Induction of cathepsin B by the CXCR3 chemokines CXCL9 and CXCL10 in human breast cancer cells

Bronger, Holger; Karge, Anne; Dreyer, Tobias; Zech, Daniela; Kraeft, Sara; Avril, Stephanie; Kiechle, Marion

doi:10.3892/ol.2017.5994

Cited by 36 publications

(24 citation statements)

References 36 publications

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“…Bannoud et al (2018) found that Cathepsin D can bind the M6PR and are co-transported in an estradiol stimulatory manner through MCF-7 cells and which linked Cathepsin D trafficking with estradioldependent EMT progression (and possible chemoresistence) [145]. Additionally, chemokines CXCL-9 and −10 were seen to upregulate Cathepsin B expression and secretion in BC cells via CXCR3 signaling [146], while the tumour suppressor Protilin was identified as a novel substrate for Cathepsin Z/X, the cleavage of which reduced its binding to Clathrin, thus linking Cathepsin Z/X activity and regulation of Clathrin-dependent endocytosis [147]. Recently, Shao et al (2018) showed that NEDD4 was needed for EGFR-dependent lung cancer cell migration and EGF-induced Cathepsin B secretion, as seen from a lack of Cathepsin B secretion in analysing a ligasedead mutant of NEDD4 and in NEDD4 knockdown experiments [148].…”

Section: Signal Transduction Intermediates and Cathepsin Regulationmentioning

confidence: 97%

‘Patchiness’ and basic cancer research: unravelling the proteases

2019

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The recent developments in Cathepsin protease research have unveiled a number of key observations which are fundamental to further our understanding of normal cellular homeostasis and disease. By far, the most interesting and promising area of Cathepsin biology stems from how these proteins are linked to the fate of living cells through the phenomenon of Lysosomal Leakage and Lysosomal Membrane Permeabilisation. While extracellular Cathepsins are generally believed to be of central importance in tumour progression, through their ability to modulate the architecture of the Extracellular Matrix, intracellular Cathepsins have been established as being of extreme significance in mediating cell death through Apoptosis. With these two juxtaposed key research areas in mind, the focus of this review highlights recent advancements in how this fastpaced area of Cathepsin research has recently evolved in the context of their mechanistic regulation in cancer research.

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Section: Signal Transduction Intermediates and Cathepsin Regulationmentioning

confidence: 97%

‘Patchiness’ and basic cancer research: unravelling the proteases

2019

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“…Finally, GAGs promote chemokine oligomerization preserving them by proteolytic cleavage and modulating chemokine-receptor linking [ 31 ]. Proteolytic cleavage can occur at either N- or C-terminal region by several proteases [ 32 ], including metalloproteases [ 33 ], dipeptidyl peptidase 4 (DPP4) [ 34 ] or cathepsin B [ 35 ]. Cleaved chemokines can display either reduced or increased activity, or different receptor selectivity.…”

Section: Regulation Of Chemokine Expression and Effectsmentioning

confidence: 99%

Role of Chemokines in the Biology of Cholangiocarcinoma

Caligiuri

Pastore

Lori

et al. 2020

Cancers

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Cholangiocarcinoma (CCA), a heterogeneous tumor with poor prognosis, can arise at any level in the biliary tree. It may derive from epithelial cells in the biliary tracts and peribiliary glands and possibly from progenitor cells or even hepatocytes. Several risk factors are responsible for CCA onset, however an inflammatory milieu nearby the biliary tree represents the most common condition favoring CCA development. Chemokines play a key role in driving the immunological response upon liver injury and may sustain tumor initiation and development. Chemokine receptor-dependent pathways influence the interplay among various cellular components, resulting in remodeling of the hepatic microenvironment towards a pro-inflammatory, pro-fibrogenic, pro-angiogenic and pre-neoplastic setting. Moreover, once tumor develops, chemokine signaling may influence its progression. Here we review the role of chemokines in the regulation of CCA development and progression, and the modulation of angiogenesis, metastasis and immune control. The potential role of chemokines and their receptors as possible biomarkers and/or therapeutic targets for hepatobiliary cancer is also discussed.

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“…induce Cathepsin B in human breast cancer cells, thereby supporting tumor invasion and metastasis [21].…”

Section: Discussionmentioning

confidence: 99%

Identification of neoadjuvant radiotherapy resistance genes in rectal cancer using integrated bioinformatics analysis

Liao

Zhang²,

Wang

et al. 2020

Preprint

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The incidence of rectal cancer is increasing year by year. And most patients have been diagnosed in the advanced stages largely because of the special anatomical location of the rectum, resulting in uneasy diagnosis in its early stage. The combination of radiotherapy and chemotherapy is widely accepted as effective treatment to the rectal cancer, significantly reduce the local recurrence rate and improve long-term survival, but the occurrence of radiotherapy resistance of rectal cancer strikingly weaken the responding of treatment. So finding reasons or factors leading to the resistance of neoadjuvant radiotherapy for rectal cancer become very urgent not just for the current clinic but also for development of new therapeutical approaches. To identify potential biomarkers associated with neoadjuvant radiotherapy resistance in rectal cancer using bioinformatics analysis. Firstly, we extracted relevant data from GEO database and analyzed the corresponding data by a series of analytic methods. Then, the candidate genes were identified by performing of the analysis of protein-protein interaction network, KEGG and GO, subsequently comfirmed at the levels of mRNA and Protein with Oncomine and The Human Protein Atlas respectively. Furthermore, these comfirmed genes were submitted to CMap analysis to identify candidate therapeutic compounds for neoadjuvant radiotherapy resistance. We found that the abnormal expression of some chemokines were tightly associated with the rectal cancer neoadjuvant radiotherapy resistance. Especially the upreuglation of Chemokines 9(CXCL9) and Chemokines 10(CXCL10) and downregulation of Chemokines 13(CXCL13) and Chemokines 5(CCL5) might be the potential biomarks of the radiotherapy resistance of rectal cancer. Through a series of analyses, the molecules that may be related to the radiotherapy resistance of rectal cancer were identified that may have a hint effect on the treatment of radiotherapy resistance of rectal cancer.

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Induction of cathepsin B by the CXCR3 chemokines CXCL9 and CXCL10 in human breast cancer cells

Cited by 36 publications

References 36 publications

‘Patchiness’ and basic cancer research: unravelling the proteases

‘Patchiness’ and basic cancer research: unravelling the proteases

Role of Chemokines in the Biology of Cholangiocarcinoma

Identification of neoadjuvant radiotherapy resistance genes in rectal cancer using integrated bioinformatics analysis

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