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1.
International Journal of Oral Science ; (4): 17-17, 2023.
Artigo em Inglês | WPRIM | ID: wpr-982475

RESUMO

Oral squamous cell carcinoma (OSCC) escape from the immune system is mediated through several immunosuppressive phenotypes that are critical to the initiation and progression of tumors. As a hallmark of cancer, DNA damage repair is closely related to changes in the immunophenotypes of tumor cells. Although flap endonuclease-1 (FEN1), a pivotal DNA-related enzyme is involved in DNA base excision repair to maintain the stability of the cell genome, the correlation between FEN1 and tumor immunity has been unexplored. In the current study, by analyzing the clinicopathological characteristics of FEN1, we demonstrated that FEN1 overexpressed and that an inhibitory immune microenvironment was established in OSCC. In addition, we found that downregulating FEN1 inhibited the growth of OSCC tumors. In vitro studies provided evidence that FEN1 knockdown inhibited the biological behaviors of OSCC and caused DNA damage. Performing multiplex immunohistochemistry (mIHC), we directly observed that the acquisition of critical immunosuppressive phenotypes was correlated with the expression of FEN1. More importantly, FEN1 directly or indirectly regulated two typical immunosuppressive phenotype-related proteins human leukocyte antigen (HLA-DR) and programmed death receptor ligand 1 (PD-L1), through the interferon-gamma (IFN-γ)/janus kinase (JAK)/signal transducer and activator transcription 1 (STAT1) pathway. Our study highlights a new perspective on FEN1 action for the first time, providing theoretical evidence that it may be a potential immunotherapy target for OSCC.


Assuntos
Humanos , Carcinoma de Células Escamosas/patologia , DNA , Regulação para Baixo , Endonucleases Flap/metabolismo , Neoplasias de Cabeça e Pescoço , Interferon gama/metabolismo , Neoplasias Bucais/patologia , Fenótipo , Carcinoma de Células Escamosas de Cabeça e Pescoço , Microambiente Tumoral , Janus Quinases/metabolismo
2.
Chinese Journal of Plastic Surgery ; (6): 513-518, 2019.
Artigo em Chinês | WPRIM | ID: wpr-805190

RESUMO

Adipose-derived stem cells (ADSCs) are adult mesenchymal stem cells, which are derived from adipose tissue. ADSCs have broad applications, due to the potential of multiple differentiation, easy sampling, wide sources and high proliferation capacity in vitro. Many researches demonstrated that ADSCs have significant effects on anti-aging. Its mechanism and therapeutic effects also become a hot topic in recent years. This review summarized the biological characteristics of ADSCs, the mechanism of skin aging, the anti-aging mechanism of ADSCs, so as to provide reference for the use of ADSCs for skin anti-aging in the future.

3.
Chinese Journal of Postgraduates of Medicine ; (36): 1002-1006, 2018.
Artigo em Chinês | WPRIM | ID: wpr-700336

RESUMO

Objective To evaluate the effectiveness and safety of pulsed radiofrequency (PRF) for postherpetic neuralgia (PHN). Methods The database was searched systematically and comprehensively, including PubMed, Cochrane library, Medalink, Embase, CNKI, Wanfang data and VIP data, from database creation to February 15, 2018. Manual retrieval was supplemented. The Cochrane Handbook 5.1 was used to evaluate the studies, and Meta-analysis was performed using RevMan 5.3. Results Seven literature were selected, including 486 patients. The Meta-analysis result showed that pain relief at 48 h, 1 week, 1 month, 3 months and 6 months after PRF was significantly better than that after traditional therapy in patients with PHN ( MD or SMD =-1.21,-1.38,-1.46,- 0.99 and- 0.95;95% CI-1.54 to-0.88,-1.58 to-1.17,-1.67 to-1.26,-1.31 to-0.67 and-1.13 to-0.77, P<0.01). The incidence of short-term complications and adverse reactions was 4.9% (12/243), and the patients were able to relieve himself after 15 d. Conclusions PRF is more effective than traditional treatment for PHN, and the treatment effect and safety is more obvious within 6 months.

4.
Chinese Journal of Pathophysiology ; (12): 289-296, 2017.
Artigo em Chinês | WPRIM | ID: wpr-506343

RESUMO

AIM:To investigate the effects of T-cell factor 3 (TCF3) expression on the growth and migratory abilities of the non-small cell lung cancer cells ( NSCLC) and the underlying mechanisms .METHODS: The non-small cell lung cancer cells A549 and H1299 were transfected with siTCF3 or negative control siRNA ( NCsiRNA) using Lipo-fectamine 2000.The expression of TCF3 at mRNA and protein levels was detected by real-time PCR and Western blot , re-spectively.The activity of TCF3 transcription was measured using luciferase reporter gene assay .The cell viability, colony formation ability, migratory ability and apoptotic rate were monitored by MTT assay , colony formation assay, Transwell method and flow cytometry with Annexin V-FITC/PI double staining , respectively .The protein expression levels of Wnt , c-Myc, matrix metalloproteinase (MMP)-9, MMP-13 and tissue inhibitor of metalloproteinase-1 (TIMP-1) were detected by Western blot.RESULTS:Compared with A549-NCsiRNA and H1299-NCsiRNA cells, the mRNA and protein levels of TCF3 were significantly inhibited in A549-siTCF3 and H1299-siTCF3 cells (P<0.01).The activity of TCF3 transcription and levels of c-Myc protein expression remarkably decreased as compared with NCsiRNA cells (P<0.05).The viability of A549-siTCF3 cells and H1299-siTCF3 cells cultured for 24 h, 48 h, 72 h and 96 h were notably lower than that of NCsi-RNA cells (P<0.05).The colony formation ability was significantly inhibited by siTCF 3 compared with NCsiRNA cells (P<0.01).The numbers of migratory A549-siTCF3 and H1299-siTCF3 cells were significantly lower than those of A549-NCsiRNA and H1299-NCsiRNA cells (P<0.05).The apoptotic rates of A549-siTCF3 cells and H1299-siTCF3 cells were notably higher than those of A549-NCsiRNA cells and H1299-NCsiRNA cells (P<0.01).Down-regulated TCF3 expres-sion inhibited the protein expression of Wnt , decreased the protein levels of MMP-9 and MMP-13 and enhanced the protein level of TCF3.CONCLUSION:siTCF3 suppresses the abilities of growth and migration , and induces apoptosis in A 549 cells and H1299 cells by down-regulating Wnt pathway and regulating expression of key MMP family genes .

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