Vinblastine, vincristine and vindesine: Anti-invasive effect on MO4 mouse fibrosarcoma cells in vitro

Mareel, Marc; Storme, Guy; Bruyne, Georges K. De; Cauwenberge, Rita M. Van

doi:10.1016/0277-5379(82)90064-5

Cited by 24 publications

(11 citation statements)

References 13 publications

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“…The process of tumor cell invasion and metastasis is conventionally understood as the migration of individual cells that detach from the primary tumor, enter lymphatic vessels or the bloodstream, and seed in distant organs. The effects of MTDs on cell migration and invasion remain very controversial, probably due to different tumor cell line behaviors, different culture conditions, but most important to different drug concentrations [205][206][207][208][209][210][211]. Both paclitaxel and nocodazole, at concentrations that signifi cantly suppress MT dynamics without modifying the MT polymer mass, reduced up to 60% the rate of locomotion of NRK fi broblasts [155,209].…”

Section: Mt Dynamics Suppression Inhibits Cell Migrationmentioning

confidence: 99%

Understanding microtubule dynamics for improved cancer therapy

Honoré¹,

Pasquier²,

Braguer³

2005

Cell. Mol. Life Sci.

297

210

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Microtubules (MTs), key components of the cytoskeleton, are dynamic polymers of tubulin that form a well-organized network of polarized tube filaments. MT dynamics are highly regulated both spacially and temporally by several MT-related proteins, themselves regulated by several kinases and phosphatases via signaling cascades, and also by coordinated interactions with actin cytoskeleton and adhesion sites. Regulation of MT dynamics is crucial for mitosis, cell migration, cell signaling and trafficking. MT-targeted drugs (MTDs), which constitute a major anticancer drug family with antimitotic and antiangiogenic properties, inhibit tumor progression mainly by altering MT dynamics in both cancer and endothelial cells. Identification of proteins regulating the MT network will lead to a better understanding of tumor progression regulators and will be helpful in improving cancer therapy.

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Section: Mt Dynamics Suppression Inhibits Cell Migrationmentioning

confidence: 99%

Understanding microtubule dynamics for improved cancer therapy

Honoré¹,

Pasquier²,

Braguer³

2005

Cell. Mol. Life Sci.

297

210

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“…In analyzing the metastatic cascade in animal tumor models several discrete stages in the metastatic process have been studied in detail (2,4,10,11) and several have been proposed as sites for therapeutic intervention (12)(13)(14). Many of these studies have been instrumental in examining the biology, pharmacology and biochemistry of tumor cell metastasis but the prospects of exploiting this information in the design of mechanism-based drugs which display improved activity against established metastases, are for reasons described above, remote, Compounds with proposed 'antimetastatic' activity like inhibitors of tumor cell invasion (protease inhibitors and disruptors of microtubule function) (15)(16)(17)(18)(19)(20)(21), antagonists of tumor cell-platelet interactions (prostacyclin thromboxane antagonists, calcium channel blockers) (22)(23) and blockers of tumor cell arrest (laminin fragments) (33, 34) may serve as useful tool compounds to yield insight into the pathogenesis of metastasis and may even find limited clinical utility in the prophylactic discouragement of tumor cell spread. However, unless and until diagnostic procedures achieve a level of sensitivity capable of detecting (and locating) malignant growths before dissemination has occurred (35), the pharmacological approaches directed at blocking tumor cell spread is inappropriate and offers little, if any, prospect of improved therapeutic strategies for cancer patients with disseminated disease.…”

Section: Therapeutic Targetmentioning

confidence: 99%

Shaping future strategies for the pharmacological control of tumor cell metastases

Greig¹,

Trainer²

1986

Cancer Metast Rev

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The eradication of established metastases in patients with malignant tumors is the single most important objective in clinical oncology. The current panel of antineoplastic agents discovered through random and semiempirical screening procedures has proven largely ineffective in treating disseminated disease and there is a clear and urgent need for more efficient antimetastatic drugs. Unfortunately, although progress has been made in examining the biology of metastatic spread, our understanding of the pharmacology, biochemistry and molecular genetics of this process is meager and insufficient to provide a rational foundation for the design of mechanism-based antineoplastic agents. Faced on the one hand with the failure of existing drugs to control metastatic spread and on the other with a dearth of alternative pharmacological approaches, the prospect of offering significantly improved therapy to the cancer patient of the 1990's is poor. The challenge of the coming decade lies in obtaining better insights into the molecular mechanisms of metastasis and using this information to identify pharmacological opportunities to curtail the proliferation of secondary tumor growths. As a first step toward this goal we need to define more rigorously what constitutes a therapeutic target in malignant disease and what steps in the pathogenesis of cancer metastasis represent the gravest risk to the patient and thus are most eligible for direct pharmacological intervention. In addressing these issues and developing future strategies for antimetastatic drugs, Paget's 100 year-old 'seed and soil' hypothesis continues to offer a useful conceptual framework for analysis of metastatic behavior. Although Paget's proposal has been validated by a century of clinical observation, efforts to define the 'seed and soil' theory in molecular terms have not been attempted. With the advent of more efficient methodologies for culturing human normal and neoplastic cells coupled with the availability of microanalytical technologies it now becomes possible to investigate and identify the complementary biochemical components of the tumor cell 'seed' and organ 'soil' that combine to encourage the proliferation of metastases. With this information the design of specific pharmacological strategies to uncouple the 'seed and soil' relationship may emerge as a potential therapeutic approach for antagonizing the growth of disseminated malignant tumors.

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“…An attribute of cells which may contribute to metastatic capability is cell motility which is, in turn, reported to be dependent on microtubule elements 381 of the cytoskeletal system (85,86,87). We therefore studied the effects of metastasis-permissive and metastasis-inhibitory temperatures on the CMTC (88) of frog renal adenocarcinoma cells and normal tadpole renal epithelial cells in vitro (89).…”

Section: The Cytoplasmic Microtubule Complex (Cmtc) : a Temperature-lmentioning

confidence: 99%

“…Mouse tumor cell spheroids, when cocultured in vitro with normal tissue fragments, will progressively invade and destroy the normal tissue and microtubule inhibitors (e.g., vinblastine, vincristine, and vindesine) inhibit malignant invasion in vitro (85,86,87,97). The in vitro invasion assay designed by Marcel and coworkers for studies on murine tumors was adapted for a study on frog renal carcinoma.…”

Section: In Vitro Invasion Of Normal Tadpole Tissue By Fragments Of Fmentioning

confidence: 99%

Temperature-dependent metastasis of the Lucke renal carcinoma and its significance for studies on mechanisms of metastasis

McKinnell

Tarin

1984

Cancer Metast Rev

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Metastasis is temperature dependent in the renal adenocarcinoma of the North American leopard frog, Rana pipiens. Widespread, multiple, metastatic colonies occur in tumor-bearing frogs kept at 28 degrees C for 50 days while tumor-bearing frogs kept at 7 degrees C for 98 days or more have either no secondary deposits or they have only an occasional small metastatic nodule. An attractive aspect of the frog tumor is that invasion and metastasis can be permitted or inhibited by the manipulation of temperature alone-no exogenous chemicals or drugs are required for the effect. Because of this, biological variables which reproducibly and specifically associate with metastasis permissive conditions when ambient temperature is cycled between permissive and inhibitory values are strong candidates for being causal elements in the multistep process leading to metastasis. Intravascularly injected labelled renal tumor cells reached all organs studied in as little as 15 minutes at both metastasis restrictive and permissive temperature. The results with tumor cell inoculation dispose of the possibility that failure of metastasis in chilled animals is due to cold-induced changes in blood flow. Histologically typical metastatic colonies developed in frogs, kept at the permissive temperature, after injection with disaggregated tumor cells which were previously cryopreserved. Frog tumors elaborate type I collagenase in a temperature dependent manner. Type IV collagenase has been demonstrated as well. Tumor cell detachment in vitro, assembly and disassembly of tumor cell cytoplasmic microtubules, and invasion in vitro, are all temperature dependent.

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Vinblastine, vincristine and vindesine: Anti-invasive effect on MO4 mouse fibrosarcoma cells in vitro

Cited by 24 publications

References 13 publications

Understanding microtubule dynamics for improved cancer therapy

Understanding microtubule dynamics for improved cancer therapy

Shaping future strategies for the pharmacological control of tumor cell metastases

Temperature-dependent metastasis of the Lucke renal carcinoma and its significance for studies on mechanisms of metastasis

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