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| Iron plays a dual and highly context-dependent role in cancer biology. It is essential for tumor proliferation due to its requirement in DNA synthesis (ribonucleotide reductase), mitochondrial respiration, and cell cycle progression. Many cancers exhibit increased iron uptake (↑ transferrin receptor, TfR1) and decreased iron export (↓ ferroportin), leading to intracellular iron accumulation that supports rapid growth. However, excess labile iron also promotes oxidative stress through Fenton chemistry (Fe²⁺ + H₂O₂ → •OH), contributing to DNA damage and genomic instability. A major therapeutic concept is ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation. Tumors with high iron dependency can be selectively vulnerable to ferroptosis induction. Conversely, chronic iron overload may promote tumor initiation through ROS-mediated mutagenesis and inflammatory signaling. Thus, iron sits at a metabolic intersection: -Pro-tumor when supporting proliferation and ROS-driven mutation -Anti-tumor when leveraged to trigger ferroptotic cell death Iron biology in cancer is best understood through three axes: -Iron uptake/storage/export balance -ROS and oxidative stress dynamics -Ferroptosis susceptibilityIron is a vital trace element that plays essential roles in various physiological processes. Its importance stems from its involvement in oxygen transport, energy production, DNA synthesis, and numerous enzymatic reactions. – Iron is a critical component of hemoglobin in red blood cells, enabling the binding and transport of oxygen from the lungs to tissues. – Iron participates in redox reactions due to its ability to alternate between ferrous (Fe²⁺) and ferric (Fe³⁺) states. Tumor cells often require increased iron to support their rapid proliferation and metabolic demands. – Elevated iron availability can promote DNA synthesis, cell division, and tumor growth. • Promotion of Reactive Oxygen Species (ROS) Formation: – Iron’s redox-active nature, while important for normal cell functions, can also lead to the generation of reactive oxygen species via reactions such as the Fenton reaction: Fe²⁺ + H₂O₂ → Fe³⁺ + •OH + OH⁻ – The hydroxyl radicals (•OH) produced are highly reactive and can cause oxidative damage to cellular components (DNA, proteins, lipids). – This oxidative damage may contribute to genomic instability, mutations, and the progression of cancer. Cancer cells often exhibit increased iron dependency, targeting iron metabolism is a strategy that is being explored for cancer therapy. – Approaches include the use of iron chelators to sequester iron and limit its availability to tumor cells, thereby inhibiting their growth. – Alternatively, therapies may aim to exploit iron’s capacity to generate toxic ROS beyond a threshold that cancer cells can manage, leading to selective cell death. Iron (Fe) – Cancer Pathway Matrix
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| Also known as CP32. Cysteinyl aspartate specific proteinase-3 (Caspase-3) is a common key protein in the apoptosis and pyroptosis pathways, and when activated, the expression level of tumor suppressor gene Gasdermin E (GSDME) determines the mechanism of tumor cell death. As a key protein of apoptosis, caspase-3 can also cleave GSDME and induce pyroptosis. Loss of caspase activity is an important cause of tumor progression. Many anticancer strategies rely on the promotion of apoptosis in cancer cells as a means to shrink tumors. Crucial for apoptotic function are executioner caspases, most notably caspase-3, that proteolyze a variety of proteins, inducing cell death. Paradoxically, overexpression of procaspase-3 (PC-3), the low-activity zymogen precursor to caspase-3, has been reported in a variety of cancer types. Until recently, this counterintuitive overexpression of a pro-apoptotic protein in cancer has been puzzling. Recent studies suggest subapoptotic caspase-3 activity may promote oncogenic transformation, a possible explanation for the enigmatic overexpression of PC-3. Herein, the overexpression of PC-3 in cancer and its mechanistic basis is reviewed; collectively, the data suggest the potential for exploitation of PC-3 overexpression with PC-3 activators as a targeted anticancer strategy. Caspase 3 is the main effector caspase and has a key role in apoptosis. In many types of cancer, including breast, lung, and colon cancer, caspase-3 expression is reduced or absent. On the other hand, some studies have shown that high levels of caspase-3 expression can be associated with a better prognosis in certain types of cancer, such as breast cancer. This suggests that caspase-3 may play a role in the elimination of cancer cells, and that therapies aimed at activating caspase-3 may be effective in treating certain types of cancer. Procaspase-3 is a apoptotic marker protein. Prognostic significance: • High Cas3 expression: Associated with good prognosis and increased sensitivity to chemotherapy in breast, gastric, lung, and pancreatic cancers. • Low Cas3 expression: Linked to poor prognosis and increased risk of recurrence in colorectal, hepatocellular carcinoma, ovarian, and prostate cancers. |
| 1762- | MF, | Fe, | Triggering the apoptosis of targeted human renal cancer cells by the vibration of anisotropic magnetic particles attached to the cell membrane |
| - | in-vitro, | RCC, | NA |
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