[Retracted] Radiosensitizing Effect of Celastrol by Inhibiting G2/M Phase Arrest Induced by the c‐myc Gene of Human SW1353 Chondrosarcoma Cells: Network and Experimental Analyses

Abstract

Objective. Studies have unveiled that the components of Tripterygium wilfordii Hook F (TWHF) such as celastrol could attenuate apoptosis and proliferation of various tumor cells. This study is focused on the radiosensitization effect and apoptotic pathways of celastrol via the inhibition of the c-myc gene and the influence of which combined with radiotherapy on the proliferation, apoptosis, invasion, and metastasis of chondrosarcoma cells. Methods. A variety of bioinformatic tools were applied to explore the expression level and prognosis of the c-myc gene in different tumor cells and chondrosarcoma cells. We used pharmacology network to analyze the components, pathways, targets, molecular functions of TWHF and explore the relevant effective components over the MYC gene. Clone formation assay, CCK-8 assay, flow cytometry, and transwell migration assay were applied to detect the effects of celastrol on the expression of c-myc gene, cell apoptosis, and cell cycle. Radiation therapy was used to observe the radiosensitization effect of celastrol on chondrosarcoma. Results. This study shows that the c-myc gene is overexpressed in various tumor cells and bone tumor cells to varying degrees. Celastrol can significantly inhibit the expression of the c-myc gene, induce G2/M phase arrest through regulation of G2/M phase-related proteins, and promote SW1353 cell apoptosis through the mitochondrial signaling pathway. In addition, we also found that the use of triptorubin to inhibit c-myc gene expression in combination with radiotherapy can increase the osteosarcoma cells’ apoptosis rate through the mitochondrial signaling pathway significantly. Conclusions. Our study validated the radiosensitization effect of celastrol through knocking down the expression of the c-myc gene to induce G2/M phase arrest and provides a new idea for the treatment of refractory or recurrent chondrosarcoma that is not sensitive to radiotherapy.

Aspirin Restores Radiosensitivity in Cervical Cancer Cells by Inducing Mitotic Catastrophe through Downregulating G2/M Effectors

“…Cells exert variations in radiosensitivity at different phases of cell-cycle making G2/M phase the most radiosensitive of them (Otani et al, 2016). Accordingly, radiosensitizers tend to arrest the cell-cycle at G2/M phase by activating cell-cycle checkpoint regulators (Morgan et al, 2015;Huang et al, 2020;Qian et al, 2022, El-Benhawy et al, 2021. But in case of radioresistant cells, these checkpoint regulators are either inactive or too deregulated thereby escape arrest and subsequent cell death (Visconti et al, 2016).…”

Retracted: Radiosensitizing Effect of Celastrol by Inhibiting G2/M Phase Arrest Induced by the c-myc Gene of Human SW1353 Chondrosarcoma Cells: Network and Experimental Analyses

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [ 1 ]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process: Discrepancies in scope Discrepancies in the description of the research reported Discrepancies between the availability of data and the research described Inappropriate citations Incoherent, meaningless and/or irrelevant content included in the article Manipulated or compromised peer review …”

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [1]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process:…”