Review




Structured Review

MetaStat Inc metastat col-3
The cancer invasion and metastasis and its targeted therapy. The tumor metastasis process consists of multiple steps. Initially, tumor cells invade the surrounding stroma and extracellular matrix from the primary tumor site, and then intravasate into the bloodstream or the lymphatics. Subsequently, tumor cells arrest in the circulation and arrive at distant organ sites, followed by extravasating and invading the parenchyma of distant tissues. Finally, tumor cells adapt to the new microenvironment and grow to form metastatic colonization. EMT is the basic embryonic developmental process that transforms polarized non-motile epithelial cells into motile and invasive mesenchymal cells. Multiple cellular stress conditions including hypoxia, inflammation, metabolic stress, and signaling cascades, can induce the expression of EMT transcription factors and prompt tumor metastasis. Meanwhile, MET amplification and mutation, the transcriptional dysregulation of c-MET, degradation deficiency, and abnormal HGF production result in the abnormal expression of HGF/c-MET and tumor progression. Various <t>inhibitors</t> including MMP inhibitors and HGF/c-MET inhibitors have been developed and emerging as promising tools in the suppression of tumor metastasis. c-MET mesenchymal-epithelial transition factor, EMT epithelial-mesenchymal transition, HGF hepatocyte growth factor, <t>MMPs</t> matrix metalloproteinases
Metastat Col 3, supplied by MetaStat Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/metastat+col-3/col+3/pmc11102923-1853-1-13
Average 90 stars, based on 1 article reviews
metastat col-3 - by Bioz Stars, 2026-10
90/100 stars

Images

1) Product Images from "Tumor biomarkers for diagnosis, prognosis and targeted therapy"

Article Title: Tumor biomarkers for diagnosis, prognosis and targeted therapy

Journal: Signal Transduction and Targeted Therapy

doi: 10.1038/s41392-024-01823-2

The cancer invasion and metastasis and its targeted therapy. The tumor metastasis process consists of multiple steps. Initially, tumor cells invade the surrounding stroma and extracellular matrix from the primary tumor site, and then intravasate into the bloodstream or the lymphatics. Subsequently, tumor cells arrest in the circulation and arrive at distant organ sites, followed by extravasating and invading the parenchyma of distant tissues. Finally, tumor cells adapt to the new microenvironment and grow to form metastatic colonization. EMT is the basic embryonic developmental process that transforms polarized non-motile epithelial cells into motile and invasive mesenchymal cells. Multiple cellular stress conditions including hypoxia, inflammation, metabolic stress, and signaling cascades, can induce the expression of EMT transcription factors and prompt tumor metastasis. Meanwhile, MET amplification and mutation, the transcriptional dysregulation of c-MET, degradation deficiency, and abnormal HGF production result in the abnormal expression of HGF/c-MET and tumor progression. Various inhibitors including MMP inhibitors and HGF/c-MET inhibitors have been developed and emerging as promising tools in the suppression of tumor metastasis. c-MET mesenchymal-epithelial transition factor, EMT epithelial-mesenchymal transition, HGF hepatocyte growth factor, MMPs matrix metalloproteinases
Figure Legend Snippet: The cancer invasion and metastasis and its targeted therapy. The tumor metastasis process consists of multiple steps. Initially, tumor cells invade the surrounding stroma and extracellular matrix from the primary tumor site, and then intravasate into the bloodstream or the lymphatics. Subsequently, tumor cells arrest in the circulation and arrive at distant organ sites, followed by extravasating and invading the parenchyma of distant tissues. Finally, tumor cells adapt to the new microenvironment and grow to form metastatic colonization. EMT is the basic embryonic developmental process that transforms polarized non-motile epithelial cells into motile and invasive mesenchymal cells. Multiple cellular stress conditions including hypoxia, inflammation, metabolic stress, and signaling cascades, can induce the expression of EMT transcription factors and prompt tumor metastasis. Meanwhile, MET amplification and mutation, the transcriptional dysregulation of c-MET, degradation deficiency, and abnormal HGF production result in the abnormal expression of HGF/c-MET and tumor progression. Various inhibitors including MMP inhibitors and HGF/c-MET inhibitors have been developed and emerging as promising tools in the suppression of tumor metastasis. c-MET mesenchymal-epithelial transition factor, EMT epithelial-mesenchymal transition, HGF hepatocyte growth factor, MMPs matrix metalloproteinases

