhibitors on the Growth of Acute Leukaemia Cells.
Anticancer Res
July 2023
Department of Laboratory Medicine, Tokyo Medical and Dental University, Tokyo, Japan
Background/aim: MYC proto-oncogene bHLH transcription factor (MYC) proteins function as transcription factors by binding to MYC-associated factor X (MAX) proteins and are involved in various cancer growth, including leukaemia. This study aimed to examine the effects of synthetic MYC inhibitors, which block the MYC-MAX complex formation, in in vitro human acute leukaemia cell lines.
Materials And Methods: Four cell lines, OCI/AML2 derived from acute myeloid leukaemia, NALM-6 from B-lymphoblastic leukaemia, and KOPT-K1 and Jurkat from notch receptor 1 (NOTCH1)-mutated T-lymphoblastic leukaemia (T-ALL), were treated with the small-molecule MYC inhibitors 10058-F4 and MYCi975.
c-MYC-Induced AP4 Attenuates DREAM-Mediated Repression by p53.
Cancers (Basel)
February 2023
Experimental and Molecular Pathology, Institute of Pathology, Ludwig-Maximilians-University München, D-80337 Munich, Germany.
Background: The deregulated expression of the c-MYC oncogene activates p53, which is presumably mediated by ARF/INK4, as well as replication-stress-induced DNA damage. Here, we aimed to determine whether the c-MYC-inducible AP4 transcription factor plays a role in this context using a genetic approach.
Methods: We used a CRISPR/Cas9 approach to generate - and/or -deficient derivatives of MCF-7 breast cancer cells harboring an ectopic, inducible c-MYC allele.
AP4 suppresses DNA damage, chromosomal instability and senescence via inducing MDC1/Mediator of DNA damage Checkpoint 1 and repressing MIR22HG/miR-22-3p.
Mol Cancer
May 2022
Experimental and Molecular Pathology, Institute of Pathology, Ludwig-Maximilians-University, Thalkirchner Strasse 36, 80337, Munich, Germany.
Background: AP4 (TFAP4) encodes a basic helix-loop-helix leucine zipper (bHLH-LZ) transcription factor and is a direct target gene of the oncogenic transcription factor c-MYC. Here, we set out to determine the relevance of AP4 in human colorectal cancer (CRC) cells.
Methods: A CRISPR/Cas9 approach was employed to generate AP4-deficient CRC cell lines with inducible expression of c-MYC.
Oridonin Dose-Dependently Modulates the Cell Senescence and Apoptosis of Gastric Cancer Cells.
Evid Based Complement Alternat Med
November 2021
Key Laboratory of Digestive Pathophysiology of Zhejiang Province, the First Affiliated Hospital of Zhejiang Chinese Medical University, 54 Youdian Road, Hangzhou 310006, China.
Gastric cancer (GC) is the fourth most lethal cancer. Effective treatments are lacking, and our knowledge of the pathogenic mechanisms in play is poor. Oridonin from the Chinese herb exerts various anticancer activities.
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