Effect of secretory leukocyte protease inhibitor on migration and invasion of human KB oral carcinoma cells

Wang, Guanlin; Lim, Do-Seon; Choi, Byeong-Dae; Park, Jin Ju; Jeong, Soon-Jeong; Jae-Duk, Kim; Park, Jungsu; Kim, Eung-Kwon; Kim, Byung–Hoon; Ham, JooHyun; Jeong, Moon‐Jin

doi:10.1080/19768354.2011.577573

Cited by 9 publications

(11 citation statements)

References 36 publications

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“…In addition, SLPI inhibits infections, accelerates epithelial cell proliferation and has anti-inflammatory action that contributes to the early inflammatory response in odontoblasts (Choi et al, 2009). The expression of SLPI is increased in human cancers including oral, breast, lung, entometrium and ovaries (Tsukishiro et al, 2005;Wang et al, 2011). In addition, SLPI inhibits the protease activity, such as neutrophil elastase, cathepsin G, trypsin, chymotrypsin, and chymase (Williams et al, 2006).…”

Section: Introductionmentioning

confidence: 96%

Induction of secretory leukocyte protease inhibitor (SLPI) in estradiol valerate (EV) induced polycystic ovary

et al. 2011

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The excessive administration of estradiol valerate induces polycystic ovary syndrome by formation of follicular cysts. Secretory leukocyte protease inhibitor (SLPI) promotes wound healing by decreasing the excessive inflammatory response, stimulating keratinocyte proliferation and increasing collagen deposition through the inhibition of protease activity. In this study, SLPI expression was high in the ovarian stroma, corpus luteum, unilaminar primary follicle, multilaminar primary follicle and granulose layer of the antral follicle in polycystic ovary (PCO) compared to the normal ovary. SLPI was expressed strongly in the theca around the cyst in PCO compared to the mature follicle in the normal ovary. The levels of SLPI mRNA and protein expression were higher in PCO than in the normal ovary, and the level of MMP-2 expression was lower in PCO. These results showed that the formation of a cyst was initiated from a multilaminar primary follicle and SLPI expression was increased depending on the morphological changes in the follicle and ovarian stroma. Therefore, an increase in SLPI may be related to the suppression of tissue disruption, and act as a protease inhibitor in PCO, suggesting that SLPI increases independently of the estrogen concentration in pathological tissues.

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Section: Introductionmentioning

confidence: 96%

Induction of secretory leukocyte protease inhibitor (SLPI) in estradiol valerate (EV) induced polycystic ovary

et al. 2011

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Section: Introductionmentioning

confidence: 99%

“…In addition, SLPI was reported to play a role not only in protecting the tissues from the protease (4) but also in promoting wound healing, cell proliferation, inhibiting HIV infections, anti-bacterial and anti-fungal activity (5,6). The overexpression of SLPI was reported to promote metastasis in lung carcinoma 3LL-S cells and oral carcinoma KB cells (7,8).Matrix metalloproteinases (MMPs) play important roles in normal physiological processes, such as embryogenesis, tissue remodeling and wound healing. The overexpression of MMPs is associated with many pathological abnormalities, such as atherosclerosis, tumor invasion and arthritic diseases (9).…”

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confidence: 99%

Secretory leukocyte protease inhibitor is associated with MMP-2 and MMP-9 to promote migration and invasion in SNU638 gastric cancer cells

