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C-Myc transcriptionally enhances MTDH (metadherin) expression and subsequently activates Twist1 expression to induce EMT.
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Mitochondrial AKAP1 supports mTOR pathway and tumor growth.
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MYC protein is expressed in variable degrees among pediatric small round blue cell tumors (SRBCT), and expression of this protein can be upregulated/deregulated in many ways. Findings provide a baseline for MYC expression in pediatric SRBCT and suggest that there may be multiple mechanisms of MYC upregulation in these different neoplasms.
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Our study highlighted the high colorectal cancer risk of people carrying MYC rs6983267 G and KBTBD11 rs11777210 C alleles
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miR-105 promotes MYC-mediated metabolic reprogramming of breast cancer stromal cells, contributing to sustained tumour growth by conditioning the shared metabolic environment.
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The high expression of c-myc may promote the invasion and metastasis of cervical cancer, and the high expression of bcat1 may promote the proliferation, invasion and metastasis of cervical cancer, which may have a synergistic effect in the pathogenesis of cervical cancer.
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MYC activity underlies intrinsic resistance to ibrutinib in MCL. As a client protein of HSP90, MYC can be inhibited via PU-H71 to overcome primary ibrutinib resistance.
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RMRP functions as a miR-34a-5p sponge to promote cell proliferation and repress cell apoptosis through upregulation of c-Myc in MM
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Authors show that loss of the tumor suppressor p53 increased MYC mRNA levels even in the absence of estrogen stimulation. However, in cells with wild-type p53, SRC acted to overcome p53-mediated inhibition of estrogen-stimulated cell cycle entry and progression.
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Study reports a high-resolution crystal structure (2.35 A) of the major quadruplex formed in the NHE III1 region of the c-MYC promoter. The crystal structure is in general agreement with the solution NMR structure, however, key differences are observed in the position of nucleotides outside the G-quartet core.
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Findings suggested that KPNA2, a potential tumor oncogene, performs its function in part via regulating cellular metabolism through c-myc signaling axis. It would provide a possible explanation for Warburg effect and thus offer a new perspective to the roles of KPNA2 in gliomagenesis.
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Blastic plasmacytoid dendritic cell neoplasm with unusual morphology, MYC rearrangement and TET2 and DNMT3A mutations.
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TXNIP is a key adaptor for c-Myc-driven aerobic glycolysis in prostate cancer
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MYC may down-regulate PD-L1 expression in the context of hepatocellular carcinoma.
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The effect of MYC gene status on breast cancer patient outcome seems to depend on the underlying chromosomal instability and appears unfavorable for tumors with MYC amplification without polysomy. Nuclear Myc protein expression seems predictive for benefit from adjuvant paclitaxel.
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NEAT1 is a direct transcriptional target of c-Myc. c-Myc represses NEAT1 expression by binding to the NEAT1 promoter, and SFPQ is required for NEAT1-mediated apoptosis in K562 cells.
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Deficiency of miR-144/451 expression may play a bona fide role in derepression of silenced c-Myc, which contributes to tumor development including B-lymphomagenesis.
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Mutational landscape of primary, metastatic, and recurrent ovarian cancer reveals c-MYC gains as potential target for BET inhibitors.
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RASSF7 competed with MAX in the formation of a heterodimeric complex with c-Myc and attenuated its occupancy on target gene promoters to regulate transcription.
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The expression of Lin28A and c-Myc was upregulated in PTC tissues and cell lines, whereas the expression of let-7a was downregulated in PTC cell lines. Clinically, Lin28A was linked to a higher tumor/node/metastasis stage and the presence of lymph node metastases.