Techniques Used: Expressing, Amplification, Mutagenesis

The typical and clinically developed  MMPs inhibitors  in cancer therapy
Figure Legend Snippet: The typical and clinically developed MMPs inhibitors in cancer therapy

Techniques Used:

Related Articles

Clinical Proteomics:

Article Title: Outline of gelatinase inhibitors as anti-cancer agents: A patent mini-review for 2010-present.
Article Snippet: Matrix metalloproteinases (MMPs) are involved in several pathological and physiological functions.. Gelatinases (MMP-2 and -9) have significant attention as therapeutic targets against cancer.. Gelatinase inhibitors have demonstrated their effectiveness in several diseases including cancer.

Article Title: Detection and modulation of slit and roundabount (robo) mediated angiogenesis and uses thereof
Article Snippet: Particular anti-angiogenic agents used in the combination include AGM-1470 (TNP-470), angiostatic steroids, angiostatin, antibodies against av 3, antibodies against bFGF, antibodies against IL-1, antibodies against TNF-a, antibodies against VEGF, auranofin, azathioprine, BB-94, BB-2516, basic FGF-soluble receptor, carboxyamido-trizole (CAI), cartilage-derived inhibitor (CDI), chitin, chloroquine, cisplatin, CM 101, cortisone/heparin, cortisone/hyaluroflan, cortexolone/heparin, CT-2584, cyclophosphamide, cyclosporin A, dexamethasone, diclofenac/hyaluronan, eosinophilic major basic protein, fibronectin peptides, glioma-derived angiogenesis inhibitory factor (GD-AIF), GM 1474, gold chloride, gold thiomalate, heparinases, hyaluronan (high and low molecular-weight species), hydrocortisone/beta-cyclodextran, ibuprofen, indomethacin, interferon-alpha, interferon gamma-inducible protein 10, interferon-gamma, IL-1, IL-2, IL-4, IL-12, laminin, levamisole, linomide, LM609, marimastat (BB-2516), medroxyprogesterone, Metastat (Col-3), methotrexate, minocycline, nitric oxide, octreotide (somatostatin analogue), Paclitaxel, D-penicillamine, pentosan polysulfate, placental proliferin-related protein, placenta Rnase inhibitor, plasminogen activator inhibitor (PAls), platelet factor-4 (PF4), prednisolone, prolactin (16-Kda fragment), proliferin-related protein, prostaglandin synthase inhibitor, protamine, retinoids, Roquinimex (LS-2616. linomide), somatostatin, substance P, suramin, SU 101, tecogalan sodium (DS-4152), tetrahydrocortisol-sthrombospondins (TSPs), tissue inhibitor of metalloproteinases (TIMP 1, 2, 3), vascular endothelial growth factor inhibitors, vitamin A, Vitaxin, vitreous fluids, thalidomide, 3-aminothalidomide, 3-hydroxythalidomide and metabolites or hydrolysis products of thalidomide, 3-aminothalidomide, or 3-hydroxythalidomide ((O'Reilly, Investigational New Drugs, 15:5-13 (1997); J. Nat'l Cancer Instit., 88:786-788 (1996); U.S. Pat.

Article Title: Kaposi Sarcoma, a Trifecta of Pathogenic Mechanisms
Article Snippet: These derivatives can serve as MMP inhibitors; of this group, metastat (COL-3), has been noted as showing promise in treating epidemic KS [ ].

Article Title: Tumor biomarkers for diagnosis, prognosis and targeted therapy
Article Snippet: Other MMPs inhibitors such as COL-3 (NSC-683551), neovastat (AE-941), prinomastat (AG3340), BMS-275291, and metastat(COL-3), have been evaluated in clinical trials (Table ).

Article Title: Bioinformatics and Molecular Insights to Anti-Metastasis Activity of Triethylene Glycol Derivatives
Article Snippet: Metastat (COL-3, CMT-3) was shown to be beneficial against nonepithelial-type malignancy and is currently under a phase II trial.

Article Title: Stromal Modulators of TGF-β in Cancer
Article Snippet: Metastat (COL-3) [ ] , Tetracycline derivative , Broad spectrum , Phase I/II.

