MYC基因参与了细胞增殖、代谢、衰老、凋亡和血管生成等多个生物学过程的调控。c-MYC癌基因在70%肿瘤中的高表达与肿瘤发生发展、侵袭、耐药和不良预后密切相关，使其成为肿瘤治疗的重要靶点。由于c-MYC具有无序结构域并且缺乏小分子药物结合口袋，靶向c ...

胃癌是常见恶性肿瘤。研究人员开展 PRSS23 参与胃癌发生发展机制的研究，发现 PRSS23 通过调节 eIF4E-c-Myc 轴影响胃癌生长，高表达与不良预后相关。该轴有望成为胃癌治疗靶点，为攻克胃癌带来新希望。

研究结果显示：在细胞质中，USP30-AS1作为"分子诱饵"与HnRNPF结合，阻断后者对p21 mRNA的稳定作用，导致p21 mRNA降解；在细胞核内，USP30-AS1与EZH2互作，减少EZH2在c-Myc启动子区的富集，降低H3K27三甲基化（H3K27me 3）修饰水平，从而解除对c-Myc的转录抑制。

C-Myc的过表达与肿瘤形成高度相关，但直接靶向c-Myc目前来说仍有较大挑战。 因此发现参与 c-Myc 失调的关键因素对于开发 c-Myc 的潜在间接靶点具有 ...

c-myc nullizygous fibroblasts (KO cells) were used to compare the abilities of c-myc, N-myc and L-myc oncoproteins to accelerate growth, promote apoptosis, revert morphology, and regulate the ...

They found that overexpression of c-Myc in Atp4b+ gastric parietal cells could induce gastric adenoma in mice. Mechanistically, c-Myc promoted tumorigenesis via the AKT/mTOR pathway.

A. 3HA-c-Myc was co-expressed with FLAG-USP17 (WT or the catalytically inactive mutant (C89S)) in COS7 cells. After 24 h, cell lysates were immunoblotted with the indicated antibodies.

c-MYC is a well-validated oncogene with broad anti-cancer potential, as c-MYC expression is dysregulated in more than 70% of cancers and a key regulator in nearly every aspect of the oncogenic ...

c-Myc plays a regular part in this protein production process—and cellular growth in general—and humans could not live without it. Occasionally, this process is disrupted.