| Field | Specification |
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| Target | |
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| Molecular weight | |
| Molecular formula | C22H23Cl2FN2RuS |
| SMILES | |
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Compound Overview
Plecstatin-1 is a metal complex that drives aggregation and collapse of the plectin network and disrupts the cytoskeletal structures of α-tubulin and F-actin. It triggers oxidative stress, mediates phosphorylation of eIF2α, and induces molecular features of immunogenic cell death, including calreticulin membrane exposure, HSP70/HSP90 membrane localization, ATP secretion and HMGB-1 release. It also induces apoptosis via the intrinsic mitochondrial pathway, exerts anti-invasive activity, and inhibits sphere proliferation while reducing clonogenicity in a 3D tumor spheroid model of colon cancer cells, making it applicable to colorectal cancer research[1]. It has a molecular formula of C22H23Cl2FN2RuS and a molecular weight of 538.47 g/mol.
Physical & Chemical Properties
| CAS Number | 2119725-22-1 |
|---|---|
| Molecular Formula | C22H23Cl2FN2RuS |
| Molecular Weight | 538.47 g/mol |
| SMILES | [Cl-][Ru+2]12345([CH]6=[CH]47)([N]8=CC=CC=C8C(NC(C=C9)=CC=C9F)=[S]5)[C]6(C(C)C)=[CH]1[CH]2=[C]37C.[Cl-] |
| Target | α-Tubulin, eIF2-α, HSP70, HSP90, Caspase 3 |
| Signaling Pathway | Cell Cycle/DNA Damage; Cytoskeleton; Metabolic Enzyme/Protease; Apoptosis; NF-κB; Immunology/Inflammation |
| Storage | Please store the product under the recommended conditions in the Certificate of Analysis. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with your institution's chemical hygiene plan.
In Vitro
Plecstatin-1 slows the growth of colon cancer cells (HCT-116, HCT-15 and HT-29) in both 2D monolayer and 3D spheroid models. Potency is lower in the spheroid model, and the effects on spheroid size and morphology depend on the cell line[1]. Plecstatin-1 (200 μM; 72 h) lowers the proliferative capacity of HCT-116 colon cancer spheroids[1]. In HCT-116 and HT-29 colon cancer cell monolayers, Plecstatin-1 (7 days) lowers long-term proliferative capacity, shown by reduced colony formation at its IC50 concentration[1]. In a cell-free system, Plecstatin-1 (50 μM; 15 min-6 h) interacts only weakly with pUC19 plasmid DNA, which indicates that its primary mechanism of action does not involve DNA damage[1]. In HT-29 and HCT-116 colon cancer spheroids, Plecstatin-1 (400 μM; 5 days) accumulates preferentially in proliferative peripheral cells, while quiescent inner cells take it up only to a limited extent[1]. In HCT-116 colon cancer spheroids, Plecstatin-1 (200 μM; 72 h) disrupts the plectin, α-tubulin and F-actin cytoskeletal structures, with weaker effects in HT-29 spheroids[1]. In Matrigel invasion assays, Plecstatin-1 (40 μM; 72 h) lowers the invasiveness of HT1080 fibrosarcoma spheroids[1]. Plecstatin-1 (200 μM; 24 h) triggers phosphorylation of the stress regulator eIF2α in HCT-116 colon cancer spheroids[1]. In HCT-116, HCT-15 and HT-29 colon cancer spheroids, Plecstatin-1 (200 μM; 24 h) triggers CRT translocation to the plasma membrane; it also triggers ATP secretion from HCT-116 and HT-29 colon cancer spheroids, and the strongest effect is seen in HCT-116 spheroids[1]. Plecstatin-1 (200 μM; 72 h) triggers HMGB-1 release from HCT-116 and HT-29 colon cancer spheroids, and the effect is stronger in HCT-116 spheroids[1]. In colon cancer spheres, Plecstatin-1 (200 μM; 24 h) raises HSP70 and HSP90 levels and promotes their translocation to the plasma membrane[1]. Plecstatin‑1 (200 μM; 72 h) causes mild apoptosis in HCT‑116 and HCT‑15 colon cancer spheroids, but does not significantly affect apoptosis in HT‑29 spheroids[1]. Plecstatin-1 (200 μM; 48-72 h) triggers apoptosis in HCT-116 colon cancer spheroids through the intrinsic mitochondrial pathway, as shown by cytochrome c release and caspase-3 cleavage[1]. Oxidative stress in HCT-116, HCT-15 and HT-29 colon cancer spheroids is caused by Plecstatin-1 (200 μM; 24 h); the effect is most potent in HCT-116 spheroids, and ROS localizes to proliferative peripheral cells[1].