Article Title: Matrix metalloproteinases (MMPs), the main extracellular matrix (ECM) enzymes in collagen degradation, as a target for anticancer drugs.
Article Snippet: The other category of MMPI are chemically modified tetracycylins – Metastat (COL-3, CMT-3) (Figure 2F), Minocycline (Figure 2G) and Doxycycline (Figure 2H).

Article Title: Potential clinical applications of matrix metalloproteinase inhibitors and their future prospects.
Article Snippet: matrix metalloproteinases (mmPs) are endopeptidases that are involved in extracellular matrix degradation. they are also implicated in a number of abnormal bioprocesses, such as tumor growth, invasion, and metastasis. therefore, controlling mmP activities has generated considerable interest as a possible therapeutic target. the tissue inhibitors of metalloproteinases (timPs) are the major naturally occurring proteins that specifically inhibit mmPs and assist in maintaining the balance between extracellular matrix destruction and formation. however, timPs are probably not suitable for pharmacological applications due to their short half-lives in vivo. during the last few decades, synthetic mmP inhibitors (mmPis) have undergone rapid clinical development in attempts to control mmP enzymatic activities in abnormal bioprocesses. although studies with these agents have met with limited clinical success, the field of mmPis is still expanding, and generation of highly effective and selective mmPis might be a promising direction of this research area.

Expressing:

Article Title: Outline of gelatinase inhibitors as anti-cancer agents: A patent mini-review for 2010-present.
Article Snippet: Matrix metalloproteinases (MMPs) are involved in several pathological and physiological functions.. Gelatinases (MMP-2 and -9) have significant attention as therapeutic targets against cancer.. Gelatinase inhibitors have demonstrated their effectiveness in several diseases including cancer.

Article Title: Detection and modulation of slit and roundabount (robo) mediated angiogenesis and uses thereof
Article Snippet: Particular anti-angiogenic agents used in the combination include AGM-1470 (TNP-470), angiostatic steroids, angiostatin, antibodies against av 3, antibodies against bFGF, antibodies against IL-1, antibodies against TNF-a, antibodies against VEGF, auranofin, azathioprine, BB-94, BB-2516, basic FGF-soluble receptor, carboxyamido-trizole (CAI), cartilage-derived inhibitor (CDI), chitin, chloroquine, cisplatin, CM 101, cortisone/heparin, cortisone/hyaluroflan, cortexolone/heparin, CT-2584, cyclophosphamide, cyclosporin A, dexamethasone, diclofenac/hyaluronan, eosinophilic major basic protein, fibronectin peptides, glioma-derived angiogenesis inhibitory factor (GD-AIF), GM 1474, gold chloride, gold thiomalate, heparinases, hyaluronan (high and low molecular-weight species), hydrocortisone/beta-cyclodextran, ibuprofen, indomethacin, interferon-alpha, interferon gamma-inducible protein 10, interferon-gamma, IL-1, IL-2, IL-4, IL-12, laminin, levamisole, linomide, LM609, marimastat (BB-2516), medroxyprogesterone, Metastat (Col-3), methotrexate, minocycline, nitric oxide, octreotide (somatostatin analogue), Paclitaxel, D-penicillamine, pentosan polysulfate, placental proliferin-related protein, placenta Rnase inhibitor, plasminogen activator inhibitor (PAls), platelet factor-4 (PF4), prednisolone, prolactin (16-Kda fragment), proliferin-related protein, prostaglandin synthase inhibitor, protamine, retinoids, Roquinimex (LS-2616. linomide), somatostatin, substance P, suramin, SU 101, tecogalan sodium (DS-4152), tetrahydrocortisol-sthrombospondins (TSPs), tissue inhibitor of metalloproteinases (TIMP 1, 2, 3), vascular endothelial growth factor inhibitors, vitamin A, Vitaxin, vitreous fluids, thalidomide, 3-aminothalidomide, 3-hydroxythalidomide and metabolites or hydrolysis products of thalidomide, 3-aminothalidomide, or 3-hydroxythalidomide ((O'Reilly, Investigational New Drugs, 15:5-13 (1997); J. Nat'l Cancer Instit., 88:786-788 (1996); U.S. Pat.

