<scp>Interleukin</scp>‐8 induces <scp>DNA</scp> synthesis, migration and down‐regulation of cleaved caspase‐3 in cultured human gingival epithelial cells

Fujita, Tsuyoshi; Yoshimoto, Tetsuya; Matsuda, Shinji; Kajiya, Mikihito; Kittaka, Mizuho; Imai, Hidenori; Iwata, Takeo; Uchida, Yuushi; Shiba, Hideki; Kurihara, Hidemi

doi:10.1111/jre.12230

Cited by 14 publications

(17 citation statements)

References 48 publications

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“…Subconfluent cells were washed three times with phosphate‐buffered saline (pH 7.4), and 10 μM BrdU was added 3 h before the end of incubation. Immunodetection of the BrdU incorporated into cells was performed according to the manufacturer's instructions …”

Section: Methodsmentioning

confidence: 99%

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DNA primase polypeptide 1 (PRIM1) involves in estrogen‐induced breast cancer formation through activation of the G2/M cell cycle checkpoint

Lee

Chen

Chia‐Jung

et al. 2018

Intl Journal of Cancer

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The DNA primase polypeptide 1 (PRIM1) is responsible for synthesizing small RNA primers for Okazaki fragments generated during discontinuous DNA replication. PRIM1 mRNA expression levels in breast tumor samples were detected by real-time PCR analysis. Xenografted tumor model was established to study the carcinogenic role of PRIM1 and its potential therapeutic applications. The average PRIM1 mRNA (copy number × 10 /μg) expression was 4.7-fold higher in tumors than in normal tissue (*p = 0.005, n = 254). PRIM1 was detected preferentially at a higher level (>40-fold) in poorly differentiated tumor tissues (n = 46) compared with more highly differentiated tumors tissues (n = 10) (*p = 0.005). Poor overall survival rate was correlated to the estrogen receptor positive (ER+, n = 20) patients with higher PRIM1 expression when compare to the ER- (n = 10) patients (Chi Square test, p = 0.03). Stable expression of PRIM1-siRNA in the ER+ BT-474 cells-xenograft tumors significantly reduced tumor volume in SCID mice (*p = 0.005). The anti-tumoral effects of inotilone isolated from Phellinus linteus was tested and had significant effects on the inhibition of PRIM1 protein expression in ER+ breast cancer cells. In vivo study was performed by administering inotilone (10 mg/kg, twice a week for 6 weeks), which resulted in significantly reduced BT-474-xenografted tumor growth volume compared with control (n =5 per group, *p < 0.05). This study provides evidences for the prognostic effects of PRIM1 with poor overall survival rate in the ER+ patients and will be valuable to test for therapeutic purpose.

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Section: Methodsmentioning

confidence: 99%

“…Immunodetection of the BrdU incorporated into cells was performed according to the manufacturer's instructions. 19 RNA interference PRIM1 expression was ablated in BT-474 and MCF-7 breast cancer cells using at least two independent siRNA clones. Scrambled sequences of each siRNA were used as controls (Supporting Information Figs.…”

Section: Dna Synthesis Analysismentioning

confidence: 99%

DNA primase polypeptide 1 (PRIM1) involves in estrogen‐induced breast cancer formation through activation of the G2/M cell cycle checkpoint

Lee

Chen

Chia‐Jung

et al. 2018

Intl Journal of Cancer

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“…P. gingivalis has the ability to invade and propagate intracellularly ( 122 ), including in gingival epithelial cells ( 123 ). It can also delay apoptosis in gingival epithelial cells through various different mechanisms, such as by activating the JAK1/STAT3/Akt pathway, downregulating caspase-3 and caspase 9 expression, upregulating microRNAs (specifically miR-203), leading to suppression of SOCS3, preventing ATP-dependent apoptosis ( 124 – 128 ). Programed cell death is one mechanism through which cells avoid replicating if DNA damage is excessive and cannot be repaired.…”

