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MYC

Non-Canonical Function of AGO2 Augments T Cell Receptor Signaling in T Cell Prolymphocytic Leukemia

[Cancer Research] A novel T cell receptor (TCR)-associated non-canonical function of AGO2 represented, in addition to TCL1A-mediated TCR signal augmentation, another enhancer mechanism of an important deregulated growth pathway in T cell prolymphocytic leukemia.

Promoters of ASCL1- and NEUROD1-Dependent Genes Are Specific Targets of Lurbinectedin in SCLC Cells

[EMBO Molecular Medicine] Investigators focused on the neuroendocrine SCLC subtypes, SCLC-A and SCLC-N, whose transcription addiction was driven by ASCL1 and NEUROD1 transcription factors which targeted E-box motifs to activate up to 40% of total genes.

WWP1 Upregulation Predicts Poor Prognosis and Promotes Tumor Progression by Regulating Ubiquitination of NDFIP1 in Intrahepatic Cholangiocarcinoma

[Cell Death Discovery] The authors investigated the expression pattern, clinical prognosis, tumor biological functions, and molecular mechanisms of WW domain-containing E3 ubiquitin protein ligase 1 (WWP1) in intrahepatic cholangiocarcinoma.

Activation of the Notch1-C-Myc-VCAM1 Signaling Axis Initiates Liver Progenitor Cell-Driven Hepatocarcinogenesis and Pulmonary Metastasis

[Oncogene] Researchers discovered that the Notch1-c-myc-VCAM1 signaling axis initiates liver progenitor cell-driven hepatocarcinogenesis and metastasis, providing a preclinical model for HCC study.

miR-32 Promotes MYC-Driven Prostate Cancer

[Oncogenesis] Scientists showed that miR-32 promoted MYC-induced prostate adenocarcinoma and identified PDK4 as a prostate cancer-relevant metabolic target of miR-32-3p.

Combination Treatment of Docetaxel with Caffeic Acid Phenethyl Ester Suppresses the Survival and the Proliferation of Docetaxel-Resistant Prostate Cancer Cells via Induction of Apoptosis...

[Journal of Biomedical Science] Combination treatment of docetaxel with caffeic acid phenethyl ester effectively suppressed the proliferation and survival of docetaxel-resistant prostate cancer cells via inhibition of Bcl-2 and c-Myc as well as induction of metabolism interference.

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