scholarly journals Physapubescin B inhibits tumorgenesis and circumvents taxol resistance of ovarian cancer cells through STAT3 signaling

Oncotarget ◽  
2017 ◽  
Vol 8 (41) ◽  
pp. 70130-70141 ◽  
Author(s):  
Xiaofeng Zhao ◽  
Lu Huang ◽  
Wanwan Xu ◽  
Xiaoyan Chen ◽  
Yan Shen ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Stat3 Signaling ◽  
Taxol Resistance

scholarly journals NCX-4016, a nitro-derivative of aspirin, inhibits EGFR and STAT3 signaling and mdulates Bcl-2 proteins in cisplatin-resistant human ovarian cancer cells and xenografts

Cell Cycle ◽  
2008 ◽  
Vol 7 (1) ◽  
pp. 81-88 ◽  
Author(s):  
Karuppaiyah Selvendiran ◽  
Anna Bratasz ◽  
Liyue Tong ◽  
Louis J. Ignarro ◽  
Periannan Kuppusamy
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Nitro Derivative ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Stat3 Signaling ◽  
Ncx 4016

scholarly journals A novel small molecule LLL12B inhibits STAT3 signaling and sensitizes ovarian cancer cell to paclitaxel and cisplatin

2020 ◽  
Author(s):  
Ruijie Zhang ◽  
Xiaozhi Yang ◽  
Dana M. Roque ◽  
Chenglong Li ◽  
Jiayuh Lin
Keyword(s):  
Ovarian Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Small Molecule ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Inhibitory Effects ◽  
Stat3 Signaling ◽  
Stat3 Phosphorylation

AbstractOvarian cancer is the fifth most common cause of cancer deaths among American women. Platinum and taxane combination chemotherapy represents the first-line approach for ovarian cancer, but treatment success is often limited by chemoresistance. Therefore, it is necessary to find new drugs to sensitize ovarian cancer cells to chemotherapy. Persistent activation of Signal Transducer and Activator of Transcription 3 (STAT3) signaling plays an important role in oncogenesis. Using a novel approach called advanced multiple ligand simultaneous docking (AMLSD), we developed a novel nonpeptide small molecule, LLL12B, which targets the STAT3 pathway. In this study, LLL12B inhibited STAT3 phosphorylation (tyrosine 705) and the expression of its downstream targets, which are associated with cancer cell proliferation and survival. We showed that LLL12B also inhibits cell viability, migration, and proliferation in human ovarian cancer cells. LLL12B combined with either paclitaxel or with cisplatin demonstrated synergistic inhibitory effects relative to monotherapy in inhibiting cell viability and LLL12B-paclitaxel or LLL12B-cisplatin combination exhibited greater inhibitory effects than cisplatin- paclitaxel combination in ovarian cancer cells. Furthermore, LLL12B-paclitaxel or LLL12B-cisplatin combination showed more significant in inhibiting cell migration and growth than monotherapy in ovarian cancer cells. In summary, our results support the novel small molecule LLL12B as a potent STAT3 inhibitor in human ovarian cancer cellsand suggest that LLL12B in combination with the current front-line chemotherapeutic drugs cisplatin and paclitaxel may represent a promising approach for ovarian cancer therapy.

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