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Abstract
We have reported the radiation could activate STAT3, which subsequently promotes the invasion of A549 cells. We here explored the dose- and time-response of STAT3 to radiation and the effect of radiation on upstream signaling molecules. A549 cells were irradiated with different doses of γ-rays. The expression of and nucleus translocation of p-STAT3 in A549 cells were detected by immunoblotting and immunofluorescence, respectively. The level of phosphorylated EGFR was also assessed by immunoblotting, and IL-6 expression was detected by real time PCR and ELISA. Radiation promoted the phosphorylation of STAT3 at Y705 in a dose- and time-dependent manner and nuclear translocation. The level of phosphorylated EGFR in A549 cells increased after radiation. In additional, the mRNA and protein levels of IL-6 in A549 cells were also up regulated by radiation. STAT3 is activated by radiation in a dose-and time-dependent manner, probably due to radiation-induced activation of EGFR or secretion of IL-6 in A549 cells.
Highlights
Radiotherapy is one of the common approaches for cancer therapy
Our previous study had proved that 2 and 4 Gy of radiation could promote the phosphorylation of Signal Transducer and Activator of Transcription 3 (STAT3) at Tyr705 significantly (Li et al, 2013)
(A), 24 h after radiation, the expression of phosphorylated STAT3 at Tyr705 in A549 cells increased with the increasing radiation dose
Summary
Radiotherapy is one of the common approaches for cancer therapy. It can be used alone or in combination with chemotherapy and/or surgery. Radiaiton can activate various radiation response genes This leads to the production of various proteins, some of which might change the radiosensitivity of cancer cell and confer survival advantage to cancer cells. Our previous study showed that radiation could promote the phosphorylation of STAT3 at Tyr705, which resulted in the increase of invasion of A549 cells by up regulating the expression of MMP2 (Li et al, 2013). This result indicated that the activation of STAT3 by radiation play an important role in recurrence and metastasis of lung adenocarcinoma. In the current study, we further investigate the relationship between the p-STAT3 and radiation, and the upstream molecular involved in radiation-induced activation of STAT3
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