Release of Proteinases by Cultures of Human Cell Lines Derived from Squamous Carcinomas of the Tongue and Larynx

Baici, Antonio; Sträuli, Peter

doi:10.1159/000163314

Cited by 5 publications

(3 citation statements)

References 8 publications

(17 reference statements)

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“…Here we show that the cysteine peptidase cathepsin B, an important mediator of tissue degradation in tumor invasion [10–13] and osteoarthritis [14,15], inactivates TIMP‐1 and TIMP‐2. This suggests a new adverse role for cathepsin B because it shares with the MMPs the same pathological sites of action.…”

Section: Introductionmentioning

confidence: 79%

“…Destruction of important antagonists of neovascularization may have a direct impact in conditions characterized by the concomitant presence of MMPs and cathepsin B in the pathological scenario. Two representative examples are tumor growth and invasion [10–13,27,28] and osteoarthritis [14,15,29]. Cathepsin B has been localized in microvascular endothelial cells around human glioblastoma and prostate carcinomas, a feature which may play a role in the malignancy of these tumors [28].…”

Section: Discussionmentioning

confidence: 99%

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Stimulation of angiogenesis through cathepsin B inactivation of the tissue inhibitors of matrix metalloproteinases

et al. 1999

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The tissue inhibitors of matrix metalloproteinases (MMPs), TIMP-1 and TIMP-2, are also angiogenesis inhibitors. Cathepsin B and MMPs are found at sites of neovascularization in pathologies such as cancer and osteoarthritis. Treatment of TIMP-1, TIMP-2, and of a mixture of both inhibitors from human articular chondrocytes with cathepsin B resulted in their fragmentation, whereby they lost their MMPinhibitory and anti-angiogenic activities. Our data suggest that, besides directly participating in tissue destruction, cathepsin B can be harmful for two further reasons: it raises the activity of the MMPs also in the absence of mechanisms up-regulating these enzymes, and it stimulates angiogenesis. This is a prerequisite for blood vessel invasion in a variety of pathological situations of which cancer and osteoarthritis are prominent examples.z 1999 Federation of European Biochemical Societies.

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Section: Introductionmentioning

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Stimulation of angiogenesis through cathepsin B inactivation of the tissue inhibitors of matrix metalloproteinases

et al. 1999

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“…The concepts discussed are summarized in Figure 2. Another enzyme that has been associated with tumor malignancy is cathepsin B (Baici and Sträuli, 1985;Graf et a/., 1981;Keppler et a/., 1996;Mort ef a/., 1980;Sloane and Honn, 1984;Sloane ef a/., 1994). One or more etiologic factors may stimulate cells in the joint space to secrete cytokines (step 1) including interleukin 1, tumor necrosisfactora and interleukin-6 (reviewed by Pelletier ef a/., 1993).…”

Section: More Than One Enzyme Acting At the Pathological Sitementioning

confidence: 99%

Review

1998

BCHM

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The replication licensing system acts to ensure that no section of the genome is replicated more than once in a single cell cycle. Experiments using Xen op us egg extracts have revealed that the licensing system consists of two components, named RLF-M and RLF-B. Whereas the function of RLF-B is still unclear, RLF-M has been shown to consist of all six members of the MCM/P1 family proteins, which appear to be the structural component of the licensing system. The origin recognition complex (ORC) and Cdc6/Cdc18 are needed on chromatin before the licensing reaction can take place, although they are not themselves components of the licensing system. Cell cycle events and cyclin-dependent protein kinases (Cdks) also seem to be involved in controlling the licensing system to ensure once per cell cycle DMA replication. The subject of this review is to detail our current understanding of the licensing system and the way that it interacts with other components of the cell cycle machinery.

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Cell, tissue and organ culture as in vitro models to study the biology of squamous cell carcinomas of the head and neck

Sacks

1996

Cancer Metast Rev

105

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In vitro models are currently being used to study head and neck squamous cell carcinoma (HNSCC). Several hundred HNSCC cell lines have been established by various investigators and used to study a broad spectrum of questions related to head and neck cancer. The head and neck model with respect to multistage carcinogenesis is now complete. Several techniques exist for the culture of normal epithelial cells from the upper aerodigestive tract (UADT). The biology of these UADT cells (oral cavity, oropharynx, hypopharynx and larynx) is being studied. Successful culture of premalignant lesions (dysplastic mucosa, leukoplakia, erythroplakia) has resulted in establishment of a limited number of premalignant cell lines and cell cultures. HPV infection of normal oral epithelial cells for immortalization (approximately premalignant cells) coupled with transformation with carcinogens (malignant cells) has established an experimental model for progression. Two in vivo models for oral carcinogenesis, the 7,12 dimethylbenz(a)anthracene-induced hamster cheek pouch model and the 4-nitroquinoline-N-oxide rat oral model, have been established in culture. Thus, multistage carcinogenesis models have been established from both human tissues and animal models and include cultures of normal, premalignant and malignant cells. Culture techniques for growing dissociated primary tumor cells for short term experimental analysis are being used. The culture of normal or tumor tissue as organ/explant cultures allows for the maintenance of normal cell-cell and cell-matrix interaction, but limits experimentation since these cultures cannot be propagated. Several three dimensional model systems are being used to obtain this histological complexity but allow for experimentation. The ability to culture normal, premalignant and malignant cells coupled with the use of a variety of culture techniques, should allow for the continued growth and experimentation in head and neck cancer research.

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Release of Proteinases by Cultures of Human Cell Lines Derived from Squamous Carcinomas of the Tongue and Larynx

Cited by 5 publications

References 8 publications

Stimulation of angiogenesis through cathepsin B inactivation of the tissue inhibitors of matrix metalloproteinases

Stimulation of angiogenesis through cathepsin B inactivation of the tissue inhibitors of matrix metalloproteinases

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Cell, tissue and organ culture as in vitro models to study the biology of squamous cell carcinomas of the head and neck

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