The effect of bone remodeling with photobiomodulation in dentistry: a review study

Le, Jie-Ren Mi; Wu, Jih-Huah; Jaw, Fu-Shan; Su, Chuan-Tsung

doi:10.1007/s10103-023-03933-9

Cited by 5 publications

(1 citation statement)

References 63 publications

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“…Secreted phosphoprotein 1 (SPP1; known as osteopontin) is a kind of secreted acidic protein ( 6 ), which is commonly expressed in osteocytes, macrophages, and endothelial cells, etc. ( 7 - 10 ) and regulates various biological functions, including bone remodeling, chemotaxis, cell activation, and apoptosis ( 6 , 11 - 15 ). Under pathological conditions, SPP1 is highly expressed in several types of cancers such as colorectal cancer, gastric cancer, liver cancer, pancreatic cancer and breast cancer, to name a few ( 16 , 17 ).…”

Section: Introductionmentioning

confidence: 99%

SPP1 promotes tumor progression in esophageal carcinoma by activating focal adhesion pathway

Sun,

Tang,

Cai

2024

J Gastrointest Oncol

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Background Recurrence and metastasis are the major obstacles affecting the therapeutic efficacy and clinical outcomes for patients with esophageal carcinoma (ESCA). Secreted phosphoprotein 1 (SPP1) is considered as a hub gene in ESCA and is negatively associated with disease-free survival (DFS) in ESCA. However, the exact roles and underlying mechanisms remain elusive. This study aims to examine the roles of SPP1 on ESCA, and elucidate the potential mechanisms. Methods Bioinformatics were used to analyze the expression of SPP1 in ESCA tissues, and its relations with clinicopathological characteristics and clinical prognosis in patients with ESCA based on The Cancer Genome Atlas (TCGA) dataset. Loss-of-function was conducted to examine the roles of SPP1 on malignant behaviors of ESCA cells by cell counting kit-8 (CCK8), plate clone, wound healing, and transwell assays. Gene set enrichment analysis (GSEA) was conducted to screen the pathways associated with SPP1 in ESCA. Then, the enriched pathway and the underlying mechanism were elucidated by western blotting, cell adhesion, and cell spreading assays. Lastly, Y15 [a specific inhibitor of focal adhesion kinase (FAK)] was used to examine its potential to inhibit tumor growth in ESCA cells. Results SPP1 was upregulated in ESCA tissues compared to the adjacent nontumorous tissues, which was closely associated with clinical stage, lymph node metastasis, histological subtype, and p53 mutation. A high expression of SPP1 indicated a poor clinical prognosis in patients with ESCA. The knockdown of SPP1 inhibited cell proliferative, migratory, and invasive capacities in ESCA cells. GSEA indicated that the focal adhesion pathway was closely related with SPP1 in ESCA. Further studies confirmed that the knockdown of SPP1 suppressed cell adhesion ability and reduced the expression of p-FAK and p-Erk in ESCA cells. In addition, Y15 inhibited FAK autophosphorylation and dramatically inhibited cell proliferation, migration, and invasion in ESCA cells. Conclusions SPP1 promotes tumor progression in ESCA by activating FAK/Erk pathway, and FAK is a potential therapeutic target to overcome tumor recurrence and metastasis of ESCA.

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