scholarly journals 1α,25‑Dihydroxyvitamin�D3 restrains stem cell‑like properties of ovarian cancer cells by enhancing vitamin�D receptor and suppressing CD44

2019 ◽  
Author(s):  
Mintao Ji ◽  
Lizhi Liu ◽  
Yongfeng Hou ◽  
Bingyan Li
Keyword(s):  
Ovarian Cancer ◽  
Vitamin D ◽  
Stem Cell ◽  
Cancer Cells ◽  
Vitamin D Receptor ◽  
Ovarian Cancer Cells ◽  
Dihydroxyvitamin D3

Role of Rb Family in Vitamin D Receptor-Mediated Anti-Tumor Effects in Ovarian Cancer Cells.

2010 ◽  
pp. P1-9-P1-9
Author(s):  
J Tang ◽  
P Li ◽  
AKW Tse ◽  
SV Nicosia ◽  
X Zhang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Vitamin D ◽  
Cancer Cells ◽  
Vitamin D Receptor ◽  
Ovarian Cancer Cells

scholarly journals Vitamin D Analogs Regulate the Vitamin D System and Cell Viability in Ovarian Cancer Cells

2021 ◽  
Vol 23 (1) ◽  
pp. 172
Author(s):  
Karina Piatek ◽  
Andrzej Kutner ◽  
Dan Cacsire Castillo-Tong ◽  
Teresa Manhardt ◽  
Nadja Kupper ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Vitamin D ◽  
Cell Viability ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Cell Line ◽  
Cell Lines ◽  
Ovarian Cancer Cells ◽  
Dihydroxyvitamin D3 ◽  
Vitamin D Analogs

Background: Ovarian cancer (OC) is one of the most lethal cancers in women. The active form of vitamin D3, 1,25-dihydroxyvitamin D3 (1,25D3, calcitriol) has anticancer activity in several cancers, including ovarian cancer, but the required pharmacological doses may cause hypercalcemia. We hypothesized that newly developed, low calcemic, vitamin D analogs (an1,25Ds) may be used as anticancer agents instead of calcitriol in ovarian cancer cells. Methods: We used two patient-derived high-grade serous ovarian cancer (HGSOC) cell lines with low (13781) and high (14433) mRNA expression levels of the gene encoding 1,25-dihydroxyvitamin D3 24-hydroxylase CYP24A1, one of the main target genes of calcitriol. We tested the effect of calcitriol and four structurally related series of an1,25Ds (PRI-1906, PRI-1907, PRI-5201, PRI-5202) on cell number, viability, the expression of CYP24A1, and the vitamin D receptor (VDR). Results: CYP24A1 mRNA expression increased in a concentration-dependent manner after treatment with all compounds. In both cell lines, after 4 h, PRI-5202 was the most potent analog (in 13781 cells: EC50 = 2.98 ± 1.10 nmol/L, in 14433 cells: EC50 = 0.92 ± 0.20 nmol/L), while PRI-1907 was the least active one (in 13781 cells: EC50 = n/d, in 14433 cells: EC50 = n/d). This difference among the analogs disappeared after 5 days of treatment. The 13781 cells were more sensitive to the an1,25Ds compared with 14433 cells. The an1,25Ds increased nuclear VDR levels and reduced cell viability, but only in the 13781 cell line. Conclusions: The an1,25Ds had different potencies in the HGSOC cell lines and their efficacy in increasing CYP24A1 expression was cell line- and chemical structure-dependent. Therefore, choosing sensitive cancer cell lines and further optimization of the analogs’ structure might lead to new treatment options against ovarian cancer.

scholarly journals HER2 decreases drug sensitivity of ovarian cancer cells via inducing stem cell-like property in an NFκB-dependent way

2019 ◽  
Vol 39 (3) ◽  
Author(s):  
Wenxiang Wang ◽  
Yuxia Gao ◽  
Jing Hai ◽  
Jing Yang ◽  
Shufeng Duan
Keyword(s):  
Ovarian Cancer ◽  
Stem Cells ◽  
Stem Cell ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Drug Sensitivity ◽  
Ovarian Cancer Cells ◽  
Her2 Overexpression ◽  
Her2 Positive ◽  
Ovarian Cancer Stem Cells