Choi

Jeong²,

Wang³

et al. 2011

Int J Mol Med

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Abstract. Secretory leukocyte protease inhibitor (SLPI) protects tissue from proteases, and promotes cell proliferation and healing during inflammatory response. SLPI is also overexpressed in gastric, lung and ovarian cancers, which accelerates the metastasis of cancer cells. Matrix metalloproteinases-2, -9 (MMP-2 and MMP-9) are overexpressed in high metastatic cancers, and promote the migration of cancer cells through collagen degradation. SLPI and MMP-2, -9 are critical factors in stimulating the metastatic processes but there are no reports of a direct correlation between these molecules. Therefore, this study examined the role of SLPI related to MMP-2 and MMP-9 using two gastric cancer cell lines, such as characterized non-metastatic SNU484 and highly metastatic SNU638 cells. SLPI, MMP-2 and MMP-9 mRNA and protein expression were higher in SNU638 cells than in SNU484 cells. In addition, the rate of cell migration and invasion was higher in the SNU638 cells than in SNU484 cells. Interestingly, after treatment with SLPI, the rate of migration and invasion was higher in the SNU484 cells than in the positive control (PC) SNU484 cells. The rate of migration was also higher in the SNU638 cells after SLPI treatment than in the SNU638 cells (PC) but the invasion rate was not changed. The expression and secretion of MMP-2 and MMP-9 as well the rate of cell migration and invasion were significantly lower in SLPIsiRNA transfected SNU638 cells (si-SLPI/SNU638) but higher in SLPI-treated SNU484 cells (SNU484 + SLPI). Strong Elk-1 phosphorylation was detected in SNU484 + SLPI and SNU638 cells but was barely detectable in SNU484 and si-SLPI/SNU638 cells. These results show that SLPI promotes the metastasis of SNU638 gastric cancer cells by increasing MMP-2 and MMP-9 expression through Elk-1 signaling, indicating its role as a signaling molecule not a protease inhibitor. IntroductionThe metastatic cascade of cancer cells is viewed as a series of sequential and interrelated steps, which include the following: epithelial-mesenchymal transition (EMT), degradation of the basement membrane; dissociation of tumor cells from the primary site; invasion of the neighboring tissue; intravasation into the blood and lymph vessels; transport through the vessels; extravasation from the vessels; and proliferation at a distant site. Among these processes, tumor cells invading the neighboring tissue after degrading the basement membrane is a major development (1).Secretory leukocyte protease inhibitor (SLPI) is an 11.7-kDa cystein-rich protein and an epithelial cell product found in saliva, seminal plasma and in the cervical, nasal, and bronchial mucus. SLPI inhibits the serine protease activity, such as chymotrypsin, trypsin, pancreatic elastase, cathepsin G, mast cell chymase (2). Recently, SLPI was reported to be an anti-inflammatory factor that contributes at the early inflammatory response in odontoblasts (3). In addition, SLPI was reported to play a role not only in protecting the tissues from the protease (4) but also in promoting wou...

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“…Estrogen receptor β (ERβ) is strongly expressed in the human stratum basal and spinosum of the scalp epithelium (29) and the increase in ERα expression is induced by estrogen in keratinocytes (30). SLPI regulates the proliferation of human endometrial epithelial cells and is expressed strongly to promote the proliferation of carcinoma cells (16,17,31). In addition, re-epithelization was delayed in the SLPI knockout mice skin wound healing model (19).…”

Section: Discussionmentioning

confidence: 99%

“…SLPI has been described as an anti-inflammatory factor during the early inflammatory response in odontoblasts (14) and plays a role not only to protect the tissues from proteases (4) but also to promote wound healing, cell proliferation and migration, and inhibition of HIV infections. It has also been described as having anti-bacterial and anti-fungal activity (15)(16)(17).…”

Section: Delayed Healing and Induction Of Secretory Leukocyte Proteasmentioning

confidence: 99%

Delayed healing and induction of secretory leukocyte protease inhibitor in polycystic ovary syndrome rat skin wounds

Jeong

Kim²,

Bae³

et al. 2011

Int J Mol Med

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Abstract. Secretory leukocyte protease inhibitor (SLPI) and estrogen promote wound healing through a decrease in the excessive inflammatory response, accelerating re-epithelialization and increasing the amount of collagen deposition. The excessive administration of estradiol valerate (EV) using hormonal therapy decreases the concentration of estrogen abruptly and induces the polycystic ovary syndrome (PCOS). In this study, the PCOS rat skin wound area was wider than that of the normal groups and the rate of keratinocyte migration in PCOS was lower than the normal group. The numbers of inflammatory cells and macrophages recruited in the PCOS group were larger than that of the normal group. More collagen was deposited in the healing area of the normal group than in the PCOS group. The level of SLPI expression was higher in the PCOS group than the normal group after wounding, with the exception of the epithelium. On the other hand, mRNA and protein expression levels of transforming growth factor-β1 (TGF-β1) were lower in the PCOS group than in the normal group. Matrix metalloproteinase-2 (MMP-2) and MMP-9 levels in the PCOS group were significantly lower than that of the normal group. Therefore, increased SLPI in PCOS skin wounds may help prevent an excessive inflammatory response and aberrant collagen deposition but not are sufficient to accelerate PCOS skin wound healing, suggesting that SLPI may act as a local rather than a systemic modulating molecule in PCOS rat skin wounds.

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Effect of secretory leukocyte protease inhibitor on migration and invasion of human KB oral carcinoma cells

Cited by 9 publications

References 36 publications

Induction of secretory leukocyte protease inhibitor (SLPI) in estradiol valerate (EV) induced polycystic ovary

Induction of secretory leukocyte protease inhibitor (SLPI) in estradiol valerate (EV) induced polycystic ovary

Secretory leukocyte protease inhibitor is associated with MMP-2 and MMP-9 to promote migration and invasion in SNU638 gastric cancer cells

Delayed healing and induction of secretory leukocyte protease inhibitor in polycystic ovary syndrome rat skin wounds

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