Blocking the Proliferation of Human Tumor Cell Lines by Peptidase Inhibitors from Bauhinia Seeds

Nakahata, Adriana Miti; Mayer, Barbara; Neth, Peter; Hansen, Daiane; Sampaio, Misako U.; Oliva, Maria Luíza Vilela

doi:10.1055/s-0032-1328156

Cited by 13 publications

(12 citation statements)

References 47 publications

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“…To date, vortioxetine has been the novel antidepressant for treatment of major depressive disorder, although its anti-tumor effects on GC have not yet been fully investigated. The main biological characteristics of a developing tumor malignancy, including GC, are the abnormal proliferation, migration and invasion of cells, [30,31]. The results of the cell function assay demonstrated that vortioxetine inhibited tumor progression of GC by inhibiting cell proliferation, invasion and migration.…”

Section: Discussionmentioning

confidence: 99%

Vortioxetine induces apoptosis and autophagy of gastric cancer AGS cells via the PI3K/AKT pathway

Wang

Zhu

et al. 2020

FEBS Open Bio

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Vortioxetine is a potent antagonist of the 5-hydroxytryptamine receptor and serotonin transporter and has been reported to function as an antidepressant in the treatment of major depressive disorder. However, its antitumor effects remain unclear. Here, we examined whether vortioxetine affects the characteristics of GC cells. Cell viability was measured by a colony formation assay and, in addition, cell invasion, migration and apoptosis assays were performed with a transwell assay and a flow cytometry assay. Protein levels were measured by western blotting. We found that vortioxetine inhibited the proliferation, invasion and migration abilities of AGS cells. Additionally, vortioxetine could induce apoptosis and autophagy by increasing the levels of Bax, active caspase-3/-9, Beclin-1 and light chain 3, as well as by downregulating Bcl-2 and P62. Further investigations indicated that vortioxetine regulated apoptosis and autophagy via activation of the phosphoinositide 3-kinase/AKT pathway. Taken together, our data suggest that vortioxetine has cytotoxic effects against GC AGS cells as a result of inhibiting proliferation, invasion and migration, as well as by inducing apoptosis and autophagy through the phosphoinositide 3-kinase/ AKT pathway.

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Section: Discussionmentioning

confidence: 99%

Vortioxetine induces apoptosis and autophagy of gastric cancer AGS cells via the PI3K/AKT pathway

Wang

Zhu

et al. 2020

FEBS Open Bio

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“…In addition, KLK6 has been identified as a marker of poor prognosis in colon and ovarian cancer patients [ 34 , 35 ]. Natural and recombinant kallikrein inhibitors are cytotoxic to a wide range of human cancer cells in vitro [ 44 , 45 ], but no data are available to demonstrate chemopreventive or chemotherapeutic efficacy in vivo . In this regard, protease inhibitors such as Bowman-Birk Inhibitor Complex (BBIC) have been demonstrated to inhibit carcinogenesis in a broad range of experimental models (reviewed in [ 46 ]), including the hamster cheek pouch model of oral neoplasia [ 47 ].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Lipocalins and Pro-Inflammatory Chemokines and Altered Methylation of PTGS2 and APC2 in Oral Squamous Cell Carcinomas Induced in Rats by 4-Nitroquinoline-1-Oxide

