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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. |
| Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression. TP53 is the most commonly mutated gene in human cancer. HH↑, GLI-1↑, SHH↑ P53↓ The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca. It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma. Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer. It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress. Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC. |
| 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 |
| 4808- | ASTX, | Anti-Tumor Effects of Astaxanthin by Inhibition of the Expression of STAT3 in Prostate Cancer |
| - | in-vitro, | Pca, | DU145 | - | in-vivo, | NA, | NA |
| 5940- | Cela, | Celastrol Suppresses Angiogenesis-Mediated Tumor Growth through Inhibition of AKT/Mammalian Target of Rapamycin Pathway |
| - | in-vivo, | Pca, | PC3 |
| 152- | CUR, | Anti-cancer activity of curcumin loaded nanoparticles in prostate cancer |
| - | in-vivo, | Pca, | NA |
| 158- | CUR, | Curcumin-targeting pericellular serine protease matriptase role in suppression of prostate cancer cell invasion, tumor growth, and metastasis |
| - | vitro+vivo, | Pca, | LNCaP | - | in-vitro, | Pca, | PC3 |
| 461- | CUR, | Curcumin inhibits prostate cancer progression by regulating the miR-30a-5p/PCLAF axis |
| - | in-vitro, | Pca, | PC3 | - | in-vitro, | Pca, | DU145 |
| 181- | CUR, | The effects of curcumin on the invasiveness of prostate cancer in vitro and in vivo |
| - | vitro+vivo, | Pca, | DU145 |
| 806- | GAR, | Garcinol exerts anti-cancer effect in human cervical cancer cells through upregulation of T-cadherin |
| - | vitro+vivo, | Pca, | HeLa | - | vitro+vivo, | Cerv, | SiHa |
| 29- | GEN, | Genistein inhibits the stemness properties of prostate cancer cells through targeting Hedgehog-Gli1 pathway |
| - | in-vivo, | Pca, | 22Rv1 | - | in-vivo, | Pca, | DU145 |
| 4687- | LT, | QC, | Dietary Flavonoids Luteolin and Quercetin Suppressed Cancer Stem Cell Properties and Metastatic Potential of Isolated Prostate Cancer Cells |
| - | in-vitro, | Pca, | DU145 |
| 4931- | PEITC, | Phenethyl isothiocyanate (PEITC) suppresses prostate cancer cell invasion epigenetically through regulating microRNA-194 |
| - | in-vitro, | Pca, | LNCaP | - | in-vitro, | Pca, | PC3 |
| - | in-vitro, | Pca, | pCSCs |
| 96- | QC, | docx, | Quercetin reverses docetaxel resistance in prostate cancer via androgen receptor and PI3K/Akt signaling pathways |
| - | vitro+vivo, | Pca, | LNCaP | - | in-vitro, | Pca, | PC3 |
| 90- | QC, | HP, | Combination of quercetin and hyperoside inhibits prostate cancer cell growth and metastasis via regulation of microRNA‑21 |
| - | in-vitro, | Pca, | PC3 |
| 85- | QC, | Quercetin inhibits invasion, migration and signalling molecules involved in cell survival and proliferation of prostate cancer cell line (PC-3) |
| - | in-vitro, | Pca, | PC3 |
| 3373- | QC, | The Effect of Quercetin in the Yishen Tongluo Jiedu Recipe on the Development of Prostate Cancer through the Akt1-related CXCL12/ CXCR4 Pathway |
| - | in-vitro, | Pca, | DU145 |
| 3086- | RES, | Resveratrol inhibits the tumor migration and invasion by upregulating TET1 and reducing TIMP2/3 methylation in prostate carcinoma cells |
| - | in-vitro, | Pca, | LNCaP | - | in-vitro, | Pca, | PC3 | - | in-vitro, | Pca, | DU145 |
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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