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| 5-FU is a chemotherapy medication used to treat various types of cancer, including colorectal, breast, stomach, and pancreatic cancer. It belongs to a class of drugs known as antimetabolites, which work by interfering with the growth and replication of cancer cells. Mechanisms: - functionally irreversibly inhibits Thymidylate Synthase (TS), thereby depleting the deoxythymidine monophosphate (dTMP) pool required for DNA synthesis. The resulting “thymineless death” prevents DNA replication and repair, particularly affecting rapidly proliferating tumor cells. 5-FU is a cornerstone in chemotherapy with a dual mechanism of action—primarily inhibiting thymidylate synthase (leading to disruption of DNA synthesis) and interfering with RNA processing by misincorporation. Its metabolism via activation (OPRT) and degradation (DPD) plays a crucial role in both its effectiveness and toxicity. Clinically, 5-FU is extensively used in treating a variety of cancers, most notably colorectal cancer, and remains a mainstay in multi-agent chemotherapeutic regimens due to its proven efficacy across diverse cancer types. 5-FU is one of the most common chemotherapeutic agents worldwide, particularly noted in gastrointestinal (GI) cancers.
Time-Scale Flag (TSF): P / R / G
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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. |
| - | in-vitro, | CRC, | NA |
| 233- | AL, | 5-FU, | Allicin sensitizes hepatocellular cancer cells to anti-tumor activity of 5-fluorouracil through ROS-mediated mitochondrial pathway |
| - | in-vivo, | Liver, | NA |
| 586- | Api, | 5-FU, | 5-Fluorouracil combined with apigenin enhances anticancer activity through mitochondrial membrane potential (ΔΨm)-mediated apoptosis in hepatocellular carcinoma |
| - | in-vivo, | HCC, | NA |
| 468- | CUR, | 5-FU, | Gut microbiota enhances the chemosensitivity of hepatocellular carcinoma to 5-fluorouracil in vivo by increasing curcumin bioavailability |
| - | vitro+vivo, | Liver, | HepG2 | - | vitro+vivo, | Liver, | 402 | - | vitro+vivo, | Liver, | Bel7 |
| 1878- | DCA, | 5-FU, | Synergistic Antitumor Effect of Dichloroacetate in Combination with 5-Fluorouracil in Colorectal Cancer |
| - | in-vitro, | CRC, | LS174T | - | in-vitro, | CRC, | LoVo | - | in-vitro, | CRC, | SW-620 | - | in-vitro, | CRC, | HT-29 |
| 1678- | PBG, | 5-FU, | sericin, | In vitro and in vivo anti-colorectal cancer effect of the newly synthesized sericin/propolis/fluorouracil nanoplatform through modulation of PI3K/AKT/mTOR pathway |
| - | in-vitro, | CRC, | Caco-2 | - | in-vivo, | NA, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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