Article Title: Kaposi Sarcoma, a Trifecta of Pathogenic Mechanisms
Article Snippet: These derivatives can serve as MMP inhibitors; of this group, metastat (COL-3), has been noted as showing promise in treating epidemic KS [ ].

Article Title: Tumor biomarkers for diagnosis, prognosis and targeted therapy
Article Snippet: Other MMPs inhibitors such as COL-3 (NSC-683551), neovastat (AE-941), prinomastat (AG3340), BMS-275291, and metastat(COL-3), have been evaluated in clinical trials (Table ).

Article Title: Bioinformatics and Molecular Insights to Anti-Metastasis Activity of Triethylene Glycol Derivatives
Article Snippet: Metastat (COL-3, CMT-3) was shown to be beneficial against nonepithelial-type malignancy and is currently under a phase II trial.

Article Title: Stromal Modulators of TGF-β in Cancer
Article Snippet: Metastat (COL-3) [ ] , Tetracycline derivative , Broad spectrum , Phase I/II.

Article Title: Matrix metalloproteinases (MMPs), the main extracellular matrix (ECM) enzymes in collagen degradation, as a target for anticancer drugs.
Article Snippet: The other category of MMPI are chemically modified tetracycylins – Metastat (COL-3, CMT-3) (Figure 2F), Minocycline (Figure 2G) and Doxycycline (Figure 2H).

Article Title: Potential clinical applications of matrix metalloproteinase inhibitors and their future prospects.
Article Snippet: matrix metalloproteinases (mmPs) are endopeptidases that are involved in extracellular matrix degradation. they are also implicated in a number of abnormal bioprocesses, such as tumor growth, invasion, and metastasis. therefore, controlling mmP activities has generated considerable interest as a possible therapeutic target. the tissue inhibitors of metalloproteinases (timPs) are the major naturally occurring proteins that specifically inhibit mmPs and assist in maintaining the balance between extracellular matrix destruction and formation. however, timPs are probably not suitable for pharmacological applications due to their short half-lives in vivo. during the last few decades, synthetic mmP inhibitors (mmPis) have undergone rapid clinical development in attempts to control mmP enzymatic activities in abnormal bioprocesses. although studies with these agents have met with limited clinical success, the field of mmPis is still expanding, and generation of highly effective and selective mmPis might be a promising direction of this research area.

Amplification:

Article Title: Outline of gelatinase inhibitors as anti-cancer agents: A patent mini-review for 2010-present.
Article Snippet: Matrix metalloproteinases (MMPs) are involved in several pathological and physiological functions.. Gelatinases (MMP-2 and -9) have significant attention as therapeutic targets against cancer.. Gelatinase inhibitors have demonstrated their effectiveness in several diseases including cancer.

Article Title: Detection and modulation of slit and roundabount (robo) mediated angiogenesis and uses thereof
Article Snippet: Particular anti-angiogenic agents used in the combination include AGM-1470 (TNP-470), angiostatic steroids, angiostatin, antibodies against av 3, antibodies against bFGF, antibodies against IL-1, antibodies against TNF-a, antibodies against VEGF, auranofin, azathioprine, BB-94, BB-2516, basic FGF-soluble receptor, carboxyamido-trizole (CAI), cartilage-derived inhibitor (CDI), chitin, chloroquine, cisplatin, CM 101, cortisone/heparin, cortisone/hyaluroflan, cortexolone/heparin, CT-2584, cyclophosphamide, cyclosporin A, dexamethasone, diclofenac/hyaluronan, eosinophilic major basic protein, fibronectin peptides, glioma-derived angiogenesis inhibitory factor (GD-AIF), GM 1474, gold chloride, gold thiomalate, heparinases, hyaluronan (high and low molecular-weight species), hydrocortisone/beta-cyclodextran, ibuprofen, indomethacin, interferon-alpha, interferon gamma-inducible protein 10, interferon-gamma, IL-1, IL-2, IL-4, IL-12, laminin, levamisole, linomide, LM609, marimastat (BB-2516), medroxyprogesterone, Metastat (Col-3), methotrexate, minocycline, nitric oxide, octreotide (somatostatin analogue), Paclitaxel, D-penicillamine, pentosan polysulfate, placental proliferin-related protein, placenta Rnase inhibitor, plasminogen activator inhibitor (PAls), platelet factor-4 (PF4), prednisolone, prolactin (16-Kda fragment), proliferin-related protein, prostaglandin synthase inhibitor, protamine, retinoids, Roquinimex (LS-2616. linomide), somatostatin, substance P, suramin, SU 101, tecogalan sodium (DS-4152), tetrahydrocortisol-sthrombospondins (TSPs), tissue inhibitor of metalloproteinases (TIMP 1, 2, 3), vascular endothelial growth factor inhibitors, vitamin A, Vitaxin, vitreous fluids, thalidomide, 3-aminothalidomide, 3-hydroxythalidomide and metabolites or hydrolysis products of thalidomide, 3-aminothalidomide, or 3-hydroxythalidomide ((O'Reilly, Investigational New Drugs, 15:5-13 (1997); J. Nat'l Cancer Instit., 88:786-788 (1996); U.S. Pat.

