To determine the radiosensitizing effect of apatinib on esophageal cancer cells, and to preliminarily investigate the underlying mechanism, KYSE-150 cells were treated with apatinib, x-ray or apatinib combined with x-ray, and compared with a blank control. It was observed that apatinib significantly inhibited vascular endothelial growth factor (VEGF) secretion and the proliferation of KYSE-150 cells in a dose-dependent manner. As the concentration of apatinib increased, the radiobiological parameters inactivation dose (D), quasi domain does (D) and survival fraction (SF) of KYSE-150 cells decreased, while the sensitization enhancement ratio SER increased. The rate of apoptosis in cells treated with apatinib and x-ray was markedly higher compared with those of the blank control, x-ray and apatinib alone groups (P<0.05). The proportion of cells in the G2/M phase was significantly increased in the apatinib, x-ray and combination groups compared with the blank control group (P<0.05). Compared with the control and x-ray groups, combination treatment did not significantly alter the expression level of polyADP-ribose polymerase (PARP), although it significantly increased the expression of cleaved-PARP (P<0.05). Moreover, the expression of cell serine/threonine-protein kinase-2 (CHK2) was downregulated (P<0.05), whilst expression of the phosphorylated form, pCHK2, was significantly increased (P<0.05) in the combination group when compared with the control and x-ray groups. In conclusion, the present study suggested that apatinib increases the radiosensitivity of KYSE-150 esophageal cancer cells by inhibiting VEGF secretion and cell proliferation, and promoting apoptosis and cell cycle redistribution.
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http://dx.doi.org/10.3892/ol.2018.9803 | DOI Listing |
Iran J Biotechnol
July 2024
Department of Pathology, The First Affiliated Hospital of Bengbu Medical University, Bengbu 233000, China.
Background: Oesophageal cancer (EC) is one of the common malignant tumors, and the prognosis of patients is poor. Further exploration of EC pathogenesis remains warranted.
Objective: The relationship between vascular epithelial cadherin (VE-cadherin) and chitinase-3-like protein 1 (CHI3L1) in EC is currently unknown.
Front Immunol
December 2024
Department of Otolaryngology, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, Jiangsu, China.
Front Oncol
December 2024
Department of Human Pathology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Background: Esophageal cancer, particularly esophageal squamous cell carcinoma (ESCC), is a leading cause of cancer-related death and has a poor prognosis. Despite the advancements in multidisciplinary therapies, resistance to conventional treatments warrants the development of novel therapeutic strategies. Ferroptosis, a form of cell death dependent on intracellular iron, has emerged as a potential mechanism for targeting cancer cells resistant to apoptosis.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Medical Department, The First Affiliated Hospital of Shihezi University, Shihezi 832008, China. Electronic address:
Exosomal microRNA (miRNA)s have been proven to affect recipient cell chemoresistance in several cancers. This research attempted to uncover the role of exosomal miRNA and the regulatory mechanism in cisplatin resistance of esophageal cancer (EC). Cisplatin-resistant EC cells (KYSE-150-CisR and TE-1-CisR) were established by the parental cells (KYSE-150 and TE-1) treated with a gradual increase of cisplatin concentration.
View Article and Find Full Text PDFBioorg Med Chem
January 2025
Department of Pharmacology, School of Pharmacy, Fujian Medical University, Fuzhou 350108, China; Fujian Key Laboratory of Drug Target Discovery and Structural and Functional Research, Fujian Medical University, Fuzhou 350108, China. Electronic address:
In this work, we successfully synthesized eight distinct compounds, comprising four chiral menthylamines and related derivatives. We evaluated their cytotoxic potential against a panel of human cancer cell lines, including human colon cancer HCT-116 cells, human esophageal squamous KYSE-150 cells, human breast cancer MCF-7 cells, and human glioma U87 cells. The U87 cells were chosen for a more in-depth investigation of their anti-tumor efficacy.
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