时间标签：数据日期 2026-11-05 · 生成时间 2026-11-05 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 ｜ 情报发生日期 2026-11-05
研究问题
Data are shown as mean ± SEM or representative of three independent experiments in (B‒J).3.3MYC promotes aggressiveness and inhibits ferroptosis of cancer cells via repressing MT2A or MT1X expressionNext, we investigated the roles of MT2A or MT1X in MYC-regulated aggressiveness and ferroptosis resistance in gastric cancer cells.
方法
Recent evidence shows the elevated copper content in gastric cancer tissues, especially in mucinous adenocarcinoma, which is associated with tumor progression and poor survival of patients8.；Meanwhile, the roles and partners of MYC in copper imbalance during cancer progression remain to be determined.In this study, we identify that MYC inhibits the expression of metallothionein (MT) genes in gastric cancer.；Cells were transfected with plasmids using Neofect™ DNA transfection reagent (Neofect Biotech Co., Ltd., Beijing, China).
核心结论
Taken together, these data indicated that MYC facilitated copper imbalance essential for cancer cell viability.3.2MYC drives expression of copper-binding proteins essential for TCA cycle and ferroptosis repressionTo explore the involvement of copper ions in MYC-modulated biological features of cancer cells, copper-binding proteins from AGS cell lysates were purified by immobilized metal ion affinity chromatography21, and subjected to mass spectrometry, which revealed 1618 potential candidates (Fig. 2A and Supporting Information Table S6).；These findings suggested that MYC drove expression of copper-binding proteins essential for TCA cycle and ferroptosis repression.Figure 2MYC drives expression of copper-binding proteins essential for TCA cycle and ferroptosis repression.；These results indicated that KIF18B-MYC interplay facilitated TCA cycle and ferroptosis repression in cancer cells.Figure 4KIF18B-MYC interplay facilitates TCA cycle and ferroptosis repression in gastric cancer cells.
局限
However, the mechanisms and intervention strategies for copper imbalance in gastric cancer are still unclear.MYC, a basic helix-loop-helix-leucine zipper transcription factor, is aberrantly activated in 70% of cancers and regulates almost 15% of human genes by binding to specific E-box consensus, which is critical for cellular growth10, differentiation11, Warburg effect12, ribonucleotide catabolism13, or immune response14.；Among them, PC, FTH1, and IDH2 were top candidates ranking by fold changes in expression levels, and were chosen for further studies.；Thus, KIF18B might modulate the roles of MBs in MYC transactivation, which warrants further investigation.Since MYC protein is lack of druggable conformation for small molecule binding10, diverse strategies have been proposed to inhibit MYC co-factors10.
对本项目的价值
中高价值：属「营养感知—自噬—蛋白稳态轴」方向；mTOR / 自噬 / 蛋白质稳态栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.0/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 62,268 字符，题名指纹 0.93，已过 PubMed PMCID 官方关联 + 题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：自噬性 CUL3 降解激活 KIF18B-MYC 轴，驱动胃癌进展必需的铜失衡
- 英文标题：Activation of KIF18B-MYC axis by autophagic CUL3 degradation promotes copper imbalance essential for gastric cancer progression.
- 期刊与标识：Acta pharmaceutica Sinica. B · PMID 42979122 · DOI 10.1016/j.apsb.2026.08.024 · PMC PMC13729720