Section: The Contribution Of the Oral Microbiomementioning

confidence: 99%

Chemokine Function in Periodontal Disease and Oral Cavity Cancer

2015

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The chemotactic cytokines, or chemokines, comprise a superfamily of polypeptides with a wide range of activities that include recruitment of immune cells to sites of infection and inflammation, as well as stimulation of cell proliferation. As such, they function as antimicrobial molecules and play a central role in host defenses against pathogen challenge. However, their ability to recruit leukocytes and potentiate or prolong the inflammatory response may have profound implications for the progression of oral diseases such as chronic periodontitis, where tissue destruction may be widespread. Moreover, it is increasingly recognized that chronic inflammation is a key component of tumor progression. Interaction between cancer cells and their microenvironment is mediated in large part by secreted factors such as chemokines, and serves to enhance the malignant phenotype in oral and other cancers. In this article, we will outline the biological and biochemical mechanisms of chemokine action in host–microbiome interactions in periodontal disease and in oral cancer, and how these may overlap and contribute to pathogenesis.

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“…However, given that the GCF originates from a complex repertoire of cells within the periodontal tissues, such as gingival epithelial cells, fibroblasts, and other immune cells (Khalaf, Lonn, & Bengtsson, ), it is not possible to pinpoint the origin of the apoptotic signals or to assign them to a specific cell type. In addition, periodontopathogens can induce apoptosis by affecting caspase‐3 in gingival epithelial cells (Fujita et al, ) and fibroblasts (Alamri et al, ), by influencing p53 in human osteoblasts (Zhang et al, ) and fibroblasts (Alikhani et al, ), and by regulating TRAIL in gingival cells (Lucas et al, ) and osteoblasts (Mori et al, ). Thus, the source of the apoptotic cells releasing caspase‐3, p53, and TRAIL into the GCF cannot be fully delineated because of the rich cellular content of the periodontal tissues and sulcus.…”

Section: Discussionmentioning

confidence: 99%

Six‐month clinical outcomes of non‐surgical periodontal treatment with antibiotics on apoptosis markers in aggressive periodontitis

Aral

Kapila³

2019

Oral Diseases

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Objective Extrinsic and intrinsic pathways of apoptosis are involved in generalized aggressive periodontitis (GAgP). The aim of this study was to evaluate 6‐month clinical outcomes relative to apoptosis of one‐stage full‐mouth disinfection (OSFMD) and systemic antibiotics (SA) in the treatment of GAgP. Methods Twenty‐six patients with GAgP were included in this prospective follow‐up intervention study. Gingival crevicular fluid (GCF) was collected from patients at baseline and 3 and 6 months after periodontal therapy, which consisted of OSFMD and SA (amoxicillin and metronidazole, 500 mg each for 7 days). The levels of p53, caspase‐3, TNF‐α, TRAIL, IL‐1β, and IL‐10 in GCF were measured via ELISA. Results Periodontal parameters were improved at 3 and 6 months compared to baseline (p < 0.05). p53 was decreased up to 6 months (p < 0.05). TRAIL, TNF‐α, and IL‐10 were similar at baseline and 3 and 6 months. Caspase‐3 and IL‐1β were decreased at 3 months (p < 0.05), but similar at 6 months compared to baseline (p > 0.05). Conclusion Although OSFMD plus SA improves clinical periodontal parameters up to 6 months, this treatment protocol differentially regulates the apoptosis markers caspase‐3 at 3 months and p53 at 6 months without influencing TRAIL in GCF.

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Interleukin‐8 induces DNA synthesis, migration and down‐regulation of cleaved caspase‐3 in cultured human gingival epithelial cells

Abstract: IL-8 may facilitate the migration of gingival junctional epithelium by enhancing DNA synthesis, migration and preventing apoptosis of gingival epithelial cells.

Cited by 14 publications

References 48 publications

DNA primase polypeptide 1 (PRIM1) involves in estrogen‐induced breast cancer formation through activation of the G2/M cell cycle checkpoint

DNA primase polypeptide 1 (PRIM1) involves in estrogen‐induced breast cancer formation through activation of the G2/M cell cycle checkpoint

Chemokine Function in Periodontal Disease and Oral Cavity Cancer

Six‐month clinical outcomes of non‐surgical periodontal treatment with antibiotics on apoptosis markers in aggressive periodontitis

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