biostudies-literatureUnknown24Fan ZPentraxin 3 (PTX3) is an inflammatory molecule that is closely related to the proliferation, invasion, and metastasis of cancer. In order to explore the role of PTX3 in the occurrence and development of esophageal carcinoma (ESCA), we modified the PTX3 gene in ESCA cell lines to obtain the model of gene knockout and overexpression and studied cell proliferation, cycle, apoptosis, migration ability, energy metabolism, and sensitivity to chemotherapy and radiotherapy. We observed the increase in cell proliferation, cycle, apoptosis, migration ability, and sensitivity to chemotherapy and radiotherapy in the PTX3 knockout model, while in the PTX3 overexpression model, these phenomena were significantly reduced. Knockout of the PTX3 also resulted in decreased cell glycolysis and increased oxidaMolecular therapy oncolytics772-787https://www.ebi.ac.uk/biostudies/studies/S-EPMC8908267biostudies-literaturePromoting role of pentraxin-3 in esophageal squamous cell carcinoma.PMC8908267Li XZheng YFan ZFeng KBa YSu JWang HLi LDeng XSuo ZfalsePromoting role of pentraxin-3 in esophageal squamous cell carcinoma.Pentraxin 3 (PTX3) is an inflammatory molecule that is closely related to the proliferation, invasion, and metastasis of cancer. In order to explore the role of PTX3 in the occurrence and development of esophageal carcinoma (ESCA), we modified the PTX3 gene in ESCA cell lines to obtain the model of gene knockout and overexpression and studied cell proliferation, cycle, apoptosis, migration ability, energy metabolism, and sensitivity to chemotherapy and radiotherapy. We observed the increase in cell proliferation, cycle, apoptosis, migration ability, and sensitivity to chemotherapy and radiotherapy in the PTX3 knockout model, while in the PTX3 overexpression model, these phenomena were significantly reduced. Knockout of the PTX3 also resulted in decreased cell glycolysis and increased oxida2022-01-01T00:00:00Z2022 Mar2025-04-04T12:57:33.472Z2025-04-04T12:57:33.472ZS-EPMC89082673531752310.1016/j.omto.2022.02.005