Silibinin Inhibits Tumor Growth through Downregulation of Extracellular Signal-Regulated Kinase and Akt in Vitro and in Vivo in Human Ovarian Cancer Cells

Novel Os(ii) arene complexes with a deprotonated ppy or ppy-CHO C^N ligand have been synthesized to selectively act on cancer cells as proteosynthesis inhibitors in vitro and exert antitumor activity in vivo in C. elegans models.

Download Full-text

The dual angiogenesis/metastasis inhibitor PG545 inhibits growth factor-induced cell migration and invasion in vitro and tumor growth in vivo of ovarian cancer cells

Gynecologic Oncology ◽

10.1016/j.ygyno.2011.12.350 ◽

2012 ◽

Vol 125 ◽

pp. S142-S143 ◽

Cited By ~ 1

Author(s):

S. Giri ◽

B. Winterhoff ◽

J. Maguire ◽

A. Teoman ◽

K. Dredge ◽

...

Keyword(s):

Ovarian Cancer ◽

Cell Migration ◽

Growth Factor ◽

Tumor Growth ◽

Cancer Cells ◽

Migration And Invasion ◽

Ovarian Cancer Cells ◽

Metastasis Inhibitor

Download Full-text

Antitumor properties of salinomycin on cisplatin-resistant human ovarian cancer cells in vitro and in vivo: Involvement of p38 MAPK activation

Oncology Reports ◽

10.3892/or.2013.2241 ◽

2013 ◽

Vol 29 (4) ◽

pp. 1371-1378 ◽

Cited By ~ 27

Author(s):

BEI ZHANG ◽

XUEYA WANG ◽

FENGFENG CAI ◽

WEIJIE CHEN ◽

ULI LOESCH ◽

...

Keyword(s):

Ovarian Cancer ◽

Cancer Cells ◽

P38 Mapk ◽

Ovarian Cancer Cells ◽

Human Ovarian Cancer ◽

Mapk Activation ◽

Antitumor Properties

Download Full-text

SPR965, a Dual PI3K/mTOR Inhibitor, as a Targeted Therapy in Ovarian Cancer

Frontiers in Oncology ◽

10.3389/fonc.2020.624498 ◽

2021 ◽

Vol 10 ◽

Author(s):

Arthur-Quan Tran ◽

Stephanie A. Sullivan ◽

Leo Li-Ying Chan ◽

Yajie Yin ◽

Wenchuan Sun ◽

...

Keyword(s):

Ovarian Cancer ◽

Tumor Growth ◽

Cancer Cells ◽

Epithelial Mesenchymal Transition ◽

Transition Process ◽

Ovarian Cancer Cells ◽

Serous Ovarian Cancer ◽

Mesenchymal Transition

SPR965 is an inhibitor of PI3K and mTOR C1/C2 and has demonstrated anti-tumorigenic activity in a variety of solid tumors. We sought to determine the effects of SPR965 on cell proliferation and tumor growth in human serous ovarian cancer cell lines and a transgenic mouse model of high grade serous ovarian cancer (KpB model) and identify the underlying mechanisms by which SPR965 inhibits cell and tumor growth. SPR965 showed marked anti-proliferative activity by causing cell cycle arrest and inducing cellular stress in ovarian cancer cells. Treatment with SPR965 significantly inhibited tumor growth in KpB mice, accompanied by downregulation of Ki67 and VEGF and upregulation of Bip expression in ovarian tumors. SPR965 also inhibited adhesion and invasion through induction of the epithelial–mesenchymal transition process. As expected, downregulation of phosphorylation of AKT and S6 was observed in SPR965-treated ovarian cancer cells and tumors. Our results suggest that SPR965 has significant anti-tumorigenic effects in serous ovarian cancer in vitro and in vivo. Thus, SPR965 should be evaluated as a promising targeted agent in future clinical trials of ovarian cancer.

Download Full-text

Forkhead Box Protein C2 (FOXC2) Promotes the Resistance of Human Ovarian Cancer Cells to Cisplatin In Vitro and In Vivo

Cellular Physiology and Biochemistry ◽

10.1159/000445620 ◽

2016 ◽

Vol 39 (1) ◽

pp. 242-252 ◽

Cited By ~ 15

Author(s):

Chanjuan Li ◽

Hongjuan Ding ◽

Jing Tian ◽

Lili Wu ◽

Yun Wang ◽

...