Article Title: Kaposi Sarcoma, a Trifecta of Pathogenic Mechanisms
Article Snippet: These derivatives can serve as MMP inhibitors; of this group, metastat (COL-3), has been noted as showing promise in treating epidemic KS [ ].

Article Title: Tumor biomarkers for diagnosis, prognosis and targeted therapy
Article Snippet: Other MMPs inhibitors such as COL-3 (NSC-683551), neovastat (AE-941), prinomastat (AG3340), BMS-275291, and metastat(COL-3), have been evaluated in clinical trials (Table ).

Article Title: Bioinformatics and Molecular Insights to Anti-Metastasis Activity of Triethylene Glycol Derivatives
Article Snippet: Metastat (COL-3, CMT-3) was shown to be beneficial against nonepithelial-type malignancy and is currently under a phase II trial.

Article Title: Stromal Modulators of TGF-β in Cancer
Article Snippet: Metastat (COL-3) [ ] , Tetracycline derivative , Broad spectrum , Phase I/II.

Article Title: Matrix metalloproteinases (MMPs), the main extracellular matrix (ECM) enzymes in collagen degradation, as a target for anticancer drugs.
Article Snippet: The other category of MMPI are chemically modified tetracycylins – Metastat (COL-3, CMT-3) (Figure 2F), Minocycline (Figure 2G) and Doxycycline (Figure 2H).

Article Title: Potential clinical applications of matrix metalloproteinase inhibitors and their future prospects.
Article Snippet: matrix metalloproteinases (mmPs) are endopeptidases that are involved in extracellular matrix degradation. they are also implicated in a number of abnormal bioprocesses, such as tumor growth, invasion, and metastasis. therefore, controlling mmP activities has generated considerable interest as a possible therapeutic target. the tissue inhibitors of metalloproteinases (timPs) are the major naturally occurring proteins that specifically inhibit mmPs and assist in maintaining the balance between extracellular matrix destruction and formation. however, timPs are probably not suitable for pharmacological applications due to their short half-lives in vivo. during the last few decades, synthetic mmP inhibitors (mmPis) have undergone rapid clinical development in attempts to control mmP enzymatic activities in abnormal bioprocesses. although studies with these agents have met with limited clinical success, the field of mmPis is still expanding, and generation of highly effective and selective mmPis might be a promising direction of this research area.

Mutagenesis:

Article Title: Outline of gelatinase inhibitors as anti-cancer agents: A patent mini-review for 2010-present.
Article Snippet: Matrix metalloproteinases (MMPs) are involved in several pathological and physiological functions.. Gelatinases (MMP-2 and -9) have significant attention as therapeutic targets against cancer.. Gelatinase inhibitors have demonstrated their effectiveness in several diseases including cancer.

