scholarly journals Minireview: Animal Models and Mechanisms of Ovarian Cancer Development

Endocrinology ◽  
2012 ◽  
Vol 153 (4) ◽  
pp. 1585-1592 ◽  
Author(s):  
Lisa K. Mullany ◽  
JoAnne S. Richards
Keyword(s):  
Ovarian Cancer ◽  
Mouse Models ◽  
Cell Transformation ◽  
Tumor Formation ◽  
Surface Epithelial Cell ◽  
Molecular Events ◽  
Ovarian Surface Epithelial ◽  
Control Tumor ◽  
Underlying Mechanisms ◽  
And Control

Ovarian cancer in women is a complex and deadly disease, where the molecular events that initiate and control tumor formation remain poorly defined. Therefore, mouse models provide one approach for determining the mechanisms by which specific oncogenic factors cause ovarian surface epithelial cell and granulosa cell transformation. This minireview summarizes the phenotypes of current mouse models that have been generated and some of the underlying mechanisms they have provided.

Morin Inhibits Ovarian Cancer Growth through the Inhibition of NF-κB Signaling Pathway

2020 ◽  
Vol 19 (18) ◽  
pp. 2243-2250 ◽  
Author(s):  
Meimei Xu ◽  
Yan Zhang
Keyword(s):  
Ovarian Cancer ◽  
Colony Formation ◽  
Cultured Cells ◽  
Tumor Formation ◽  
Cancer Growth ◽  
Ovarian Cancer Cells ◽  
Therapeutic Drugs ◽  
Underlying Mechanisms

Background &Objective: Ovarian cancer has the highest mortality in gynecological tumors without effective therapeutic drugs as a result of drug-resistance for long-term utilization. Morin has been reported to possess powerful anti-tumor effects in several cancers. The present study aims to investigate whether Morin could influence ovarian cancer growth and underlying mechanisms. Methods: Morin was administered to cultured cells in vitro and formed tumors in vivo. MTT and colony formation assays were performed to explore the effects of Morin on the proliferation and colony formation of OVCAR3 and SKOV3 ovarian cancer cells. Western blot, RT-qPCR, immunofluorescence as well as ELISA were used to detect protein and mRNA expression of target factors. Tumor formation was performed to investigate tumorigenesis ability of drug-treated cells. Results: The proliferation and colony size of OVCAR3 and SKOV3 were significantly decreased after Morin administration. The expression of NF-κB and inflammatory cytokine IL6/8 induced by TNF-α can be inhibited by Morin. Furthermore, Morin inhibited the volume of ovarian cancer tumors in nude mice. Conclusion: Morin effectively alleviates ovarian cancer growth, inhibits the inflammatory response, and reduces tumor size via modulation of the NF-κB pathway.

scholarly journals miR-200b/200a/429 Cluster Stimulates Ovarian Cancer Development by Targeting ING5

2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
Wei Guan ◽  
Huiling Cui ◽  
Ping Huang ◽  
Wan Joo Chun ◽  
Jin-Won Lee ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Transformation ