CTRP1 Knockout Attenuates Tumor Progression in A549 and HCT116 Cancer Cells

Park, Rackhyun; Park, Yea-In; Park, Yeonjeong; Lee, Siyun; So, Jaeyeon; Park, Junsoo

doi:10.3390/cancers14184495

Cited by 7 publications

(3 citation statements)

References 24 publications

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“…Cell migration is a vital part of ocular surface wound healing and essential to restore integrity of the physiological barrier of the eye [ 1 , 60 ]. Several studies have described enhanced cell proliferation and migration as well as tumor invasion through CTRP1, CTRP6, or CTRP8 [ 5 , 7 , 19 , 20 , 21 , 30 , 31 , 63 ]. For example, CTRP8 promotes cell migration in human glioblastoma cells by activation of the RXFP1 involving the N-terminal “YAAFSVG” peptide motif present in the C1q globular domain of CTRP8 [ 5 ].…”

Section: Discussionmentioning

confidence: 99%

C1q/TNF-Related Proteins 1, 6 and 8 Are Involved in Corneal Epithelial Wound Closure by Targeting Relaxin Receptor RXFP1 In Vitro

Nicolaus

Klonisch

Paulsen

et al. 2023

IJMS

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Inadequate wound healing of ocular surface injuries can lead to permanent visual impairment. The relaxin ligand-receptor system has been demonstrated to promote corneal wound healing through increased cell migration and modulation of extracellular matrix formation. Recently, C1q/tumor necrosis factor-related protein (CTRP) 8 was identified as a novel interaction partner of relaxin receptor RXFP1. Additional data also suggest a role for CTRP1 and CTRP6 in RXFP1-mediated cAMP signaling. However, the role of CTRP1, CTRP6 and CTRP8 at the ocular surface remains unclear. In this study, we investigated the effects of CTRP1, CTRP6, and CTRP8 on epithelial ocular surface wound closure and their dependence on the RXFP1 receptor pathway. CTRP1, CTRP6, and CTRP8 expression was analyzed by RT-PCR and immunohistochemistry in human tissues and cell lines derived from the ocular surface and lacrimal apparatus. In vitro ocular surface wound modeling was performed using scratch assays. We analyzed the effects of recombinant CTRP1, CTRP6, and CTRP8 on cell proliferation and migration in human corneal and conjunctival epithelial cell lines. Dependence on RXFP1 signaling was established by inhibiting ligand binding to RXFP1 using a specific anti-RXFP1 antibody. We detected the expression of CTRP1, CTRP6, and CTRP8 in human tissue samples of the cornea, conjunctiva, meibomian gland, efferent tear ducts, and lacrimal gland, as well as in human corneal, conjunctival, and meibomian gland epithelial cell lines. Scratch assays revealed a dose-dependent increase in the closure rate of surface defects in human corneal epithelial cells after treatment with CTRP1, CTRP6, and CTRP8, but not in conjunctival epithelial cells. Inhibition of RXFP1 fully attenuated the effect of CTRP8 on the closure rate of surface defects in human corneal epithelial cells, whereas the CTRP1 and CTRP6 effects were not completely suppressed. Conclusions: Our findings demonstrate a novel role for CTRP1, CTRP6, and CTRP8 in corneal epithelial wound closure and suggest an involvement of the relaxin receptor RXFP1 signaling pathway. This could be a first step toward new approaches for pharmacological and therapeutic intervention.

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Section: Discussionmentioning

confidence: 99%

C1q/TNF-Related Proteins 1, 6 and 8 Are Involved in Corneal Epithelial Wound Closure by Targeting Relaxin Receptor RXFP1 In Vitro

Nicolaus

Klonisch

Paulsen

et al. 2023

IJMS

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show abstract

“…In addition, it has been shown that C1QTNF1 expression is increased in obese mice, and overexpression of C1QTNF1 can inhibit the transcription and protein expression of the tumor suppressor gene P53, leading to tumor progression ( Park et al, 2021 ). Knockdown of C1QTNF1 in A549 and HCT116 resulted in tumor cell proliferation, invasion, and growth ( Park et al, 2022 ).…”

Section: Discussionmentioning

confidence: 99%

High C1QTNF1 expression mediated by potential ncRNAs is associated with poor prognosis and tumor immunity in kidney renal clear cell carcinoma

Qiu

Wang

Zhao

et al. 2023

Front. Mol. Biosci.

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Background: Kidney renal clear cell carcinoma (KIRC) originates from proximal tubular cells and is the most common subtype of renal cell carcinoma. KIRC is characterized by changes in lipid metabolism, and obesity is a risk factor for it. C1q And TNF Related 1 (C1QTNF1), a novel adipokine and member of the C1q and TNF-related protein (CTRP) family, has been shown to affect the progression of various cancers. However, the role of C1QTNF1 in KIRC has not been studied.Methods: The Wilcoxon rank sum test was used to analyze the expression of C1QTNF1 in KIRC tissues and normal tissues. The relationship between clinicopathological features and C1QTNF1 levels was also examined by logistic regression and the Wilcoxon rank sum test. In addition, the effect of C1QTNF1 on the prognosis of KIRC patients was analyzed by Kaplan-Meier (KM). The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to analyze the potential signaling pathways and biological functions of differential genes. A nomogram was constructed to predict the prognosis of KIRC patients. Spearman correlation analysis was performed to determine the association between C1QTNF1 expression and immune cell infiltration and immune checkpoint genes. The upstream miRNAs and lncRNAs of C1QTNF1 were predicted by the ENCORI online tool. Finally, we examined the proliferation, invasion, and migration abilities of KIRC cells after C1QTNF1 knockdown.Results: The expression of C1QTNF1 in KIRC tissues was significantly higher than in normal renal tissues. Patients with higher C1QTNF1 expression had a poor prognosis, a finding supported by Kaplan-Meier survival analysis. C1QTNF1 expression was significantly correlated with TNM and pathologic stages, age, and gender (p < 0.05). The C1QTNF1 expression level was significantly correlated with immune cell infiltration and immune checkpoint genes in KIRC. Additionally, high C1QTNF1 expression was associated with poor prognosis in stage I and II, T1 and T2, T3 and T4, N0, and M0 patients (HR > 1, p < 0.05). The calibration diagram shows that the C1QTNF1 model has effective predictive performance for the survival of KIRC patients. Knockdown of C1QTNF1 inhibited KIRC cell proliferation, cell migration, and cell invasion. In addition, CYTOR and AC040970.1/hsa-miR-27b-3p axis were identified as the most likely upstream ncRNA-related pathways of C1QTNF1 in KIRC.Conclusion: In conclusion, our study suggests that high expression of C1QTNF1 is associated with KIRC progression and immune infiltration. The increased expression of C1QTNF1 suggests a poor prognosis in KIRC patients.

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“…Previous studies have highlighted the diverse functions of C1QTNF1 in immunity, metabolism and endocrine. It has been demonstrated that knockout of C1QTNF1 inhibits cell proliferation and invasion as well as tumor growth by generating C1QTNF1 knockout human lung cancer and human colon cancer cell lines ( Park et al, 2022 ). Meanwhile, C1QTNF1 has also been found to be widely involved in the regulation of a variety of inflammatory responses, such as the association of C1QTNF1 levels with coronary artery disease ( Shen et al, 2019 ); C1QTNF1 suppressed porcine circovirus type 2 ( PCV2 ) replication ( Cao et al, 2023 ).…”

Section: Introductionmentioning

confidence: 99%

Potential regulator of meat quality in geese: C1QTNF1 implications on cell proliferation and muscle growth

Ni,

Zhang,

et al. 2024

Poultry Science

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CTRP1 Knockout Attenuates Tumor Progression in A549 and HCT116 Cancer Cells

Cited by 7 publications

References 24 publications

C1q/TNF-Related Proteins 1, 6 and 8 Are Involved in Corneal Epithelial Wound Closure by Targeting Relaxin Receptor RXFP1 In Vitro

C1q/TNF-Related Proteins 1, 6 and 8 Are Involved in Corneal Epithelial Wound Closure by Targeting Relaxin Receptor RXFP1 In Vitro

High C1QTNF1 expression mediated by potential ncRNAs is associated with poor prognosis and tumor immunity in kidney renal clear cell carcinoma

Potential regulator of meat quality in geese: C1QTNF1 implications on cell proliferation and muscle growth

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