• Journal of the Society of Cosmetic Scientists of Korea
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• v.39 no.3
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• pp.177-186
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• 2013

Skin dermal fibroblast is the major collagen-producing cell type in human skin. As aging process continues in human skin, collagen production is reduced and fragmentation is increased, which is initiated by matrix metalloproteinase-1 (MMP-1). This imbalance of collagen homeostasis impairs the structure and function of dermal collagenous extracellular matrix (ECM), thereby promoting skin aging. Cysteine-rich protein 61 (CCN1), a member of the CCN family, negatively regulates collagen homeostasis in primary human skin dermal fibroblast cells. It is known in aging fibroblast cells that elevated CCN1 expression substantially reduces type I procollagen and concurrently increases MMP-1, which initiates fibrillar collagen degradation. And proliferation rate of aging fibroblast cells is reduced compared to the pre-aging fibroblast cells. In this study, we confirmed that the replicative senescence dermal fibroblast cells increased the expression levels of MMP-1 and decreased the production of type I procollagen. Our results also showed that the replicative senescence dermal fibroblast cells increased in the expression of CCN1 and decreased in the proliferation rate. Hydrolyzed Ulva pertusa extracts are the materials to improve photo-aging by reducing the expression of MMP-1 that was increased by ultraviolet and by promoting the synthesis of new collagen from fibroblast cells. In this study, we also investigated the hydrolyzed U. pertusa extract to see whether it inhibits CCN1 protein expression in the senescence fibroblasts. Results showed that the hydrolyzed U. pertusa extract inhibited the expression of MMP-1 and increased the production of type I procollagen in the aging skin fibroblast cells cultured. In addition, the proteins that regulate collagen homeostasis CCN1 expression were greatly reduced. The hydrolyzed U. pertusa extract increased the proliferation rate of the aging fibroblast cells. These results suggest that replicative senescent fibroblast cells may be used in the study of cosmetic ingredients as a model of the natural aging. In conclusion, the hydrolyzed U. pertusa extract can be used in anti-wrinkle functional cosmetic material to improve the natural aging skin care as well as photo-aging.

• Molecules and Cells
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• v.39 no.12
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• pp.909-914
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• 2016

Epithelial-mesenchymal transition (EMT) is a critical step in the acquisition of the migratory and invasive capabilities associated with metastatic competence. Cysteine-rich protein 61 (CCN1/Cyr61) has been implicated as an important mediator in the proliferation and metastasis of breast cancer. Hence, Cyr61 and associated pathways are attractive targets for therapeutic interventions directed against the EMT. In the present study, we report that baicalein significantly inhibits the expression of Cyr61 and migration and invasion of MDA-MB231 human breast cancer cells. Exposure to baicalein led to increased E-cadherin expression, possibly due to the ubiquitination of Snail and Slug, which was mediated by the Cyr61/Akt/glycogen synthase kinase $3{\beta}$ ($GSK3{\beta}$) pathway. Further analysis revealed that baicalein inhibited the expression of lysyl oxidase like-2 (LOXL-2), which is a functional collaborator of Snail and Slug, and subsequently attenuated the direct interaction between LOXL-2 and Snail or Slug, thereby enhancing $GSK3{\beta}$-dependent Snail and Slug degradation. Our findings provide new insights into the antimetastatic mechanism of baicalein and may contribute to its beneficial use in breast cancer therapies.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.7
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• pp.2659-2664
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• 2015

Background: To examine the expression of cysteine-rich 61 (Cyr61/CCN1) protein in laryngeal squamouscell carcinoma (LSCC) tissues, and its relationship with the tumor epithelial-mesenchymal transition (EMT), invasion, metastasis, and prognosis. Materials and Methods: Immunohistochemistry was used to detect the expressions of Cyr61, Vimentin (Vim), and E-cadherin (E-cad) in 88 cases of LSCC tissues and 30 cases of tumor-adjacent normal tissues. Vim and E-cad were used as mesenchymal and epithelial markers, respectively, to determine the relationship between Cyr61 expression and the EMT of LSCC cells. In addition, clinical and histopathological data were combined to analyze the relationship between the positive-expression rates of Cyr61, Vim and E-cad and LSCC invasion, metastasis and prognosis. Results: In LSCC tissues, Vim expression rate was significantly higher than that of the tumor-adjacent tissues, whereas E-cad expression rate was significantly lower than that of the tumor-adjacent tissues. The Vim expression rate was significantly higher in stages T3 and T4 than in stages T1 and T2 LSCC tissues, whereas E-cad expression rate was significantly lower in stages T3 and T4 than in stages T1 and T2 LSCC tissues. Compared to the group without lymph node metastasis, the Vim expression rate was significantly higher and the E-cad expression rate was significantly lower in the group with lymph node metastasis. The expression rate of Cyr61 was significantly higher in LSCC tissues than in the tumor-adjacent normal tissues. In addition, the Cyr61 expression rate was higher in stages T3 and T4 than in stages T1 and T2 LSCC, and higher in the group with lymph node metastasis than in the group without lymph node metastasis. The Vim expression rate was significantly higher in the Cyr61 positive group than in the Cyr61 negative group, whereas the E-cad expression rate was significantly higher in the Cyr61 negative group than in the Cyr61 positive group. Survival analysis indicated that survival rates of Cyr61 positive, Vim positive and E-cad negative groups were significantly lower than that of Cyr61 negative, Vim negative and E-cad positive groups, respectively. Conclusions: Cyr61 expression is closely associated with LSCC invasion and lymph node metastasis. Overexpression of Cyr61 may induce EMT and therefore leads to LSCC invasion and metastasis and poor prognosis. Cyr61 may become a new maker for clinical prediction of LSCC invasion and metastasis and a new target for LSCC treatment.