Article Title: Detection and modulation of slit and roundabount (robo) mediated angiogenesis and uses thereof
Article Snippet: Particular anti-angiogenic agents used in the combination include AGM-1470 (TNP-470), angiostatic steroids, angiostatin, antibodies against av 3, antibodies against bFGF, antibodies against IL-1, antibodies against TNF-a, antibodies against VEGF, auranofin, azathioprine, BB-94, BB-2516, basic FGF-soluble receptor, carboxyamido-trizole (CAI), cartilage-derived inhibitor (CDI), chitin, chloroquine, cisplatin, CM 101, cortisone/heparin, cortisone/hyaluroflan, cortexolone/heparin, CT-2584, cyclophosphamide, cyclosporin A, dexamethasone, diclofenac/hyaluronan, eosinophilic major basic protein, fibronectin peptides, glioma-derived angiogenesis inhibitory factor (GD-AIF), GM 1474, gold chloride, gold thiomalate, heparinases, hyaluronan (high and low molecular-weight species), hydrocortisone/beta-cyclodextran, ibuprofen, indomethacin, interferon-alpha, interferon gamma-inducible protein 10, interferon-gamma, IL-1, IL-2, IL-4, IL-12, laminin, levamisole, linomide, LM609, marimastat (BB-2516), medroxyprogesterone, Metastat (Col-3), methotrexate, minocycline, nitric oxide, octreotide (somatostatin analogue), Paclitaxel, D-penicillamine, pentosan polysulfate, placental proliferin-related protein, placenta Rnase inhibitor, plasminogen activator inhibitor (PAls), platelet factor-4 (PF4), prednisolone, prolactin (16-Kda fragment), proliferin-related protein, prostaglandin synthase inhibitor, protamine, retinoids, Roquinimex (LS-2616. linomide), somatostatin, substance P, suramin, SU 101, tecogalan sodium (DS-4152), tetrahydrocortisol-sthrombospondins (TSPs), tissue inhibitor of metalloproteinases (TIMP 1, 2, 3), vascular endothelial growth factor inhibitors, vitamin A, Vitaxin, vitreous fluids, thalidomide, 3-aminothalidomide, 3-hydroxythalidomide and metabolites or hydrolysis products of thalidomide, 3-aminothalidomide, or 3-hydroxythalidomide ((O'Reilly, Investigational New Drugs, 15:5-13 (1997); J. Nat'l Cancer Instit., 88:786-788 (1996); U.S. Pat.

Article Title: Kaposi Sarcoma, a Trifecta of Pathogenic Mechanisms
Article Snippet: These derivatives can serve as MMP inhibitors; of this group, metastat (COL-3), has been noted as showing promise in treating epidemic KS [ ].

Article Title: Tumor biomarkers for diagnosis, prognosis and targeted therapy
Article Snippet: Other MMPs inhibitors such as COL-3 (NSC-683551), neovastat (AE-941), prinomastat (AG3340), BMS-275291, and metastat(COL-3), have been evaluated in clinical trials (Table ).

Article Title: Bioinformatics and Molecular Insights to Anti-Metastasis Activity of Triethylene Glycol Derivatives
Article Snippet: Metastat (COL-3, CMT-3) was shown to be beneficial against nonepithelial-type malignancy and is currently under a phase II trial.

Article Title: Stromal Modulators of TGF-β in Cancer
Article Snippet: Metastat (COL-3) [ ] , Tetracycline derivative , Broad spectrum , Phase I/II.

Article Title: Matrix metalloproteinases (MMPs), the main extracellular matrix (ECM) enzymes in collagen degradation, as a target for anticancer drugs.
Article Snippet: The other category of MMPI are chemically modified tetracycylins – Metastat (COL-3, CMT-3) (Figure 2F), Minocycline (Figure 2G) and Doxycycline (Figure 2H).

Article Title: Potential clinical applications of matrix metalloproteinase inhibitors and their future prospects.
Article Snippet: matrix metalloproteinases (mmPs) are endopeptidases that are involved in extracellular matrix degradation. they are also implicated in a number of abnormal bioprocesses, such as tumor growth, invasion, and metastasis. therefore, controlling mmP activities has generated considerable interest as a possible therapeutic target. the tissue inhibitors of metalloproteinases (timPs) are the major naturally occurring proteins that specifically inhibit mmPs and assist in maintaining the balance between extracellular matrix destruction and formation. however, timPs are probably not suitable for pharmacological applications due to their short half-lives in vivo. during the last few decades, synthetic mmP inhibitors (mmPis) have undergone rapid clinical development in attempts to control mmP enzymatic activities in abnormal bioprocesses. although studies with these agents have met with limited clinical success, the field of mmPis is still expanding, and generation of highly effective and selective mmPis might be a promising direction of this research area.



