Nrf3 alleviates oxidative stress and promotes the survival of colon cancer cells by activating AKT/BCL-2 signal pathway.

Oxidative stress is closely linked to tumor initiation and development, conferring a survival advantage to cancer cells. Therefore, understanding cancer cells' antioxidant molecular mechanisms is crucial to cancer therapy. In this study, we discovered that HO-induced oxidative stress increased Nrf3 expression in colon cancer cells.

Homocysteine Suppresses Autophagy Through AMPK-mTOR-TFEB Signaling in Human THP-1 Macrophages.

Hyperhomocysteinemia is an independent risk factor for atherosclerosis. It is known that macrophage autophagy plays a protective role in atherosclerosis and that hyperhomocysteinemia is strongly linked to autophagy. Therefore, it is of great significance to study the molecular mechanisms underlying the effect of homocysteine (Hcy) on macrophage autophagy.

Nrf3 Promotes 5-FU Resistance in Colorectal Cancer Cells via the NF-B/BCL-2 Signaling Pathway In Vitro and In Vivo.

Increasing evidence indicates that nuclear factor, erythroid 2-like 3 (Nrf3) is connected with tumorigenesis. However, the relationship between Nrf3 and tumor drug resistance remains elusive. In this study, we investigated the effect and mechanism of action by which Nrf3 regulated the sensitivity of colon cancer cells to 5-fluorouracil (5-FU).

12--Napelline Inhibits Leukemia Cell Proliferation via the PI3K/AKT Signaling Pathway and .

This study aimed to investigate the inhibitory effect of 12--napelline on leukemia cells and its possible mechanisms. The inhibitory effects of 12--napelline on K-562 and HL-60 cells were evaluated using the CCK-8 assay, cell cycle arrest and apoptosis were detected by flow cytometry, and the expression of related proteins was measured by western blot. A K-562 tumor model was established to evaluate the antitumor effect of 12--napelline .