Timosaponin AIII inhibits metastasis of renal carcinoma cells through suppressing cathepsin C expression by AKT/miR‐129‐5p axis

Chiang, Kuang‐Chung; Lai, Chung‐Yu; Chiou, Hui‐Ling; Lin, Chia‐Liang; Chen, Yong-Syuan; Kao, Shao‐Hsuan; Hsieh, Yi‐Hsien

doi:10.1002/jcp.28010

Cited by 36 publications

(20 citation statements)

References 39 publications

(68 reference statements)

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“…The shLuc and shMTA2 cells were seeded into 6 cm dishes at a density of 2 × 10 5 cells/well for 24 h and transfected with the miR-133b antagomir and MTA2 plasmid by using the TurboFect transfection reagent (Thermo Fisher Scientific, Waltham, MA USA) as previously reported [45].…”

Section: Mir-133b Antagomir and Mta2 Plasmid Transfectionmentioning

confidence: 99%

MTA2 as a Potential Biomarker and Its Involvement in Metastatic Progression of Human Renal Cancer by miR-133b Targeting MMP-9

Chen

Hung

et al. 2019

Cancers

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Metastasis-associated protein 2 (MTA2) was previously known as a requirement to maintain malignant potentials in several human cancers. However, the role of MTA2 in the progression of renal cell carcinoma (RCC) has not yet been delineated. In this study, MTA2 expression was significantly increased in RCC tissues and cell lines. Increased MTA2 expression was significantly associated with tumour grade (p = 0.002) and was an independent prognostic factor for overall survival with a high RCC tumour grade. MTA2 knockdown inhibited the migration, invasion, and in vivo metastasis of RCC cells without effects on cell proliferation. Regarding molecular mechanisms, MTA2 knockdown reduced the activity, protein level, and mRNA expression of matrix metalloproteinase-9 (MMP-9) in RCC cells. Further analyses demonstrated that patients with lower miR-133b expression had poorer survival rates than those with higher expression from The Cancer Genome Atlas database. Moreover, miR-133b modulated the 3 untranslated region (UTR) of MMP-9 promoter activities and subsequently the migratory and invasive abilities of these dysregulated expressions of MTA2 in RCC cells. The inhibition of MTA2 could contribute to human RCC metastasis by regulating the expression of miR-133b targeting MMP-9 expression.

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Section: Mir-133b Antagomir and Mta2 Plasmid Transfectionmentioning

confidence: 99%

MTA2 as a Potential Biomarker and Its Involvement in Metastatic Progression of Human Renal Cancer by miR-133b Targeting MMP-9

Chen

Hung

et al. 2019

Cancers

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“…In addition, studies have indicated that CTSB and CTSS mediate cancer progression and metastasis in lung cancer, renal cancer, and gastric cancer [33][34][35]. In our previous study, we discovered that CTSC is highly expressed in RCC cells and involved in inhibited the migratory and invasive ability in timosaponin AIII-treated RCC cells [24]. Our present results also demonstrate that the expression of CTSC and CTSV is inhibited by Pra-B as well as involved in the migration and invasion of RCC cells.…”

Section: Discussionmentioning

confidence: 93%

“…Cathepsin-related proteins have been broadly implicated in cancer [23], and we even previously reported CTSC as being a target in the suppression of RCC migration and invasion [24]. To identify the effect of Pra-B on CTS-related mRNA expression, we treated 786-O cells with Pra-B (30 μM) for 24 h and used qRT-PCR analysis to screen the expression of CTS-related gene expression.…”

Section: Pra-b Inhibits the Expression Of Ctsc And Ctsv In 786-o Cellsmentioning

confidence: 99%

Praeruptorin B Mitigates the Metastatic Ability of Human Renal Carcinoma Cells through Targeting CTSC and CTSV Expression