et al. 2015

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Oral squamous cell carcinomas (OSCC) induced in F344 rats by 4-nitroquinoline-1-oxide (4-NQO) demonstrate considerable phenotypic similarity to human oral cancers. Gene expression studies (microarray and PCR) were coupled with methylation analysis of selected genes to identify molecular markers of carcinogenesis in this model and potential biochemical and molecular targets for oral cancer chemoprevention. Microarray analysis of 11 pairs of OSCC and site-matched phenotypically normal oral tissues from 4-NQO-treated rats identified more than 3500 differentially expressed genes; 1735 genes were up-regulated in rat OSCC versus non-malignant tissues, while 1803 genes were down-regulated. In addition to several genes involved in normal digestion, genes demonstrating the largest fold increases in expression in 4-NQO-induced OSCC include three lipocalins (VEGP1, VEGP2, LCN2) and three chemokines (CCL, CXCL2, CXCL3); both classes are potentially druggable targets for oral cancer chemoprevention and/or therapy. Down-regulated genes in 4-NQO-induced OSCC include numerous keratins and keratin-associated proteins, suggesting that alterations in keratin expression profiles may provide a useful biomarker of oral cancer in F344 rats treated with 4-NQO. Confirming and extending our previous results, PTGS2 (cyclooxygenase-2) and several cyclooxygenase-related genes were significantly up-regulated in 4-NQO-induced oral cancers; up-regulation of PTGS2 was associated with promoter hypomethylation. Rat OSCC also demonstrated increased methylation of the first exon of APC2; the increased methylation was correlated with down-regulation of this tumor suppressor gene. Overexpression of pro-inflammatory chemokines, hypomethylation of PTGS2, and hypermethylation of APC2 may be causally linked to the etiology of oral cancer in this model.

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“…BbKI is the first plant-derived inhibitor of the primary structure set described that is an inhibitor of tissue kallikrein [ 17 , 18 ]. Indeed, rBbKI was effective in inhibiting the viability of tumor cell lines [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

The Plant-DerivedBauhinia bauhinioidesKallikrein Proteinase Inhibitor (rBbKI) Attenuates Elastase-Induced Emphysema in Mice

Martins-Olivera

Almeida-Reis

Theodoro-Junior

et al. 2016

Mediators of Inflammation

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Background. Elastase mediates important oxidative actions during the development of chronic obstructive pulmonary disease (COPD). However, few resources for the inhibition of elastase have been investigated. Our study evaluated the ability of the recombinant plant derived Bauhinia bauhinioides Kallikrein proteinase Inhibitor (rBbKI) to modulate elastase-induced pulmonary inflammation. Methods. C57Bl/6 mice were given intratracheal elastase (ELA group) or saline (SAL group) and were treated intraperitoneally with rBbKI (ELA-rBbKI and SAL-rBbKI groups). At day 28, the following analyses were performed: (I) lung mechanics, (II) exhaled nitric oxide (ENO), (III) bronchoalveolar lavage fluid (BALF), and (IV) lung immunohistochemical staining. Results. In addition to decreasing mechanical alterations and alveolar septum disruption, rBbKI reduced the number of cells in the BALF and decreased the cellular expression of TNF-α, MMP-9, MMP-12, TIMP-1, eNOS, and iNOS in airways and alveolar walls compared with the ELA group. rBbKI decreased the volume proportion of 8-iso-PGF2α, collagen, and elastic fibers in the airways and alveolar walls compared with the ELA group. A reduction in the number of MUC-5-positive cells in the airway walls was also observed. Conclusion. rBbKI reduced elastase-induced pulmonary inflammation and extracellular matrix remodeling. rBbKI may be a potential pharmacological tool for COPD treatment.

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Blocking the Proliferation of Human Tumor Cell Lines by Peptidase Inhibitors from Bauhinia Seeds

Cited by 13 publications

References 47 publications

Vortioxetine induces apoptosis and autophagy of gastric cancer AGS cells via the PI3K/AKT pathway

Vortioxetine induces apoptosis and autophagy of gastric cancer AGS cells via the PI3K/AKT pathway

Overexpression of Lipocalins and Pro-Inflammatory Chemokines and Altered Methylation of PTGS2 and APC2 in Oral Squamous Cell Carcinomas Induced in Rats by 4-Nitroquinoline-1-Oxide

The Plant-DerivedBauhinia bauhinioidesKallikrein Proteinase Inhibitor (rBbKI) Attenuates Elastase-Induced Emphysema in Mice

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