A novel approach for reliable detection of cathepsin S activities in mouse antigen presenting cells

Steimle, Alex; Kalbacher, Hubert; Maurer, Andreas; Beifuss, Brigitte; Bender, Annika; Schäfer, Andrea; Müller, Ricarda; Autenrieth, Ingo B.; Frick, Julia-Stefanie

doi:10.1016/j.jim.2016.02.015

Cited by 10 publications

(6 citation statements)

References 29 publications

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“…Cathepsin S (CTSS), a lysosomal cysteine protease of papain subfamily, has a series of functions under extracellular conditions, unlike other family members [14]. Like matrix metalloproteinases, members of the histone family have been associated with metastasis and cancer recurrence [15]. Cathepsin S is highly expressed in renal clear cell carcinoma [16], hepatocellular carcinoma [17], cervical cancer [18], lung cancer [19] and other tumours and is an essential regulator of tumour growth and invasion.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of CD44 inhibits proliferation, migration and invasion of osteosarcoma cells accompanied by downregulation of cathepsin S

Ji¹,

Gan

Cao

et al. 2022

J Orthop Surg Res

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Background Osteosarcoma (OS) is a malignant bone tumour of mesenchymal origin. These tumours are characterised by rich vascularisation, therefore promoting rapid proliferation and facilitating metastasis. CD44 has been reported to be involved in OS, but its role and molecular mechanisms in the pathogenesis of the disease are not fully determined. Methods In this study, we investigated the antitumor effect of CD44 on the development of OS and further explored the molecular mechanisms. The expression of CD44, cathepsin S and MMP-9 was detected by Western blot (WB) and reverse transcription-polymerase chain reaction (RT-qPCR) in different cell lines (MG63, U2OS OS and hFOB 1.19). To elucidate the role of CD44 in OS, MG63 and U2OS cells were treated with small interference RNA (siRNA) to knock down CD44, and the knockdown efficiency was validated with GFP and RT-qPCR. Furthermore, cell proliferation was assayed using Cell Counting Kit‑8 (CCK-8) and colony formation assays, and cell migration and invasion were assayed by transwell and wound-healing assays. Results We found that CD44 expression in the MG63 and U2OS OS cell lines was markedly increased compared to that of the human osteoblast hFOB 1.19 cell line. Knockdown of CD44 inhibited proliferation, migration and invasion of MG63 and U2OS cells. Cathepsin S expression in the MG63 and U2OS OS cell lines was increased compared to that of the human osteoblast hFOB 1.19 cell line. When CD44 was knocked down, its expression level went down. Conclusion Taken together, our data reinforced the evidence that CD44 knockdown inhibited cell proliferation, migration and invasion of OS cells accompanied by altered expression of cathepsin S. These findings offer new clues for OS development and progression, suggesting CD44 as a potential therapeutic target for OS.

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Section: Introductionmentioning

confidence: 99%

Knockdown of CD44 inhibits proliferation, migration and invasion of osteosarcoma cells accompanied by downregulation of cathepsin S

Ji¹,

Gan

Cao

et al. 2022

J Orthop Surg Res

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“…To know more about the molecular mechanisms, we next investigated the expression of cathepsin S. Like matrix metalloproteinases, members of the histone family have been associated with metastasis and cancer recurrence [24]. Cathepsin S (CTSS), a member of the histone family of enzymes, is highly expressed in renal clear cell carcinoma [25], hepatocellular carcinoma [26], cervical cancer [27], lung cancer [28] and other tumours and is an essential regulator of tumour growth and invasion.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of CD44 Inhibits Proliferation, Invasion and Migration of Osteosarcoma Cells by Regulating the Expression of Cathepsin S

Kong

Gan

et al. 2021

Preprint

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BackgroundOsteosarcoma (OS) is a malignant bone tumour of mesenchymal origin. These tumours are characterised by rich vascularisation, therefore promoting rapid proliferation and facilitating metastasis. CD44 has been reported to be involved in OS, but its role and molecular mechanisms in the pathogenesis of the disease are not fully determined. MethodsIn this study, we investigated the antitumor effect of CD44 on the development of OS and further explored the molecular mechanisms. The expression of CD44, cathepsin S and MMP-9 was detected by Western blot (WB) and reverse transcription-polymerase chain reaction (RT-qPCR) in different cell lines (MG63, U2OS OS and hFOB 1.19). To elucidate the role of CD44 in OS, MG63 and U2OS cells were treated with small interference RNA (siRNA) to knock down CD44, and the knockdown efficiency was validated with GFP and RT-qPCR. Furthermore, cell proliferation was assayed using Cell Counting Kit‑8 (CCK-8) and colony formation assays, and cell migration and invasion were assayed by transwell and wound-healing assays. ResultsWe found that CD44 expression in the MG63 and U2OS OS cell lines was markedly increased compared to that of the human osteoblast hFOB 1.19 cell line. Knockdown of CD44 inhibited proliferation, migration, and invasion of MG63 and U2OS cells, possibly by regulating the expression of cathepsin S in OS. ConclusionTaken together, our data reinforced the evidence that CD44 knockdown inhibited cell proliferation, migration, and invasion of OS cells accompanied by altered expression of cathepsin S. These findings offer new clues for OS development and progression, suggesting CD44 as a potential therapeutic target for OS.

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“…Cathepsin S is produced by immune cells presenting antigen, which are activated by inflammatory mediators. The distinctive properties of this protein from other cathepsins are the stability beyond the lysosome and the catalytic activity at neutral pH [ 60 , 61 ]. Inhibition of this enzyme can be effective in the treatment of immune related diseases such as rheumatism or psoriasis.…”

Section: Biological Properties Of Imidazo[45- B mentioning

confidence: 99%

Pharmacological Potential and Synthetic Approaches of Imidazo[4,5-b]pyridine and Imidazo[4,5-c]pyridine Derivatives

2017

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The structural resemblance between the fused imidazopyridine heterocyclic ring system and purines has prompted biological investigations to assess their potential therapeutic significance. They are known to play a crucial role in numerous disease conditions. The discovery of their first bioactivity as GABAA receptor positive allosteric modulators divulged their medicinal potential. Proton pump inhibitors, aromatase inhibitors, and NSAIDs were also found in this chemical group. Imidazopyridines have the ability to influence many cellular pathways necessary for the proper functioning of cancerous cells, pathogens, components of the immune system, enzymes involved in carbohydrate metabolism, etc. The collective results of biochemical and biophysical properties foregrounded their medicinal significance in central nervous system, digestive system, cancer, inflammation, etc. In recent years, new preparative methods for the synthesis of imidazopyridines using various catalysts have been described. The present manuscript to the best of our knowledge is the complete compilation on the synthesis and medicinal aspects of imidazo[4,5-b]pyridines and imidazo[4,5-c]pyridines reported from the year 2000 to date, including structure–activity relationships.

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A novel approach for reliable detection of cathepsin S activities in mouse antigen presenting cells

Cited by 10 publications

References 29 publications

Knockdown of CD44 inhibits proliferation, migration and invasion of osteosarcoma cells accompanied by downregulation of cathepsin S

Knockdown of CD44 inhibits proliferation, migration and invasion of osteosarcoma cells accompanied by downregulation of cathepsin S

Downregulation of CD44 Inhibits Proliferation, Invasion and Migration of Osteosarcoma Cells by Regulating the Expression of Cathepsin S

Pharmacological Potential and Synthetic Approaches of Imidazo[4,5-b]pyridine and Imidazo[4,5-c]pyridine Derivatives

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