Similar Products

90
MetaStat Inc metastat col-3
The cancer invasion and metastasis and its targeted therapy. The tumor metastasis process consists of multiple steps. Initially, tumor cells invade the surrounding stroma and extracellular matrix from the primary tumor site, and then intravasate into the bloodstream or the lymphatics. Subsequently, tumor cells arrest in the circulation and arrive at distant organ sites, followed by extravasating and invading the parenchyma of distant tissues. Finally, tumor cells adapt to the new microenvironment and grow to form metastatic colonization. EMT is the basic embryonic developmental process that transforms polarized non-motile epithelial cells into motile and invasive mesenchymal cells. Multiple cellular stress conditions including hypoxia, inflammation, metabolic stress, and signaling cascades, can induce the expression of EMT transcription factors and prompt tumor metastasis. Meanwhile, MET amplification and mutation, the transcriptional dysregulation of c-MET, degradation deficiency, and abnormal HGF production result in the abnormal expression of HGF/c-MET and tumor progression. Various <t>inhibitors</t> including MMP inhibitors and HGF/c-MET inhibitors have been developed and emerging as promising tools in the suppression of tumor metastasis. c-MET mesenchymal-epithelial transition factor, EMT epithelial-mesenchymal transition, HGF hepatocyte growth factor, <t>MMPs</t> matrix metalloproteinases
Metastat Col 3, supplied by MetaStat Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/metastat+col-3/col+3/pmc11102923-1853-1-13
Average 90 stars, based on 1 article reviews
metastat col-3 - by Bioz Stars, 2026-10
90/100 stars
  Buy from Supplier

90
MetaStat Inc metastat(col-3)
The cancer invasion and metastasis and its targeted therapy. The tumor metastasis process consists of multiple steps. Initially, tumor cells invade the surrounding stroma and extracellular matrix from the primary tumor site, and then intravasate into the bloodstream or the lymphatics. Subsequently, tumor cells arrest in the circulation and arrive at distant organ sites, followed by extravasating and invading the parenchyma of distant tissues. Finally, tumor cells adapt to the new microenvironment and grow to form metastatic colonization. EMT is the basic embryonic developmental process that transforms polarized non-motile epithelial cells into motile and invasive mesenchymal cells. Multiple cellular stress conditions including hypoxia, inflammation, metabolic stress, and signaling cascades, can induce the expression of EMT transcription factors and prompt tumor metastasis. Meanwhile, MET amplification and mutation, the transcriptional dysregulation of c-MET, degradation deficiency, and abnormal HGF production result in the abnormal expression of HGF/c-MET and tumor progression. Various <t>inhibitors</t> including MMP inhibitors and HGF/c-MET inhibitors have been developed and emerging as promising tools in the suppression of tumor metastasis. c-MET mesenchymal-epithelial transition factor, EMT epithelial-mesenchymal transition, HGF hepatocyte growth factor, <t>MMPs</t> matrix metalloproteinases
Metastat(col 3), supplied by MetaStat Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/metastat+col-3/col+3/pmc11102923-172-4-0
Average 90 stars, based on 1 article reviews
metastat(col-3) - by Bioz Stars, 2026-10
90/100 stars
  Buy from Supplier

90
MetaStat Inc chemical modified tetracyclines metastat (col-3)
Different Types of MMPIs Used in Cancer Treatment.
Chemical Modified Tetracyclines Metastat (Col 3), supplied by MetaStat Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/metastat+col-3/col+3/pmc10707261-33-0-4
Average 90 stars, based on 1 article reviews
chemical modified tetracyclines metastat (col-3) - by Bioz Stars, 2026-10
90/100 stars
  Buy from Supplier

90
MetaStat Inc col-3 (metastat)
Different Types of MMPIs Used in Cancer Treatment.
Col 3 (Metastat), supplied by MetaStat Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/metastat+col-3/col+3/pm37068243-672-11-12
Average 90 stars, based on 1 article reviews
col-3 (metastat) - by Bioz Stars, 2026-10
90/100 stars
  Buy from Supplier

90
MetaStat Inc metastat/col-3
Different Types of MMPIs Used in Cancer Treatment.
Metastat/Col 3, supplied by MetaStat Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/metastat+col-3/col+3/pm35969157-40-16-17
Average 90 stars, based on 1 article reviews
metastat/col-3 - by Bioz Stars, 2026-10
90/100 stars
  Buy from Supplier

