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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. |
| Stomach/Gastric Cancer |
| 2741- | BetA, | Betulinic acid triggers apoptosis and inhibits migration and invasion of gastric cancer cells by impairing EMT progress |
| - | in-vitro, | GC, | SNU16 | - | in-vitro, | GC, | NCI-N87 | - | in-vivo, | NA, | NA |
| 3258- | CHr, | PBG, | Chrysin Induced Cell Apoptosis and Inhibited Invasion Through Regulation of TET1 Expression in Gastric Cancer Cells |
| - | in-vitro, | GC, | MKN45 |
| 16- | CP, | RES, | Resveratrol inhibits the hedgehog signaling pathway and epithelial-mesenchymal transition and suppresses gastric cancer invasion and metastasis |
| - | in-vitro, | GC, | SGC-7901 |
| 456- | CUR, | Curcumin Promoted miR-34a Expression and Suppressed Proliferation of Gastric Cancer Cells |
| - | vitro+vivo, | GC, | SGC-7901 |
| 802- | GAR, | Garcinol acts as an antineoplastic agent in human gastric cancer by inhibiting the PI3K/AKT signaling pathway |
| - | in-vitro, | GC, | HGC27 |
| 2898- | HNK, | Honokiol Suppression of Human Epidermal Growth Factor Receptor 2 (HER2)-Positive Gastric Cancer Cell Biological Activity and Its Mechanism |
| - | in-vitro, | GC, | AGS | - | in-vitro, | GC, | NCI-N87 | - | in-vitro, | BC, | MGC803 | - | in-vitro, | GC, | SGC-7901 |
| 2375- | MET, | Metformin inhibits gastric cancer via the inhibition of HIF1α/PKM2 signaling |
| - | in-vitro, | GC, | SGC-7901 |
| 4965- | PSO, | Cisplatin, | The synergistic antitumor effects of psoralidin and cisplatin in gastric cancer by inducing ACSL4-mediated ferroptosis |
| - | vitro+vivo, | GC, | HGC27 | - | vitro+vivo, | GC, | MKN45 |
| 1238- | PTS, | Pterostilbene suppresses gastric cancer proliferation and metastasis by inhibiting oncogenic JAK2/STAT3 signaling: In vitro and in vivo therapeutic intervention |
| - | in-vitro, | GC, | NA | - | in-vivo, | NA, | NA |
| 101- | RES, | Resveratrol inhibits the hedgehog signaling pathway and epithelial-mesenchymal transition and suppresses gastric cancer invasion and metastasis |
| - | in-vitro, | GC, | SGC-7901 |
| 5035- | SAS, | Sulfasalazine, a potent suppressor of gastric cancer proliferation and metastasis by inhibition of xCT: Conventional drug in new use |
| - | Human, | GC, | NA | - | in-vitro, | GC, | NCI-N87 | - | in-vitro, | GC, | SGC-7901 |
| 1452- | SFN, | Sulforaphane Suppresses the Nicotine-Induced Expression of the Matrix Metalloproteinase-9 via Inhibiting ROS-Mediated AP-1 and NF-κB Signaling in Human Gastric Cancer Cells |
| - | in-vitro, | GC, | AGS |
| 2234- | SK, | Shikonin Suppresses Cell Tumorigenesis in Gastric Cancer Associated with the Inhibition of c-Myc and Yap-1 |
| - | in-vitro, | GC, | NA |
| 5080- | SSE, | Sodium Selenite Regulates the Proliferation and Apoptosis of Gastric Cancer Cells by Suppressing the Expression of LncRNA HOXB-AS1 |
| - | in-vitro, | GC, | HGC27 | - | in-vitro, | GC, | NCI-N87 |
| 4849- | Uro, | Urolithin A suppresses tumor progression and induces autophagy in gastric cancer via the PI3K/Akt/mTOR pathway |
| - | vitro+vivo, | GC, | NA |
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