Plecstatin-1

Plecstatin-1 inhibits the growth of HCT-116, HCT-15 and HT-29 colon cancer cells in both 2D monolayer and 3D spheroid models. Its potency is lower in the spheroid model, and its effects on spheroid size and morphology are cell line-dependent^[1].
Plecstatin-1 (200 μM; 72 h) reduces the proliferative capacity of HCT-116 colon cancer spheroids^[1].
Plecstatin-1 (7 days) reduces the long-term proliferation capacity of HCT-116 and HT-29 colon cancer cell monolayers, as evidenced by decreased colony formation at its IC₅₀ concentration^[1].
Plecstatin-1 (50 μM; 15 min-6 h) only weakly interacts with pUC19 plasmid DNA in a cell-free system, indicating that DNA damage is not its primary mechanism of action^[1].
Plecstatin-1 (400 μM; 5 days) preferentially accumulates in the proliferative peripheral cells of HT-29 and HCT-116 colon cancer spheroids, with limited uptake by quiescent inner cells^[1].
Plecstatin-1 (200 μM; 72 h) disrupts the cytoskeletal structures of plectin, α-tubulin and F-actin in HCT-116 colon cancer spheroids, while exerts weaker effects in HT-29 spheroids^[1].
Plecstatin-1 (40 μM; 72 h) reduces the invasiveness of HT1080 fibrosarcoma spheroids in Matrigel invasion assays^[1].
Plecstatin-1 (200 μM; 24 h) induces phosphorylation of the stress regulator eIF2α in HCT-116 colon cancer spheroids^[1].
Plecstatin-1 (200 μM; 24 h) induces CRT translocation to the plasma membrane of HCT-116, HCT-15 and HT-29 colon cancer spheroids; it also induces ATP secretion from HCT-116 and HT-29 colon cancer spheroids, with the strongest effect observed in HCT-116 spheroids^[1].
Plecstatin-1 (200 μM; 72 h) induces HMGB-1 release from HCT-116 and HT-29 colon cancer spheroids, with a stronger effect observed in HCT-116 spheroids^[1].
Plecstatin-1 (200 μM; 24 h) increases the levels of HSP70 and HSP90 and promotes their translocation to the plasma membrane of colon cancer spheres^[1].
Plecstatin‑1 (200 μM; 72 h) induces mild apoptosis in HCT‑116 and HCT‑15 colon cancer spheroids, but exerts no significant effect on apoptosis in HT‑29 spheroids^[1].
Plecstatin-1 (200 μM; 48-72 h) induces apoptosis in HCT-116 colon cancer spheroids via the intrinsic mitochondrial pathway, as evidenced by cytochrome c release and caspase-3 cleavage^[1].
Plecstatin-1 (200 μM; 24 h) induces oxidative stress in HCT-116, HCT-15 and HT-29 colon cancer spheroids, with the most potent effect observed in HCT-116 spheroids, and ROS localizes to proliferative peripheral cells^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.