Clinical Characteristics of Coronary Interventions in Old Aged Patients

Park, Jong Chul; Jeong, Myung Ho; Kim, Ju Han; Kim, Sung Hee; Kim, Jun Yoo; Bae, Youl; Ahn, Young Keun; Soo, Kwang; Seo, Jeong Pyeong; Kim, In Soo; Choi, Myung Ja; Park, Joo Hyung; Cho, Jeong Gwan; Park, Jong Chun; Kang, Jung Chaee; Park, Ock Kyu

doi:10.4070/kcj.1998.28.2.256

Cited by 7 publications

(3 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Hence, downstream genes (excluding WT1) that could be regulated by WT1-AS were investigated by RNA-sEq. Combined with the KEGG enrichment data and cluster analyzes, 10 genes (PSPH [34,35], PHGDH [36,37], GSTO2 [38], CACNA2D1 [39,40], FYN [41], MAOB [42,43], ANPEP [44,45], ITGA2 [46,47], CTSS [48] and PRKCA [49] were selected for further explorations in view of their close association with cancer progression and prognosis. Our RT-qPCR assay validated that PSPH, GSTO2, FYN, and PHGDH could be regulated by WT1-AS, but not WT1 in GSCs.…”

Section: Discussionmentioning

confidence: 99%

Investigations into the effects and related upstream/downstream regulatory mechanisms of long non-coding RNA WT1-AS in the maintenance and development of gastric cancer stem cells in vitro and in vivo

Zhang¹,

Jin²,

Liu³

et al. 2021

Preprint

View full text Add to dashboard Cite

Background Cancer stem cells (CSCs) are proposed to be responsible for almost all malignant phenotypes (e.g. heterogeneity, uncontrolled growth, metastasis, recurrence, chemoresistance) of tumors. Long non-coding RNA WT1 antisense RNA (WT1-AS) has been found to be involved in the regulation of lung cancer cell stemness. However, the roles and molecular mechanisms of WT1-AS in the maintenance and development of gastric cancer stem cells (GSCs) have not been investigated. Methods mRNA and protein expression was measured by RT-qPCR and western blot. CCK8 and Soft agar colony formation assays were performed to assess cell viability and colony clone formation ability. Cell cycle and apoptosis were determined by flow cytometry analysis. Cell transwell and wound healing analyses were carried out to assess cell migration ability. In vitro angiogenesis and 3D spheroid cultures assays were also performed. Moreover, in vitro experiments were carried out to explore the function of WT1-AS on tumor growth, metastasis and cell stemness. The upstream transcription factors or downstream genes of WT1-AS were screened through Bioinformatics, dual-luciferase assays and RNA-sequencing (RNA-seq) technology. Results Our present study demonstrated that WT1-AS knockdown or wilms tumor 1 (WT1) overexpression improved GSC proliferative and migratory capacities, promoted GSC EMT, enhanced GSC stemness, inhibited GSC apoptosis, potentiated the resistance of GSCs to 5-FU and induced HUVEC angiogenesis in vitro. WT1-AS loss or WT1 increase facilitated the formation of in-vitro 3D GSC aggregates. WT1-AS ameliorated the malignant phenotypes of GSCs by down-regulating WT in vitro. Additionally, WT1-AS inhibited tumor growth and metastasis, and reduced tumor stemness in GSCs-derived xenografts (s.c., i.p., and i.v.) in vivo. Furthermore, XBP1 was identified as an upstream regulator of WT1-AS in GSCs. RNA-seq and RT-qPCR data suggested that PSPH, GSTO2, FYN, and PHGDH might be the downstream targets of WT1-AS in GSCs. Conclusions Our data demonstrated that WT1-AS weakened the stem-cell like behaviors and characteristics of GSCs in vitro and in vivo by down-regulating WT1. Also, some upstream regulators and downstream targets of WT1-AS were identified in GSCs. Investigations on the molecular mechanisms underlying the complex phenotypes of GSCs might contribute to the better management of headaches in cancers.

show abstract

Section: Discussionmentioning

confidence: 99%

Investigations into the effects and related upstream/downstream regulatory mechanisms of long non-coding RNA WT1-AS in the maintenance and development of gastric cancer stem cells in vitro and in vivo

Zhang¹,

Jin²,

Liu³

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…It is the most important treatment for preventing a fatal complication, stent thrombosis 9)10). Since the number of patients with ischemic heart disease is increasing, and many of them are elderly and have arthritis, there are more and more candidates for treatment with both celecoxib and antiplatelet agents 11). However, the safety profile of celecoxib with concomitant administration of aspirin and clopidogrel has not been evaluated.…”

Section: Introductionmentioning

confidence: 99%

“… 9) 10) Since the number of patients with ischemic heart disease is increasing, and many of them are elderly and have arthritis, there are more and more candidates for treatment with both celecoxib and antiplatelet agents. 11) However, the safety profile of celecoxib with concomitant administration of aspirin and clopidogrel has not been evaluated. We conducted the current study to evaluate 1) whether celecoxib can be used safely with antiplatelet agents, and 2) whether celecoxib interferes with the antiplatelet activity of aspirin and clopidogrel.…”

Section: Introductionmentioning

confidence: 99%

Celecoxib Does Not Attenuate the Antiplatelet Effects of Aspirin and Clopidogrel in Healthy Volunteers

et al. 2010

View full text Add to dashboard Cite

Background and ObjectivesThe prevalence of arthritis, which is often treated with celecoxib, is high in patients with coronary artery disease. Furthermore, celecoxib has been reported to reduce restenosis after coronary stenting by inhibiting expression of the proto-oncogene Akt. A concern is that celecoxib increases thrombogenicity by inhibiting the synthesis of prostacyclin in endothelial cells. However, it is not known whether the administration of celecoxib will attenuate the antiplatelet effects of aspirin and clopidogrel, which are used after stenting. We addressed this gap in our knowledge.Subjects and MethodsWe recruited healthy volunteers (n=40) and randomized them into five subgroups (n=8 for each group: aspirin, celecoxib, aspirin+celecoxib, aspirin+clopidogrel, and aspirin+clopidogrel+celecoxib). Each subject received their medications for 6 days and blood samples were taken on day 0 and day 7. Celecoxib (200 mg twice a day), and/or aspirin (100 mg daily), and/or clopidogrel (75 mg daily) were administered. We compared platelet function among subgroups using light transmittance aggregometry and arachidonic acid metabolite assays.ResultsCelecoxib treatment alone did not significantly affect platelet aggregation. The reduction in adenosine diphosphase (ADP)-induced platelet aggregation by aspirin+clopidogrel was not affected by addition of celecoxib (31.3±6.9% vs. 32.4±12.2%, p=0.83). Inhibition of collagen-induced platelet aggregation by aspirin+clopidogrel was not affected by addition of celecoxib (47.6±13.4% vs. 51.6±3.7%, p=0.69). Drug-induced changes in prostacyclin and thromboxane levels did not differ among treatment groups.ConclusionCelecoxib treatment does not interfere with the antiplatelet effects of aspirin or clopidogrel, suggesting that celecoxib can be safely administered in combination with dual antiplatelet therapy in patients with coronary stenting without increased thrombogenicity.

show abstract