OLEANOLIC ACID CONJUGATED CHITOSAN NANOCOMPLEX EXERTS ANTI-TUMOR EFFECTS BY INHIBITING AUTOPHAGY IN LUNG CANCER CELLS THROUGH THE SIGNAL TRANSDUCERS AND ACTIVATORS OF TRANSCRIPTION 3/B CELL LYMPHOMA-2 SIGNALING PATHWAY

被引:1
作者
Abulaiti, A. [1 ]
Sun, X. H. [1 ]
Yibulayin, W. [1 ]
He, D. [1 ]
Xu, K. M. [1 ]
Yibulayin, X. [1 ]
机构
[1] Xinjiang Med Univ, Affiliated Canc Hosp, Dept Thorac Surg Ward 1, 789 Suzhou East St, Urumqi 830011, Xinjiang Uygur, Peoples R China
来源
JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY | 2024年 / 75卷 / 03期
关键词
lung cancer; oleanolic acid conjugated chitosan nanocomplex; autophagy; apoptosis; signal transducers and activators of transcription 3; B cell lymphoma-2; cell transfection; anti-inflammation; cell migration; HEPATOCELLULAR-CARCINOMA CELLS; STAT3; INFLAMMATION;
D O I
10.26402/jpp.2024.3.08
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The current study reveals the anticancer potential of oleanolic acid conjugated chitosan nanocomplex (OAC) in lung cancer (LC). Cell counting kit-8 (CCK-8) and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium (MTT) assay were used to detect cell viability, 5-ethynyl-2'-deoxyuridine (EdU) assay to detect cell proliferation, flow cytometry and TUNEL assay to detect cell apoptosis in A549 (ATCC (R) CCL-185TM) (R) CCL-185 TM ) and NCIH460 cells. Transwell evaluated cell migration and invasion ability, transmission electron microscopy and immunofluorescence observed autophagy, and Western blotting detected apoptosis- and autophagy-associated proteins. OAC inhibited LC cell viability, migration, and invasion, and induced apoptosis and autophagy depending on the concentration. The phosphorylation of signal transducers and activators of transcription 3 (STAT3) in cells was weakened after OAC treatment. STAT3 activation restored the inhibition of cell viability and induction of apoptosis by OAC. We conclude that OAC induces apoptosis and inhibits cell viability, which may be related to the STAT inactivation. Therefore, OAC is a promising compound for LC therapy.
引用
收藏
页码:315 / 326
页数:12
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