Image Search Results


The cancer invasion and metastasis and its targeted therapy. The tumor metastasis process consists of multiple steps. Initially, tumor cells invade the surrounding stroma and extracellular matrix from the primary tumor site, and then intravasate into the bloodstream or the lymphatics. Subsequently, tumor cells arrest in the circulation and arrive at distant organ sites, followed by extravasating and invading the parenchyma of distant tissues. Finally, tumor cells adapt to the new microenvironment and grow to form metastatic colonization. EMT is the basic embryonic developmental process that transforms polarized non-motile epithelial cells into motile and invasive mesenchymal cells. Multiple cellular stress conditions including hypoxia, inflammation, metabolic stress, and signaling cascades, can induce the expression of EMT transcription factors and prompt tumor metastasis. Meanwhile, MET amplification and mutation, the transcriptional dysregulation of c-MET, degradation deficiency, and abnormal HGF production result in the abnormal expression of HGF/c-MET and tumor progression. Various inhibitors including MMP inhibitors and HGF/c-MET inhibitors have been developed and emerging as promising tools in the suppression of tumor metastasis. c-MET mesenchymal-epithelial transition factor, EMT epithelial-mesenchymal transition, HGF hepatocyte growth factor, MMPs matrix metalloproteinases

Journal: Signal Transduction and Targeted Therapy

Article Title: Tumor biomarkers for diagnosis, prognosis and targeted therapy

doi: 10.1038/s41392-024-01823-2

Figure Lengend Snippet: The cancer invasion and metastasis and its targeted therapy. The tumor metastasis process consists of multiple steps. Initially, tumor cells invade the surrounding stroma and extracellular matrix from the primary tumor site, and then intravasate into the bloodstream or the lymphatics. Subsequently, tumor cells arrest in the circulation and arrive at distant organ sites, followed by extravasating and invading the parenchyma of distant tissues. Finally, tumor cells adapt to the new microenvironment and grow to form metastatic colonization. EMT is the basic embryonic developmental process that transforms polarized non-motile epithelial cells into motile and invasive mesenchymal cells. Multiple cellular stress conditions including hypoxia, inflammation, metabolic stress, and signaling cascades, can induce the expression of EMT transcription factors and prompt tumor metastasis. Meanwhile, MET amplification and mutation, the transcriptional dysregulation of c-MET, degradation deficiency, and abnormal HGF production result in the abnormal expression of HGF/c-MET and tumor progression. Various inhibitors including MMP inhibitors and HGF/c-MET inhibitors have been developed and emerging as promising tools in the suppression of tumor metastasis. c-MET mesenchymal-epithelial transition factor, EMT epithelial-mesenchymal transition, HGF hepatocyte growth factor, MMPs matrix metalloproteinases

Article Snippet: Other MMPs inhibitors such as COL-3 (NSC-683551), neovastat (AE-941), prinomastat (AG3340), BMS-275291, and metastat(COL-3), have been evaluated in clinical trials (Table ).

Techniques: Expressing, Amplification, Mutagenesis

The typical and clinically developed  MMPs inhibitors  in cancer therapy

Journal: Signal Transduction and Targeted Therapy

Article Title: Tumor biomarkers for diagnosis, prognosis and targeted therapy

doi: 10.1038/s41392-024-01823-2

Figure Lengend Snippet: The typical and clinically developed MMPs inhibitors in cancer therapy

Article Snippet: Other MMPs inhibitors such as COL-3 (NSC-683551), neovastat (AE-941), prinomastat (AG3340), BMS-275291, and metastat(COL-3), have been evaluated in clinical trials (Table ).

Techniques:

Different Types of MMPIs Used in Cancer Treatment.

Journal: International Journal of Molecular Sciences

Article Title: Hypoxic Effects on Matrix Metalloproteinases’ Expression in the Tumor Microenvironment and Therapeutic Perspectives

doi: 10.3390/ijms242316887

Figure Lengend Snippet: Different Types of MMPIs Used in Cancer Treatment.

Article Snippet: Chemical modified tetracyclines , Metastat (COL-3) , MMP-1, MMP-2, MMP-8, MMP-9, MMP-13 , [ , , , , ] .

Techniques: Modification, Bioprocessing