Keyword(s):

Ovarian Cancer ◽

Cancer Cells ◽

Cell Line ◽

Mapk Signaling ◽

Ovarian Cancer Cells ◽

Human Ovarian Cancer ◽

Cancer Tissues ◽

Mapk Signaling Pathways

Background/Aims: FOXC2 has been reported to play a role in tumor progression, but the correlations of FOXC2 with the cisplatin (CDDP) resistance of ovarian cancer cells are still unclear. The purpose of the present study is to investigate the roles of FOXC2 in the CDDP resistance of ovarian cancer cells and its possible mechanisms. Methods: Quantitative real-time PCR (qRT-PCR) was performed to detect the expression of FOXC2 mRNA in CDDP-resistant or sensitive ovarian cancer tissues and cell lines (SKOV3/CDDP and SKOV3). Gain- and loss-of-function assays were performed to analyze the effects of FOXC2 knockdown or overexpression on the in vitro and in vivo sensitivity of ovarian cancer cells to CDDP and its possible molecular mechanisms. Results: The relative expression level of FOXC2 mRNA in CDDP-resistant ovarian cancer tissues was higher than that in CDDP-sensitive tissues. Also, the expression of FOXC2 mRNA and protein in CDDP-resistant ovarian cancer cell line (SKOV3/CDDP) cell line was higher than that in its parental cell line (SOKV3). Small hairpin RNA (shRNA)-mediated FOXC2 knockdown significantly increased the in vitro and in vive sensitivity of SKOV3/CDDP cells to CDDP by enhancing apoptosis, while upregulation of FOXC2 significantly decreased the in vitro and in vivo sensitivity of SKOV3 cells to CDDP by reducing apoptosis. Furthermore, FOXC2 activates the Akt and MAPK signaling pathways, and then induced the decreased expression of Bcl-2 protein and the increased expression of Bax and cleaved caspase-3 proteins. Conclusions: FOXC2 mediates the CDDP resistance of ovarian cancer cells by activation of the Akt and MAPK signaling pathways, and may be a potential novel therapeutic target for overcoming CDDP resistance in human ovarian cancer.

Download Full-text

WISP2 promotes cell proliferation via targeting ERK and YAP in ovarian cancer cells

10.21203/rs.3.rs-18963/v2 ◽

2020 ◽

Author(s):

Zi-Qing Shi ◽

Zi-Yan Chen ◽

Yao Han ◽

Heng-Yan Zhu ◽

Meng-Dan Lyu ◽

...

Keyword(s):

Ovarian Cancer ◽

Cell Proliferation ◽

Cancer Cells ◽

Signaling Pathway ◽

Inhibitory Effect ◽

Ovarian Cancer Cells ◽

Extracellular Signal ◽

And Migration

Abstract Background: Wnt-inducible signaling pathway protein 2 (WISP2) is a wnt1-induced signaling pathway protein 2. Although studies indicate that WISP2 may promote the development of various tumors, its role in ovarian cancer remains unclear. The objective of the current study was to analyze the effects of WISP2 on the proliferation and migration of ovarian cancer cells in vitro and in vivo.Results: Immunohistochemistry and western blotting indicated that WISP2 was highly expressed in various ovarian cancer tissues and cell lines，but weakly expressed in normal ovary tissue. WISP2 deletion inhibited cell growth, clone formation, and migration of ovarian cancer cells while promoting cell apoptosis and affecting the cell cycle. This growth inhibitory effect caused by WISP2 loss is due to the inhibition of phosphorylated extracellular signal-related kinase (p-ERK)1/2, as well as CCAAT/enhancer-binding protein α (CEBPα) and CEPBβ. In addition, WISP2 deletion also activated the Yes-associated protein (YAP).Conclusion: WISP2 deletion inhibits ovarian cancer cell proliferation by affecting ERK signaling pathways.

Download Full-text

WISP2 promotes cell proliferation via targeting ERK and YAP in ovarian cancer cells

10.21203/rs.3.rs-18963/v1 ◽

2020 ◽

Author(s):

Zi-Qing Shi ◽

Zi-Yan Chen ◽

Yao Han ◽

Heng-Yan Zhu ◽

Meng-Dan Lyu ◽

...

Keyword(s):

Ovarian Cancer ◽

Cell Proliferation ◽

Cancer Cells ◽

Inhibitory Effect ◽

Ovarian Cancer Cells ◽

Growth Inhibitory ◽

Extracellular Signal ◽

And Migration

Abstract Background Wnt inducible signaling protein 2 (WISP2) is a wnt1-induced signaling pathway protein 2. Although studies indicate that WISP2 may promote the development of various tumors, its role in ovarian cancer remains unclear. The objective of the current study was to analyze the effects of WISP2 on proliferation and migration of ovarian cancer cells in vitro and in vivo . Results Immunohistochemistry and western blot results indicated that WISP2 was highly expressed in various ovarian tissues and cell lines. WISP2 deletion inhibited cell growth, clone formation, and migration of ovarian cancer cells. WISP2 deletion promoted cell apoptosis and affected the cell cycle. This growth inhibitory effect caused by WISP2 loss is due to the inhibition of extracellular signal-related kinase (p-ERK)1/2, as well as CEBPα and CEBPβ. In addition, WISP2 deletion also activated the Yes-associated protein (YAP). Conclusion WISP2 deletion inhibits ovarian cancer cell proliferation by affecting ERK signaling pathways.

Download Full-text