Immunofluorescence[1]
| Cell Line | HCT-116 human colon carcinoma multicellular tumour spheroids |
|---|---|
| Concentration | 200 μM |
| Incubation Time | 72 h |
| Result | Caused an approximately 3-fold decrease in the number of KI67+ cells compared to untreated controls. |
Apoptosis Analysis[1]
| Cell Line | HCT-116, HCT-15, HT-29 human colon carcinoma multicellular tumour spheroids |
|---|---|
| Concentration | 200 μM |
| Incubation Time | 72 h |
| Result | Induced a minor apoptotic response in HCT-15 and HCT-116 spheroids, with cell death levels reaching approximately 30% in HCT-15 spheroids. Caused no significant change in apoptotic cell number (10% cell death) in HT-29 spheroids compared to untreated controls. |
Immunofluorescence[1]
| Cell Line | HCT-116, HT-29 human colon carcinoma multicellular tumour spheroids |
|---|---|
| Concentration | 200 μM |
| Incubation Time | 48 h (cytochrome-c analysis) 72 h (cleaved caspase-3 analysis) |
| Result | Caused cytochrome-c release from mitochondria into the cytosol and induced cleavage of caspase-3 in HCT-116 spheroids. Showed less pronounced cytochrome-c release and caspase-3 cleavage effects in HT-29 spheroids. |
Immunofluorescence[1]
| Cell Line | HCT-116, HT-29 human colon carcinoma multicellular tumour spheroids |
|---|---|
| Concentration | 200 μM |
| Incubation Time | 72 h |
| Result | Caused collapse of the punctuated plectin network into larger aggregates and reduced plectin mean fluorescence intensity (MFI) in HCT-116 spheroids. Induced collapse of the α-tubulin microtubule network, with a 5-fold reduction in α-tubulin MFI in HCT-116 spheroids. Disrupted the F-actin cytoskeleton, forming aggregates with reduced fluorescence signal in HCT-116 spheroids. Showed less pronounced cytoskeletal disruption effects in HT-29 spheroids. |
Cell Invasion Assay[1]
| Cell Line | HT1080 human fibrosarcoma multicellular tumour spheroids |
|---|---|
| Concentration | 40 μM |
| Incubation Time | 72 h, monitored up to 144 h |
| Result | Prevented spheroid invasion into the Matrigel matrix, with treated spheroids remaining smaller and non-invasive compared to larger, invasive untreated spheroids, and this trend maintained up to 144 h. |
Western Blot Analysis[1]
| Cell Line | HCT-116 human colon carcinoma multicellular tumour spheroids |
|---|---|
| Concentration | 200 μM |
| Incubation Time | 24 h |
| Result | Induced phosphorylation of eIF2α, while total eIF2α levels remained consistent with untreated controls. |
Immunofluorescence[1]
| Cell Line | HCT-116, HCT-15, HT-29 human colon carcinoma multicellular tumour spheroids |
|---|---|
| Concentration | 200 μM |
| Incubation Time | 24 h |
| Result | Increased CRT expression and promoted CRT translocation to the cell membrane (evidenced by colocalization with membrane marker) in HCT-116 spheroids. Caused up to a 4-fold increase in CRT+ cells compared to untreated controls, with the highest percentage (20%) in HCT-116 spheroids and lowest responsiveness in HT-29 spheroids. |
ELISA Assay[1]
| Cell Line | HCT-116, HT-29 human colon carcinoma multicellular tumour spheroids |
|---|---|
| Concentration | 200 μM |
| Incubation Time | 72 h |
| Result | Increased extracellular HMGB-1 levels by approximately 5-fold in HCT-116 spheroids and approximately 3-fold in HT-29 spheroids compared to untreated controls. Induced translocation of HMGB-1 from the nucleus to the cytoplasm and extracellular space in treated spheroids, with a stronger effect in HCT-116 spheroids. |
Immunofluorescence[1]
| Cell Line | HCT-116, HT-29 human colon carcinoma multicellular tumour spheroids |
|---|---|
| Concentration | 200 μM |
| Incubation Time | 24 h |
| Result | Increased fluorescence signals for HSP70 and HSP90, with preferred co-localization to the plasma membrane compared to untreated controls. |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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The umbrella cell keratin network: organization as a tile-like mesh, formation of a girded layer in response to bladder filling, and dependence on the plectin cytolinker. bioRxiv 2024 Jun 13:2024.06.11.598498. PMID: 38915686
