Glycididazole Sodium

In this study, we construct a subcutaneous tumor mice model of U14 cells, observe the tumor growth, and detect the expression of Foxp3 and VISTA in cervical cancer tissues and adjacent tissues during CMNa-enhancing radiotherapy.From the 15th day, compared with the control group, the tumor volume changes in each treatment group were significant (P < 0.01). CMNa combined with radiotherapy had an interactive effect and a positive effect in inhibiting tumor volume growth. There was no significant difference in the expression of Foxp3 and VISTA in mouse cervical cancer tissues and adjacent tissues in each group. The Foxp3 level in the RT group was the highest, and the CMNa group was the lowest. The VISTA level of the CMNa+RT group was the highest, the RT group is followed by, and the Control group is the lowest. The Foxp3 level of the CMNa group did not change much at each different point. The Foxp3 level in RT and CMNa+RT group gradually decreased after a transient increase, and the VISTA level in the CMNa+RT group increased more.Our results show that CMNa can enhance the efficacy of radiotherapy, and at the same time can reduce the compensatory increase in regulatory T cell Foxp3 levels caused by radiotherapy, and reduce the radiotherapy response. However, in the course of the treatment of the two, there may be a substantial increase in the level of VISTA, and the combined application of VISTA inhibitors may increase the anti-tumor response.

Chemoresistance to cisplatin in lung cancer treatment remains prevalent. Since targeting excision repair cross-complementing 1 (ERCC1) may be a viable strategy to reestablish the therapeutic sensitivity to platinum-based agents in chemoresistant cases, and low ERCC1 level is beneficial to metastatic lung cancer patients undergoing platinum-based chemotherapy, we hypothesized that metastasis-associated process is involved in ERCC1-dependent cisplatin-resistance in lung adenocarcinoma.

We performed an RNA-Sequencing (RNA-Seq) analysis to identify differentially expressed genes in ERCC1-deficient cells co-treated with cisplatin and sodium glycididazole (CMNa). Differentially expressed genes and the hub genes in the cisplatin/CMNa-treated cells were identified by systematic network analysis. Oncomine expression analysis was also performed to evaluate the clinical implication of the identified hub gene.

Platelet-derived growth factor receptor (PDGF/PDGFR) and focal adhesion genes were downregulated in ERCC1-defective non-small cell lung cancer (NSCLC) cells undergoing combined cisplatin/CMNa treatment. Consistent with the finding, cell migration was reduced in these cells. PDGFRB was identified as the hub gene in the process by differential expressed gene network analysis. Importantly, elevated PDGFRB level was observed in advanced lung adenocarcinoma patients with metastases.

PDGF/PDGFR and focal adhesion signaling may serve as another mechanism in addition to ERCC1-mediated cisplatin-resistance in lung adenocarcinoma. Multiple pro-invasion/pro-migration/proliferation and DNA damage repair pathways may be integrated to confer growth advantages on tumor cells.