Lin

Hung

Ying

et al. 2020

IJMS

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Renal cell carcinoma (RCC) is the most common adult kidney cancer, and accounts for 85% of all cases of kidney cancers worldwide. Praeruptorin B (Pra-B) is a bioactive constituent of Peucedanum praeruptorum Dunn and exhibits several pharmacological activities, including potent antitumor effects. However, the anti-RCC effects of Pra-B and their underlying mechanisms are unclear; therefore, we explored the effects of Pra-B on RCC cells in this study. We found that Pra-B nonsignificantly influenced the cell viability of human RCC cell lines 786-O and ACHN at a dose of less than 30 μM for 24 h treatment. Further study revealed that Pra-B potently inhibited the migration and invasion of 786-O and ACHN cells, as well as downregulated the mRNA and protein expression of cathepsin C (CTSC) and cathepsin V (CTSV) of 786-O and ACHN cells. Mechanistically, Pra-B also reduced the protein levels of phospho (p)-epidermal growth factor receptor (EGFR), p-mitogen-activated protein kinase kinase (MEK), and p-extracellular signal-regulated kinases (ERK) in RCC cells. In addition, Pra-B treatment inhibited the effect of EGF on the upregulation of EGFR–MEK–ERK, CTSC and CTSV expression, cellular migration, and invasion of 786-O cells. Our findings are the first to demonstrate that Pra-B can reduce the migration and invasion ability of human RCC cells through suppressing the EGFR-MEK-ERK signaling pathway and subsequently downregulating CTSC and CTSV. This evidence suggests that Pra-B can be developed as an effective antimetastatic agent for the treatment of RCC.

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“…Cell cycle assay as previously report [ 27 ]. HeLa-Luc or HeLa-shPROK2 cells were collected and fixed with 75% ice ethanol for overnight.…”

Section: Methodsmentioning

confidence: 99%

Silencing PROK2 Inhibits Invasion of Human Cervical Cancer Cells by Targeting MMP15 Expression

Hsieh

et al. 2020

IJMS

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Cervical cancer is the second most frequent type of gynecologic cancer worldwide. Prokineticin 2 (PROK2) is reported to be involved in tumor progression in some malignant tumors. However, the role of PROK2 in the development of cervical cancer remains unknown. Our results indicate that PROK2 is overexpressed in the human cervical cancer. Cervical cancer patients with high PROK2 expression have a shorter overall survival rate (OS) and disease-free survival rate (DFS). PROK2 acts as a potential biomarker for predicting OS and DFS of cervical cancer patients. We further show that PROK2 is important factor for oncogenic migration and invasion in human cervical cancer cells. Knockdown PROK2 significantly inhibited cell migration, invasion, and MMP15 protein expression in HeLa cells. High expression of MMP15 is confirmed in the human cervical cancer, is significantly associated with the shorter overall survival rate (OS) and is correlated with PROK2 expression. Overexpression of PROK2 using PROK2 plasmid significantly reverses the function of knockdown PROK2, and further upregulates MMP15 expression, migration and invasion of human cervical cancer cells. In conclusion, our findings are the first to demonstrate the role of PROK2 as a novel and potential biomarker for clinical use, and reveal the oncogenic functions of PROK2 as therapeutic target for cervical cancer.

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Timosaponin AIII inhibits metastasis of renal carcinoma cells through suppressing cathepsin C expression by AKT/miR‐129‐5p axis

Cited by 36 publications

References 39 publications

MTA2 as a Potential Biomarker and Its Involvement in Metastatic Progression of Human Renal Cancer by miR-133b Targeting MMP-9

MTA2 as a Potential Biomarker and Its Involvement in Metastatic Progression of Human Renal Cancer by miR-133b Targeting MMP-9

Praeruptorin B Mitigates the Metastatic Ability of Human Renal Carcinoma Cells through Targeting CTSC and CTSV Expression

Silencing PROK2 Inhibits Invasion of Human Cervical Cancer Cells by Targeting MMP15 Expression

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