Pharmacological inhibition of cathepsin C (CatC) as a potential approach for cancer therapeutics

Abideen, Syed Ainul; Khan, Murad; Al-Harbi, Alhanouf I.; Ahmad, Sajjad

doi:10.1080/07391102.2022.2135603

Cited by 2 publications

(1 citation statement)

References 34 publications

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“…Growing evidence has implied that the expression level of CTSC in several tissues and cells gleaned from tumors is different from that in normal adjacent tissues and cells, and its mechanism of action is markedly linked to the occurrence, development, metastasis, and recurrence of cancers, including breast cancer (Xiao et al 2021), colorectal cancer (Dang et al 2023), glioma (Cheng et al 2022;Li et al 2024), and hepatocellular carcinoma (Zhang et al 2020). Pharmacological suppression of CTSC is considered a possible strategy in cancer treatment (Abideen et al 2022). In 2024, the latest research found that CTSC could promote tumor development in non-small cell lung cancer by activating the Yes-associated protein signaling pathway (Kim et al 2024).…”

Section: Introductionmentioning

confidence: 99%

CTSC promotes tumorigenesis in bladder cancer by activating Wnt/β-Catenin signaling

Wang,

Jia,

Wang

2024

Preprint

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Cathepsin C (CTSC) participates in the development of numerous cancers. The function of bladder cancer (BCa) is still largely unknown. Bioinformatics prediction, RT-qPCR assay, and Western blotting assay determined the level of expression of CTSC in BCa tissues, para-cancer tissues, BCa cells, and normal uroepithelial cells (SV-HUC-1). Colony formation assay, CCK-8 assay, and Transwell assay were utilized to ascertain the involvement of CTSC in BCa. In addition, the effect of CTSC on BCa was further studied by animal experiments in vivo. The findings affirmed that CTSC exhibited a heightened expression level in BCa cells and tissues, and the overexpression of CTSC substantially enhanced the activity, proliferation, migration, and invasion of BCa cells, while suppression of CTSC repressed the above biological phenotypes. CTSC could both activate the Wnt/β-Catenin signaling pathway and up-regulate DIAPH3 expression. Overexpression of CTSC combined with knockdown of DIAPH3 could partially reverse the impact of CTSC on the biological behavior of BCa cells and the Wnt/β-Catenin signaling pathway activation. CTSC could up-regulate DIAPH3 and activate the aforementioned pathway to enhance the activity, proliferation, migration, and invasion of cells from BCa.

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Section: Introductionmentioning

confidence: 99%

CTSC promotes tumorigenesis in bladder cancer by activating Wnt/β-Catenin signaling

Wang,

Jia,

Wang

2024

Preprint

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Cathepsin C Promotes Tumorigenesis in Bladder Cancer by Activating the Wnt/β-catenin Signalling Pathway

Wang,

Jia,

Wang

2024

Front. Biosci. (Landmark Ed)

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Background: Cathepsin C (CTSC) participates in the development of numerous cancers; however, its function in bladder cancer (BCa) remains largely unknown. Methods: Bioinformatics prediction, quantitative reverse transcription polymerase chain reaction (RT-qPCR) assay, and Western blot assay were used to determine CTSC expression in BCa tissues, paracancer tissues, BCa cells, and normal uroepithelial cells (SV-HUC-1). Colony formation, cell counting kit-8 (CCK-8), and Transwell assays were utilised to ascertain the involvement of CTSC in BCa. The effect of CTSC on BCa was further studied in vivo via animal experiments. Results: CTSC exhibited a heightened expression in BCa cells and tissues; meanwhile, bladder urothelial carcinoma (BLCA) patients with enhanced CTSC expression had a remarkably reduced overall survival than those with low CTSC expression. The overexpression of CTSC substantially enhanced the activity, proliferation, migration, and invasion of BCa cells, whereas its suppression repressed the above biological phenotypes. CTSC could activate the Wnt/β-catenin signalling pathway and upregulate diaphanous-related formin 3 (DIAPH3). CTSC overexpression combined with DIAPH3 knockdown partially reversed the impact of CTSC overexpression on the biological behaviour of BCa cells and the activation of the Wnt/β-catenin signalling pathway. Conclusions: CTSC was upregulated in tissues and BCa cells, and high CTSC expression was associated with poor overall survival. CTSC could enhance the activity, proliferation, migration, and invasion of BCa cells via upregulating DIAPH3 and activating the Wnt/β-catenin pathway.

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Pharmacological inhibition of cathepsin C (CatC) as a potential approach for cancer therapeutics

Cited by 2 publications

References 34 publications

CTSC promotes tumorigenesis in bladder cancer by activating Wnt/β-Catenin signaling

CTSC promotes tumorigenesis in bladder cancer by activating Wnt/β-Catenin signaling

Cathepsin C Promotes Tumorigenesis in Bladder Cancer by Activating the Wnt/β-catenin Signalling Pathway

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