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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. |
| Normal Healthy |
| 359- | AgNPs, | Anti-cancer & anti-metastasis properties of bioorganic-capped silver nanoparticles fabricated from Juniperus chinensis extract against lung cancer cells |
| - | in-vitro, | Lung, | A549 | - | in-vitro, | Nor, | HEK293 |
| 3442- | ALA, | α‑lipoic acid modulates prostate cancer cell growth and bone cell differentiation |
| - | in-vitro, | Pca, | 22Rv1 | - | in-vitro, | Pca, | C4-2B | - | in-vitro, | Nor, | 3T3 |
| 1565- | Api, | Apigenin-7-glucoside induces apoptosis and ROS accumulation in lung cancer cells, and inhibits PI3K/Akt/mTOR pathway |
| - | in-vitro, | Lung, | A549 | - | in-vitro, | Nor, | BEAS-2B | - | in-vitro, | Lung, | H1975 |
| 3172- | Ash, | Implications of Withaferin A for the metastatic potential and drug resistance in hepatocellular carcinoma cells via Nrf2-mediated EMT and ferroptosis |
| - | in-vitro, | HCC, | HepG2 | - | in-vitro, | Nor, | HL7702 |
| 1173- | Ash, | Withaferin A inhibits proliferation of human endometrial cancer cells via transforming growth factor-β (TGF-β) signalling |
| - | in-vitro, | EC, | K1 | - | in-vitro, | Nor, | THESCs |
| 2700- | BBR, | Cell-specific pattern of berberine pleiotropic effects on different human cell lines |
| - | in-vitro, | GBM, | U343 | - | in-vitro, | GBM, | MIA PaCa-2 | - | in-vitro, | Nor, | HDFa |
| 5757- | CAPE, | Caffeic acid phenethyl ester (CAPE): pharmacodynamics and potential for therapeutic application |
| - | Review, | Nor, | NA |
| 5885- | CAR, | Inhibition of TRPM7 by carvacrol suppresses glioblastoma cell proliferation, migration and invasion |
| - | in-vitro, | GBM, | U87MG | - | in-vitro, | Nor, | HEK293 |
| 5912- | CAR, | Inhibition of TRPM7 by carvacrol suppresses glioblastoma cell proliferation migration and invasion |
| - | in-vitro, | GBM, | U87MG | - | in-vitro, | Nor, | HEK293 |
| 6010- | CGA, | The Biological Activity Mechanism of Chlorogenic Acid and Its Applications in Food Industry: A Review |
| - | Review, | Nor, | NA |
| 6030- | CGA, | Chlorogenic acid induces apoptosis, inhibits metastasis and improves antitumor immunity in breast cancer via the NF‑κB signaling pathway |
| - | vitro+vivo, | BC, | MDA-MB-231 | - | in-vitro, | BC, | MDA-MB-453 | - | in-vitro, | Nor, | MCF10 |
| 1186- | Gb, | Ginkgolic acid suppresses the development of pancreatic cancer by inhibiting pathways driving lipogenesis |
| - | in-vitro, | PC, | NA | - | in-vitro, | Nor, | HUVECs | - | in-vivo, | PC, | NA |
| 4528- | MAG, | Pharmacology, Toxicity, Bioavailability, and Formulation of Magnolol: An Update |
| - | Review, | Nor, | NA |
| 3478- | MF, | One Month of Brief Weekly Magnetic Field Therapy Enhances the Anticancer Potential of Female Human Sera: Randomized Double-Blind Pilot Study |
| - | Trial, | BC, | NA | - | in-vitro, | BC, | MCF-7 | - | in-vitro, | Nor, | C2C12 |
| 3353- | QC, | Quercetin triggers cell apoptosis-associated ROS-mediated cell death and induces S and G2/M-phase cell cycle arrest in KON oral cancer cells |
| - | in-vitro, | Oral, | KON | - | in-vitro, | Nor, | MRC-5 |
| - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | BC, | 4T1 | - | in-vitro, | Nor, | MCF12A | - | in-vivo, | NA, | NA |
| 962- | TQ, | Thymoquinone affects hypoxia-inducible factor-1α expression in pancreatic cancer cells via HSP90 and PI3K/AKT/mTOR pathways |
| - | in-vitro, | PC, | PANC1 | - | in-vitro, | Nor, | hTERT-HPNE | - | in-vitro, | PC, | AsPC-1 | - | in-vitro, | PC, | Bxpc-3 |
| 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 |
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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