scholarly journals WITHDRAWN: Metformin antagonizes MPS-1-mediated IL-6/Stat3 signaling in ovarian cancer cells: possible mechanisms of stemness and angiogenesis inhibition

Oncotarget ◽  
2018 ◽  
Vol 0 (0) ◽  
Author(s):  
Xu Yang ◽  
Yingling Ding ◽  
Mengyuan Yang
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Angiogenesis Inhibition ◽  
Stat3 Signaling

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.

scholarly journals Inhibition of STAT3 signaling as critical molecular event in resveratrol-suppressed ovarian cancer cells

2015 ◽  
Vol 8 (1) ◽  
Author(s):  
Li-Xia Zhong ◽  
Hong Li ◽  
Mo-Li Wu ◽  
Xiao-Yu Liu ◽  
Ming-Jun Zhong ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Molecular Event ◽  
Stat3 Signaling

scholarly journals Metformin Antagonizes Ovarian Cancer Cells Malignancy Through MSLN Mediated IL-6/STAT3 Signaling

2021 ◽  
Vol 30 ◽  
pp. 096368972110278
Author(s):  
Xu Yang ◽  
Mei Huang ◽  
Qin Zhang ◽  
Jiao Chen ◽  
Juan Li ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Ovarian Cancer Cells ◽  
Metformin Treatment ◽  
Antitumor Effects ◽  
Cancer Management ◽  
Stat3 Signaling ◽  
Skov3 Cells

Background: Ovarian cancer is the most lethal gynecological malignancy, and chemotherapy remains the cornerstone for ovarian cancer management. Due to the unsatisfactory prognosis, a better understanding of the underlying molecular carcinogenesis is urgently required. Methods: Assays for determining cell growth, cell motility, and apoptosis were employed to evaluate the potential antitumor effects of metformin against ovarian cancer cells. Molecular biological methods were employed to explore the underlying mechanism. Human ovarian cancer samples and Gene Expression Profiling Interactive Analysis (GEPIA) dataset were used for uncovering the clinical significances of mesothelin (MSLN) on ovarian cancer. Results: In the present work, we found that metformin treatment led to cell growth and cell migration inhibition, and induced cell apoptosis. Metformin administration also impaired cancer cell stemness and the capillary-like structure formation capacity of SKOV3 cells. On mechanism, metformin treatment remarkably reduced mesothelin (MSLN) expression, downregulated IL-6/STAT3 signaling activity, subsequently resulted in VEGF and TGFβ1 expression. We also observed an oncogenic function of MSLN on ovarian cancer. Conclusions: Collectively, our findings suggested that metformin exerts anticancer effects by suppressing ovarian cancer cell malignancy, which attributed to MSLN inhibition mediated IL6/STAT3 signaling and VEGF and TGFβ1 downregulation.

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
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