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| Tumor cell invasion is a critical process in cancer progression and metastasis, where cancer cells spread from the primary tumor to surrounding tissues and distant organs. This process involves several key steps and mechanisms: 1.Epithelial-Mesenchymal Transition (EMT): Many tumors originate from epithelial cells, which are typically organized in layers. During EMT, these cells lose their epithelial characteristics (such as cell-cell adhesion) and gain mesenchymal traits (such as increased motility). This transition is crucial for invasion. 2.Degradation of Extracellular Matrix (ECM): Tumor cells secrete enzymes, such as matrix metalloproteinases (MMPs), that degrade the ECM, allowing cancer cells to invade surrounding tissues. This degradation facilitates the movement of cancer cells through the tissue. 3.Cell Migration: Once the ECM is degraded, cancer cells can migrate. They often use various mechanisms, including amoeboid movement and mesenchymal migration, to move through the tissue. This migration is influenced by various signaling pathways and the tumor microenvironment. 4.Angiogenesis: As tumors grow, they require a blood supply to provide nutrients and oxygen. Tumor cells can stimulate the formation of new blood vessels (angiogenesis) through the release of growth factors like vascular endothelial growth factor (VEGF). This not only supports tumor growth but also provides a route for cancer cells to enter the bloodstream. 5.Invasion into Blood Vessels (Intravasation): Cancer cells can invade nearby blood vessels, allowing them to enter the circulatory system. This step is crucial for metastasis, as it enables cancer cells to travel to distant sites in the body. 6.Survival in Circulation: Once in the bloodstream, cancer cells must survive the immune response and the shear stress of blood flow. They can form clusters with platelets or other cells to evade detection. 7.Extravasation and Colonization: After traveling through the bloodstream, cancer cells can exit the circulation (extravasation) and invade new tissues. They may then establish secondary tumors (metastases) in distant organs. 8.Tumor Microenvironment: The surrounding microenvironment plays a significant role in tumor invasion. Factors such as immune cells, fibroblasts, and signaling molecules can either promote or inhibit invasion and metastasis. |
| 5911- | TV, | Thymol Isolated from Thymus vulgaris L. Inhibits Colorectal Cancer Cell Growth and Metastasis by Suppressing the Wnt/β-Catenin Pathway |
| - | vitro+vivo, | CRC, | NA |
| 5019- | UA, | Ursolic acid in colorectal cancer: mechanisms, current status, challenges, and future research directions |
| - | Review, | Var, | NA |
| 4856- | Uro, | Study on the biological mechanism of urolithin a on nasopharyngeal carcinoma in vitro |
| - | in-vitro, | NPC, | CNE1 | - | in-vitro, | NPC, | CNE2 |
| 4844- | Uro, | Urolithin A Inhibits Epithelial–Mesenchymal Transition in Lung Cancer Cells via P53-Mdm2-Snail Pathway |
| - | in-vitro, | Lung, | A549 | - | in-vitro, | Lung, | H460 |
| 4849- | Uro, | Urolithin A suppresses tumor progression and induces autophagy in gastric cancer via the PI3K/Akt/mTOR pathway |
| - | vitro+vivo, | GC, | NA |
| 4851- | Uro, | Urolithin A suppressed osteosarcoma cell migration and invasion via targeting MMPs and AKT1 |
| - | in-vitro, | OS, | MG63 |
| 3143- | VitC, | ATO, | Vitamin C enhances the sensitivity of osteosarcoma to arsenic trioxide via inhibiting aerobic glycolysis |
| - | in-vitro, | OS, | NA |
| 3130- | VitC, | Effect of high-dose vitamin C on MMP2 expression and invasive ability in human pancreatic cancer cell line PANC-1 |
| - | in-vitro, | PC, | PANC1 |
| 1817- | VitK2, | Research progress on the anticancer effects of vitamin K2 |
| - | Review, | Var, | NA |
| 1820- | VitK3, | Vitamin K3 (menadione) suppresses epithelial-mesenchymal-transition and Wnt signaling pathway in human colorectal cancer cells |
| - | in-vitro, | CRC, | SW480 | - | in-vitro, | CRC, | SW-620 |
| 7909- | VT, | Vitexin Inhibits Gastric Cancer Growth and Metastasis through HMGB1-mediated Inactivation of the PI3K/AKT/mTOR/HIF-1α Signaling Pathway |
| - | vitro+vivo, | GC, | NA |
| 1761- | WBV, | Low Intensity Vibration Mitigates Tumor Progression and Protect Bone Quantity and Quality in a Murine Model of Myeloma |
| - | in-vivo, | Melanoma, | NA |
| 1755- | WBV, | Reduction of breast cancer extravasation via vibration activated osteocyte regulation |
| 1751- | WBV, | Yoda1 Enhanced Low-Magnitude High-Frequency Vibration on Osteocytes in Regulation of MDA-MB-231 Breast Cancer Cell Migration |
| - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | AML, | RAW264.7 |
| 1222- | Z, | Zinc regulates primary ovarian tumor growth and metastasis through the epithelial to mesenchymal transition |
| - | in-vitro, | Ovarian, | NA |
| 961- | Z, | Zinc Downregulates HIF-1α and Inhibits Its Activity in Tumor Cells In Vitro and In Vivo |
| - | in-vitro, | RCC, | RCC4 | - | vitro+vivo, | GBM, | U373MG | - | in-vitro, | Nor, | HUVECs |
| 2414- | β‐Ele, | Beta‐elemene inhibits breast cancer metastasis through blocking pyruvate kinase M2 dimerization and nuclear translocation |
| - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | BC, | MCF7 | - | in-vivo, | NA, | NA |
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