Experimental immunology Effects of sufentanil on human gastric cancer cell line SGC-7901 in vitro

Wu, Weidong; Wei, Ningxian; Jiang, Chun-Yi; Cui, Suyang; Yuan, Jiaqing

doi:10.5114/ceji.2014.45939

Cited by 17 publications

(19 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…phosphatidylserine. The binding of Annexin V to phosphatidylserine demonstrates the feasibility of using FITC-conjugated Annexin V to identify apoptotic cells [28,29] . Thus, Annexin-V-FITC/PI dual staining was used to detect apoptosis of Caco-2 cells in the present study.…”

Section: Changes In the Cell Membrane During Early Apoptosis Results Imentioning

confidence: 99%

Matrine Treatment Triggers Apoptosis in Colon Cancer Cells

Chang¹,

LIU²

2020

pharmaceutical-sciences

View full text Add to dashboard Cite

Chang and Liu: Matrine Triggers Apoptosis in Colon Cancer Cells The aim of the present study was to investigate the role of matrine, a natural alkaloid from Sophora flavescens with antiproliferative and proapoptotic activities, in human colon cancer using in vitro studies. Caco-2 cell line was treated with increasing doses (2.0 and 32 mg/ml) of matrine for 24 h. The MTT assay was used to measure abnormal cell multiplication, while flow cytometry was applied to determine the degree of apoptosis and cell growth. Western blot analysis was also used to detect the expression of various proteins. The results indicated that matrine blocked Caco-2 cell division in a dose-dependent and time-dependent manner. Matrine triggered apoptosis and blocked mitosis by altering the protein expression levels of B-cell lymphoma-2, B-cell lymphoma-2-associated X protein, cytochrome c, caspase-9 and caspase-3. In conclusion, matrine is found to interfere with the proliferation of colon cancer cells in vitro by triggering apoptosis through enhancing the expression of X protein, caspase-3 and caspase-9, as well as suppressing B-cell lymphoma-2 expression. Therefore, matrine is a potential natural compound that could be used in colon cancer treatment..

show abstract

Section: Changes In the Cell Membrane During Early Apoptosis Results Imentioning

confidence: 99%

Matrine Treatment Triggers Apoptosis in Colon Cancer Cells

Chang¹,

LIU²

2020

pharmaceutical-sciences

View full text Add to dashboard Cite

show abstract

“…ere are also reports that fentanyl can inhibit tumor growth, proliferation, and metastasis in mouse bone cancer models, and morphine can reduce tumor cell spread before and after operation [25][26][27]. Sufentanil, as a newly synthesized receptor agonist, has an analgesic potency 5-10 times that of fentanyl and 500-1000 times that of morphine [28][29][30]. Continuous administration has a more stable time-volume-dependent half-life than fentanyl.…”

Section: Discussionmentioning

confidence: 99%

Sufentanil Inhibits the Proliferation and Metastasis of Esophageal Cancer by Inhibiting the NF-κB and Snail Signaling Pathways

Tang

Wang

et al. 2021

Journal of Oncology

View full text Add to dashboard Cite

Sufentanil is a μ-opioid receptor agonist, widely used in intraoperative and postoperative analgesia of esophageal cancer. This study investigated the effects of sufentanil on the proliferation, invasion, and metastasis of esophageal carcinoma cells and its molecular mechanisms. Human esophageal carcinoma cells CaES-17 and Eca-109 were cultured in vitro. Different concentrations of sufentanil (1 and 10 μmol/L) were added to the experimental group. MTT was used to detect the proliferative activity of esophageal carcinoma cells. The migration ability of esophageal carcinoma cells was measured by the scratch test. Transwell was used to detect the invasive ability of esophageal carcinoma cells. The EMT marker expression was detected by qPCR. Meanwhile, effects of sufentanil on NF-κB and Snail expression and nucleation were evaluated. Establish a subcutaneous xenograft tumor model of nude mice with esophageal carcinoma cells and evaluate the antitumor effect of sufentanil. Sufentanil can inhibit the proliferation, invasion, and migration of CaES-17 and Eca-109 cells and has a dose-dependent relationship. The molecular mechanism showed that sufentanil could upregulate the expression of E-cadherin and inhibit the expression of vimentin. Sufentanil can inhibit the expression of NF-κB and Snail, as well as the nuclear expression of NF-κB and Snail. Xenograft tumor model results showed that sufentanil could inhibit tumor proliferation and NF-κB and Snail expression in tumor tissues of nude mice. Sufentanil inhibits esophageal cancer epithelial-mesenchymal transition (EMT) by acting on NF-κB and Snail signaling pathways to inhibit proliferation and metastasis of esophageal cancer.

show abstract

“…G protein-coupled receptors are involved in ligand recognition and subsequent activation or inactivation, because of their most essential characteristic, conformational flexibility (28,29). Compared with fentanyl and remifentanil, sufentanil is highest affinity agonist targeting the µ opioid receptor (30). This suggests that sufentanil and µ opioid receptors may activate downstream signaling pathways of G proteins, resulting in Cx43 GJ function alternation.…”

Section: Discussionmentioning

confidence: 99%

Sufentanil attenuates oxaliplatin cytotoxicity via inhibiting connexin 43-composed gap junction function

Zhang

2017

Molecular Medicine Reports

View full text Add to dashboard Cite

Comprehensive strategies for the treatment of colorectal cancer (CRC) have become increasingly important. One of the most important factors is pain relief. Therefore, patients with CRC are concurrently treated with analgesics and chemotherapeutic agents; however, the effects of analgesics on the therapeutic activity of chemotherapeutic agents remain largely unknown. The present study investigated the effects of three widely used analgesics in clinics: Fentanyl, remifentanil and sufentanil, on the cytotoxicity of oxaliplatin, a commonly used chemotherapeutic agent for CRC. Furthermore, the underlying mechanisms of those effects in association with connexin 43 (Cx43)‑composed gap junction (GJ) function were analyzed. The Lovo, Colo320, HCT116 and HT29 human CRC cell lines, with or without Cx43 expression, were used to examine the effects of the three analgesics on the cytotoxicity of oxaliplatin. The results demonstrated that in the cell lines expressing Cx43 (Lovo and Colo320), the cytotoxicity of oxaliplatin was attenuated and Cx43 GJ function was inhibited. Sufentanil, not fentanyl or remifentanil, inhibited Cx43 GJ function effectively, and reduced the cytotoxicity of oxaliplatin. In contrast, these effects were not observed in the other two colon cancer cell lines not expressing Cx43 (HCT116 and HT29). These results suggested that alternation of Cx43 GJ function may regulate the cytotoxicity of oxaliplatin in regard to CRC. Furthermore, sufentanil, not fentanyl or remifentanil, suppressed the cytotoxicity of oxaliplatin through inhibition of Cx43 GJ function. These results may be beneficial for the treatment of CRC and reduction of treatment resistance.

show abstract

Experimental immunology Effects of sufentanil on human gastric cancer cell line SGC-7901 in vitro

Cited by 17 publications

References 20 publications

Matrine Treatment Triggers Apoptosis in Colon Cancer Cells

Matrine Treatment Triggers Apoptosis in Colon Cancer Cells

Sufentanil Inhibits the Proliferation and Metastasis of Esophageal Cancer by Inhibiting the NF-κB and Snail Signaling Pathways

Sufentanil attenuates oxaliplatin cytotoxicity via inhibiting connexin 43-composed gap junction function

Contact Info

Product

Resources

About