An adiponectin paralog protein, CTRP6 decreased the proliferation and invasion activity of oral squamous cell carcinoma cells: possible interaction with laminin receptor pathway

Hano, Kimika; Hatano, Kiichi; Saigo, Chiemi; Kito, Yusuke; Shibata, Toshiyuki; Takeuchi, Tamotsu

doi:10.1007/s11033-019-04947-9

Cited by 9 publications

(16 citation statements)

References 35 publications

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“…Some of the other upregulated genes have been found to be similarly associated with features of other cancers. For example, overexpression of C1QTNF6 was found in gastric carcinoma 23 (although it has been reported that the C1QTNF6 protein significantly suppresses the proliferation of oral squamous cell carcinoma cells) 24 ; PARP12 upregulation was associated with the inhibition of metastasis in hepatocellular carcinoma cell lines 25 .…”

Section: Discussionmentioning

confidence: 99%

Genes and pathways monotonically dysregulated during progression from normal through leukoplakia to gingivo-buccal oral cancer

et al. 2021

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Oral squamous cell carcinoma of the gingivo-buccal region (OSCC-GB) accounts for the highest cancer morbidity and mortality among men in India. It has been observed that about one-third of individuals with oral leukoplakia, a dysplastic precancerous lesion in the oral cavity, progress to oral cancer. We aimed to identify systematic transcriptomic changes as a normal tissue in the oral cavity progresses to frank OSCC-GB. Seventy-two OSCC-GB patients, from multiple hospitals, were recruited, and transcriptome analysis of tumor and adjacent normal tissue (of all patients) and adjacent leukoplakia tissue (of a subset of 25 unselected patients with concomitant leukoplakia) was performed. We have identified many differences in the transcriptomic profiles between OSCC-GB and squamous cell carcinoma of the head and neck regions. Compared to the normal/precancerous tissue, significant enrichment of ECM−receptor interaction, PI3K-Akt signaling, cytokine−cytokine receptor interaction, focal adhesion, and cell cycle pathways were observed in OSCC-GB. Using gene set enrichment analysis, we identified a profound role of interferon receptor signaling in tumor growth by activating immune evasion mechanisms. The role of tumor-infiltrating immune cells further supported the growth and immunosuppressive mechanism of tumor tissues. Some immune evasion genes—CD274, CD80, and IDO1—were found to be activated even in the precancerous tissue. Taken together, our findings provide a clear insight into the sequential genetic dysregulation associated with progression to oral cancer. This insight provides a window to the development of predictive biomarkers and therapeutic targets for gingivo-buccal oral cancer.

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Section: Discussionmentioning

confidence: 99%

Genes and pathways monotonically dysregulated during progression from normal through leukoplakia to gingivo-buccal oral cancer

et al. 2021

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“…It plays different roles in different physiological or pathological processes, and has been proven to be involved in inflammation, diabetes, and cardiovascular disease [ 11 ]. In addition, a previous study revealed that CTRP6 could inhibit the proliferation, invasion and migration of squamous cell carcinoma cells [ 12 ]. And another study deemed that CTRP6 could inhibit the proliferation of vascular smooth muscle cells induced by platelet-derived growth factor-bb [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

C1q/tumor necrosis factor related protein 6 (CTRP6) regulates the phenotypes of high glucose-induced gestational trophoblast cells via peroxisome proliferator-activated receptor gamma (PPARγ) signaling

Zhang

Bai

2021

Bioengineered

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Multiple studies have confirmed that adipokines are compactly relevant to insulin resistance and participate in the pathogenesis of gestational diabetes mellitus (GDM). This paper aimed to study the effects of C1q/tumor necrosis factor related protein (CTRP)6 on the phenotypes of trophoblast cells, covering cell proliferation, invasion and migration, and initially explore the mechanism. High glucose was used to induce trophoblast cells to establish an in vitro model. The expression levels of CTRP6 were firstly determined, and then the effects of CTRP6 knockdown on cell viability, apoptosis, migration and invasion were assessed using CCK8, TUNEL, wound healing, Transwell assays. Moreover, the role of peroxisome proliferator-activated receptor gamma (PPARγ), probable target of CTRP6, was evaluated through co-transfection with PPARγ overexpression vector. The results of the present study revealed that CTRP6 and PPARγ were both upregulated in high glucose-induced cells. And CTRP6 knockdown could significantly elevate the abilities of cell viability, migration and invasion, and avoid cell apoptosis. In addition, PPARγ overexpression was found to restrain the protective effects of CTRP6 knockdown on the above aspects, indicating CTRP6 played a role in trophoblast cells via inhibiting PPARγ expression. In conclusion, CTRP6 regulated the viability, migration and invasion of high glucose-induced gestational trophoblast cells through PPARγ signaling.

