Cloning and characterization of human cathepsin L promoter

Bakhshi, Radhika; Goel, Ashish; Seth, Puneet; Chhikara, Poonam; Chauhan, Shyam S.

doi:10.1016/s0378-1119(01)00650-3

Cited by 18 publications

(14 citation statements)

References 22 publications

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“…Upon cotransfections with empty vector, fulllength promoter and all deletion constructs exhibited a trend in the promoter activity (Fig. 4), which was similar to that observed by us earlier (Bakhshi et al, 2001). We observed that deletion of bases till − 133 in the pRB5 construct retained the responsiveness to VEGF.…”

Section: Discussionsupporting

confidence: 87%

“…Both these motifs were found in hCATL promoter sequence by TRANSFAC analysis (Bakhshi et al, 2001). Interestingly, deletion of these NF-AT elements did not affect the responsiveness of hCATL promoter to VEGF (Fig.…”

Section: Discussionmentioning

confidence: 81%

“…In the present study, we employed this strategy for the identification of VRE in hCATL promoter. For this, various deletion constructs of hCATL promoter used in an earlier study (Bakhshi et al 2001) were cotransfected with VEGF expression vector or the empty vector. Upon cotransfections with empty vector, fulllength promoter and all deletion constructs exhibited a trend in the promoter activity (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…The construction of hCATL promoter reporter plasmids (pRB1.75, pRB9, pRB8, pRB4.75, pRB5, pRB14 and pRB13) by cloning different lengths of hCATL promoter fragments, varying in their 5′ ends, upstream to the luciferase gene in the pGL-3 basic vector (Promega) has been described earlier (Bakhshi et al, 2001). Same plasmids were used in the present study for deletion mapping of VEGF response elements.…”

Section: Luciferase Promoter Constructs and Site Directed Mutagenesismentioning

confidence: 99%

“…In an earlier study, a series of promoter reporter deletion constructs were generated to characterize the hCATL promoter (Bakhshi et al, 2001). The promoter activities of these deletion constructs in VEGF induced and control cells were compared.…”

Section: Identification Of Vre In Hcatl Promotermentioning

confidence: 99%

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Transcriptional upregulation of human cathepsin L by VEGF in glioblastoma cells

Keerthivasan

Mittal

et al. 2007

Gene

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Section: Luciferase Promoter Constructs and Site Directed Mutagenesismentioning

confidence: 99%

Section: Identification Of Vre In Hcatl Promotermentioning

confidence: 99%

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Transcriptional upregulation of human cathepsin L by VEGF in glioblastoma cells

Keerthivasan

Mittal

et al. 2007

Gene

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Cathepsin B: Multiple roles in cancer

Aggarwal

Sloane

2014

Proteomics Clinical Apps

326

236

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Proteases, including intracellular proteases, play roles at many different stages of malignant progression. Our focus here is cathepsin B, a lysosomal cysteine cathepsin. High levels of cathepsin B are found in a wide variety of human cancers, levels that often induce secretion and association of cathepsin B with the tumor cell membrane. In experimental models, such as transgenic models of murine pancreatic and mammary carcinomas, causal roles for cathepsin B have been demonstrated in initiation, growth/tumor cell proliferation, angiogenesis, invasion, and metastasis. Tumor growth in transgenic models is promoted by cathepsin B in tumor-associated cells, for example, tumor-associated macrophages, as well as in tumor cells. In transgenic models, the absence of cathepsin B has been associated with enhanced apoptosis, yet cathepsin B also has been shown to contribute to apoptosis. Cathepsin B is part of a proteolytic pathway identified in xenograft models of human glioma; targeting only cathepsin B in these tumors is less effective than targeting cathepsin B in combination with other proteases or protease receptors. Understanding the mechanisms responsible for increased expression of cathepsin B in tumors and association of cathepsin B with tumor cell membranes is needed to determine whether targeting cathepsin B could be of therapeutic benefit.

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