Abstract Increasing evidence shows that cancer stem cells are responsible for drug resistance and relapse of tumors. In breast cancer, human epidermal growth factor receptor 2 (HER2) induces Herceptin resistance by inducing cancer stem cells. In the present study, we explored the effect of HER2 on cancer stem cells induction and drug sensitivity of ovarian cancer cell lines. First, we found that HER2 overexpression (HER2 OE) induced, while HER2 knockdown (HER2 KD) decreased CD44+/CD24− population. Consistently, HER2 expression was closely correlated with the sphere formation efficiency (SFE) of ovarian cancer cells. Second, we found that NFκB inhibition by specific inhibitor JSH23 or siRNA targetting subunit p65 dramatically impaired the induction of ovarian cancer stem cells by HER2, indicating that NFκB mediated HER2-induced ovarian cancer stem cells. Third, we found that HER2 KD significantly attenuated the tumorigenicity of ovarian cancer cells. Further, we found that HER2 inhibition increased drastically the sensitivity of ovarian cancer cells to doxorubicin (DOX) or paclitaxel (PTX). Finally, we examined the correlation between HER2 status and stem cell-related genes expression in human ovarian tumor tissues, and found that expressions of OCT4, COX2, and Nanog were higher in HER2 positive tumors than in HER2 negative tumors. Consistently, the 5-year tumor-free survival rate of HER2 positive patients was dramatically lower than HER2 negative patients. Taken together, our data indicate that HER2 decreases drug sensitivity of ovarian cancer cells via inducing stem cell-like property.

scholarly journals Autophagy Is Indispensable for the Self-Renewal and Quiescence of Ovarian Cancer Spheroid Cells with Stem Cell-Like Properties

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Qian Wang ◽  
Shixia Bu ◽  
Dedong Xin ◽  
Boning Li ◽  
Lan Wang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Stem Cell ◽  
Cancer Cells ◽  
Feedback Regulation ◽  
Soft Agar ◽  
The Self ◽  
Ovarian Cancer Cells ◽  
Quiescent State ◽  
Bafilomycin A1 ◽  
Self Renewal

Epithelial ovarian cancer has the highest mortality rate of all gynecologic cancers. Cancer stem cells are considered to be the initiating cells of tumors. It is known that spheroid culture promotes ovarian cancer cells to acquire stem cell characteristics and to become stem cell-like. But the mechanisms remain largely unclear. Our data show that autophagy is sustainably activated in ovarian cancer spheroid cells. Inhibition of autophagy by knockdown of ATG5 abolishes the self-renewal ability of ovarian cancer spheroid cells. Knockdown of ATG5 prevents ovarian cancer spheroid cells to enter quiescent state. Autophagy is critical for quiescent ovarian cancer spheroid cells to reenter the cell cycle because rapamycin can promote quiescent ovarian cancer spheroid cells to form colonies on soft agar and knockdown of ATG5 can arrest ovarian cancer cells in G0/G1. Autophagy and NRF2 form a positive feedback regulation loop to regulate reactive oxygen species (ROS) levels in ovarian cancer spheroid cells. The optimal ROS level, neither too high nor too low, facilitates the self-renewal marker, NOTCH1, to reach to the highest level. Bafilomycin A1 can impair the self-renewal of ovarian cancer spheroid cells by disturbing ROS levels.

scholarly journals MUC4 stabilizes HER2 expression and maintains the cancer stem cell population in ovarian cancer cells

2011 ◽  
Vol 4 (1) ◽  
pp. 7 ◽  
Author(s):  
Moorthy P Ponnusamy ◽  
Parthasarathy Seshacharyulu ◽  
ArokiaPriyanka Vaz ◽  
Parama Dey ◽  
Surinder K Batra
Keyword(s):  
Ovarian Cancer ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Cancer Cells ◽  
Cell Population ◽  
Stem Cell Population ◽  
Ovarian Cancer Cells ◽  
Her2 Expression ◽  
Cancer Stem Cell Population

scholarly journals Stem cell characteristics of dormant cells and cisplatin-induced effects on the stemness of epithelial ovarian cancer cells

2014 ◽  
Vol 10 (5) ◽  
pp. 2495-2504 ◽  
Author(s):  
NAN ZHOU ◽  
XIAOHUA WU ◽  
BO YANG ◽  
XU YANG ◽  
DINGDING ZHANG ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Stem Cell ◽  
Epithelial Ovarian Cancer ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Dormant Cells
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