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“…It is expressed mainly in placenta, and also in heart, adipose tissue, and uterus . Studies have shown that it is involved in cell proliferation and differentiation, apoptosis, lipolysis and adipogenesis, insulin sensitivity, fibrogenesis, inflammation, embryogenesis, and tumorigenesis . Recently, it was identified in ovarian cells, indicating a possible role in modulating reproductive system function .…”

Section: Introductionmentioning

confidence: 99%

“…17 Studies have shown that it is involved in cell proliferation and differentiation, apoptosis, 26 lipolysis and adipogenesis, [27][28][29][30][31] insulin sensitivity, 32 fibrogenesis, 33,34 inflammation, 35 embryogenesis, and tumorigenesis. [36][37][38] Recently, it was identified in ovarian cells, indicating a possible role in modulating reproductive system function. 39 It has been associated with a number of disorders including, type 1 diabetes mellitus, rheumatoid arthritis, 40 and Graves' disease.…”

Section: Introductionmentioning

confidence: 99%

Circulating levels of C1q/TNF‐α‐related protein 6 (CTRP6) in polycystic ovary syndrome

et al. 2020

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Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders affecting females of reproductive age. It has been associated with cardiometabolic disorders including diabetes mellitus and cardiovascular disorders, and increases the risk of developing fecundity pathologies including recurrent pregnancy loss (RPL) and infertility. C1q/tumor necrosis factor‐α‐related protein‐6 (CTRP6) is a novel adipokine involved in glucose and lipid metabolism, host inflammation, and organogenesis. In the present study, we aimed to determine the association of serum CTRP6 levels with some components of metabolic syndrome in PCOS patients (infertile PCOS [inf‐PCOS] and PCOS‐RPL). This case–control study included 120 PCOS patients (60 inf‐PCOS and 60 PCOS‐RPL) and 60 healthy controls. Serum high‐sensitivity C‐reactive protein (hs‐CRP) and homocysteine were measured using commercial kits, while adiponectin and CTRP6 levels were assessed using ELISA technique. Inf‐PCOS and PCOS‐RPL individuals had higher levels of serum CTRP6 than controls (546.15 ± 125.02 ng/ml and 534.04 ± 144.19 ng/ml vs. 440.16 ± 159.24 ng/ml; both p < .001). Moreover, serum adiponectin levels were significantly reduced, while fasting insulin, homeostasis model assessment of insulin resistance, free testosterone, and hs‐CRP levels were significantly elevated in PCOS group, when compared with controls. Furthermore, serum CTRP6 positively associated with body mass index in all subjects. It showed an inverse correlation with adiponectin in PCOS group and subgroups. However, it had a direct association with hs‐CRP in PCOS group and inf‐PCOS subgroup, but not PCOS‐RPL subgroup. These findings unravel a probable role of CTRP6 in PCOS pathogenesis, which poses a possibility to be a good diagnostic target. However, further investigation is needed.

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An adiponectin paralog protein, CTRP6 decreased the proliferation and invasion activity of oral squamous cell carcinoma cells: possible interaction with laminin receptor pathway

Cited by 9 publications

References 35 publications

Genes and pathways monotonically dysregulated during progression from normal through leukoplakia to gingivo-buccal oral cancer

Genes and pathways monotonically dysregulated during progression from normal through leukoplakia to gingivo-buccal oral cancer

C1q/tumor necrosis factor related protein 6 (CTRP6) regulates the phenotypes of high glucose-induced gestational trophoblast cells via peroxisome proliferator-activated receptor gamma (PPARγ) signaling

Circulating levels of C1q/TNF‐α‐related protein 6 (CTRP6) in polycystic ovary syndrome

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