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Inhibition of STAT3 signaling induces apoptosis and suppresses growth of lung cancer: good and bad

Authors
강주희장영수이하정이창영신동윤오승현
Issue Date
21-Dec-2019
Publisher
한국실험동물학회
Keywords
STX-0119; STAT3 inhibitor; NSCLC; Xenograft; Cancer
Citation
Laboratory Animal Research, v.35, no.4, pp.221 - 229
Journal Title
Laboratory Animal Research
Volume
35
Number
4
Start Page
221
End Page
229
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/19387
DOI
10.1186/s42826-019-0030-0
ISSN
1738-6055
Abstract
Signal transducer and activator of transcription 3 (STAT3) modulates a variety of genes involved in the regulation of critical functions, including cell proliferation, differentiation, apoptosis, angiogenesis, metastasis, and immunity. For many cancers, elevated levels of STAT3 signaling have been associated with a poor prognosis and the development of chemotherapy resistance. In this study, we investigated the inhibitory effects of a novel small-molecule inhibitor of STAT3, STX-0119, on the cell viability and survival of human lung cancer cells. STX-0119 inhibited activated STAT3 and the expression of STAT3-regulated oncoproteins such as c-Myc, cyclin D1, and survivin in lung cancer cells. STX-0119 also decreased the amount of STAT3 in the nuclear fraction as well as induced apoptosis of these lung cancer cell lines as evidenced by increases in apoptotic cells (Annexin V positive) and poly (ADP-ribose) polymerase (PARP) cleavage. The efficacy of STX-0119 in a mouse xenograft model was confirmed. However, a hematological side effect, which had not been previously reported, was observed. The level of white blood cells was significantly lowered when treated at the dose at which STX-0119 alone showed a significant tumor-suppressive effect. In conclusion, we suggest that STX-0119 may be a potent therapeutic agent against lung cancer. Consideration of the side effect suggests, it is necessary to study whether low-dose STX-0119 is effective for lung treatment with a combination of classic lung cancer therapeutics.
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