Parecoxib prevents complications in hepatocellular carcinoma patients receiving hepatic transarterial chemoembolization: a prospective score-matched cohort study

Zhou, Zhou Zhong-Guo; Chen, J. B.Jin Bin; Qiu, Hai Bo; Wang, Ruo Jing; Chen, Jian Cong; Xu, Li; Chen, Min Shan; Zhang, Yaojun

doi:10.18632/oncotarget.8560

Cited by 5 publications

(2 citation statements)

References 24 publications

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“…HCC is a common malignant tumor with high morbidity and mortality, particularly in China 17 . Compared with other cancers, risk factors for HCC are relatively well known; however, the mechanisms of hepatocarcinogenesis are not well understood at present 18 . Some studies have suggested that B7-H4 is involved in the developmental mechanisms of some types of cancer including pancreatic and breast cancers 11,19 .…”

Section: Discussionmentioning

confidence: 99%

Downregulation of B7-H4 suppresses tumor progression of hepatocellular carcinoma

Dong

Xie

et al. 2019

Sci Rep

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B7-H4, as a member of the B7 superfamily, was overexpressed in various types of cancers. However, the effects of B7-H4 on the aggressiveness of HCC and the underlying mechanisms have not yet been fully explored. For this purpose, B7-H4 expression was detected by Flow cytometry and Western blotting, it was highly expressed in several HCC cell lines but not in normal LO2 cell line. Knockdown B7-H4 expression induced HCC cells apoptosis by flow cytometry and colony formation assays and increased several apoptosis-related proteins, including survivin, cleaved caspase-3, cleaved caspase-7, and Bax, while the pro-growth protein survivin was reduced. Then the proliferation and cell cycle were suppressed after treated by siB7-H4. Moreover, the level of B7-H4 was significantly correlated with cell migration. In vivo, intra-tumor injection of siRNA targeting B7-H4 can significantly inhibited the growth of HepG2 cells in nude mice. Finally, regions of interest were manually traced on T1WI, T2WI, DWI and ADC of MR images. ADC values were increased in HCC xenografts after B7-H4 siRNA treatment. These data indicated that downregulation of B7-H4 suppressed the proliferation and migration and promoted apoptosis in vitro and in vivo. Blocking the B7-H4 channel might be a potential therapeutic strategy for HCC.

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Section: Discussionmentioning

confidence: 99%

Downregulation of B7-H4 suppresses tumor progression of hepatocellular carcinoma

Dong

Xie

et al. 2019

Sci Rep

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“…Several analgesics, such as oxycodone and parecoxib sodium, have been required to alleviate the postembolization pain. 10 , 11 Despite the good adjuvant analgesic effect on post-TACE pain, there are still a fraction of patients who are not sensitive to analgesic medications or suffer from side effects. It is, therefore, necessary to develop non-pharmacologic approaches to improve the patient’s painful experience.…”

Section: Introductionmentioning

confidence: 99%

Health education helps to relieve postembolization pain during hepatic arterial chemoembolization therapy

Wang

Tao

2018

JPR

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AimPsychological intervention has been proved a complementary approach to drug analgesia. Another study suggested that health knowledge is associated with psychological symptoms in patients with liver cancer. This study is conducted to assess whether improving the health education (HE) alleviates the postembolization pain during transarterial chemoembolization (TACE).Materials and methodsOne hundred and fifteen patients, who required TACE for hepatocellular carcinoma (HCC) and suffered postembolization pain, were randomized into control group (n=63) and HE group (n=52). The health knowledge was scaled with the health knowledge questionnaire (HKQ). The postembolization pain was scored using a 0–10 numeric rating scale (NRS-10) after arterial embolization in both groups.ResultsThere were no statistical differences between male and female in all HKQ scores (P>0.05). The HKQ scores of young people (≤45 years old) were significantly higher than those of elders (>45 years old; P<0.05). After teaching HE, the HKQ scores were significantly increased in patients of the HE group (P<0.01). The postembolization pain score in the HE group was significantly lower than that in the control group (P<0.05). The HKQ scores of question 1, 3, and total were negatively correlated with the pain score in this sample (P<0.05).ConclusionImproving the HE among HCC patients before TACE is beneficial for the pain relief during interventional procedure.

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Parecoxib inhibits tumorigenesis and angiogenesis in hepatocellular carcinoma through ERK–VEGF/MMPs signaling pathway

Tian,

Huang,

Liu

et al. 2024

IUBMB Life

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Parecoxib, a well‐recognized nonsteroidal anti‐inflammatory drug, has been reported to possess anticancer properties in various tumor types. In this work, we aimed to investigate the potential anticancer effects of parecoxib on hepatocellular carcinoma (HCC) cells. To assess the impact of parecoxib on HCC cell proliferation, we employed Cell Counting Kit‐8, colony formation, and 5‐ethynyl‐2′‐deoxyuridine assays. Hoechst/propidium iodide (PI) double staining and flow cytometry were performed to evaluate apoptosis and cell cycle analysis. Wound healing and transwell assays were utilized to assess cell migration and invasion. Tube formation assay was employed to analyze angiogenesis. Protein levels were determined using western blotting, and mRNA expression levels were assessed using quantitative real‐time polymerase chain reaction (PCR). A xenograft mouse model was used to confirm the antitumor effects of parecoxib on HCC tumors in vivo. Our data demonstrated that parecoxib effectively inhibited the proliferation of HCC cells in a dose‐ and time‐dependent manner. In addition, parecoxib induced cell cycle arrest in the G2 phase and promoted apoptosis. Moreover, parecoxib hindered tumor migration and invasion by impeding the epithelial–mesenchymal transition process. Further investigation showed that parecoxib could significantly suppress angiogenesis through the inhibition of extracellular signal‐regulated kinase (ERK)–vascular endothelial growth factor (VEGF) axis. Notably, treatment with the ERK activator phorbol myristate acetate upregulated the expression of matrix metalloproteinase (MMP)‐2, MMP‐9, and VEGF and reversed the function of parecoxib in HCC cells. Besides, parecoxib displayed its antitumor efficacy in vivo. Collectively, our results suggest that parecoxib ameliorates HCC progression by regulating proliferation, cell cycle, apoptosis, migration, invasion, and angiogenesis through the ERK–VEGF/MMPs signaling pathway.

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Parecoxib prevents complications in hepatocellular carcinoma patients receiving hepatic transarterial chemoembolization: a prospective score-matched cohort study

Cited by 5 publications

References 24 publications

Downregulation of B7-H4 suppresses tumor progression of hepatocellular carcinoma

Downregulation of B7-H4 suppresses tumor progression of hepatocellular carcinoma

Health education helps to relieve postembolization pain during hepatic arterial chemoembolization therapy

Parecoxib inhibits tumorigenesis and angiogenesis in hepatocellular carcinoma through ERK–VEGF/MMPs signaling pathway

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