Abstract
BackgroundLocal recurrence is the main cause of treatment failure for esophageal cancer and a large part of them require re-irradiation which needs to face the two major challenges of radioresistance and radiation-induced lung injury (RILI). This study aimed to evaluate the effects of irradiation with different fractionations on inhibition in radioresistant esophageal cancer cells in vitro and RILI in vivo. MethodsEC109R was selected from the human esophageal squamous carcinoma cell line EC109 by multiple exposures and verified to be radioresistant through colony forming assay and cell proliferation assay. EC109R was irradiated with different fractionations (conventional radiotherapy, CR: 2 Gy/d, 5 d; pulsed low dose-rate radiotherapy, PLDR: 0.2 Gy x 10 pulses with 3-min intervals/d, 5 d; hypo-fractionated radiotherapy, HR: 5 Gy/d, 2 d) to verify their inhibition by CCK-8. The protection of PLDR on RILI was assessed by H&E-staining paraffin sections and mice serum TGF-β1 levels. ResultsEC109R exhibited much better radioresistance (p < 0.0001) than EC109 in colony forming and cell proliferation assays. For EC109R, PLDR showed slightly lower inhibition by detection of optical density than HR (p = 0.0025) but similar to CR (p = 0.1155). In addition, pathological sections of lung tissues from PLDR group showed less alveolar structural damage and inflammatory cells infiltration, and serum TGF-β1 levels were significantly lower than those in the other two fractionations (vs CR: p = 0.0092; vs HR: p = 0.0045). ConclusionPLDR could effectively inhibit the proliferation of radioresistant esophageal cancer cells in vitro and mitigate RILI in vivo.
Published Version
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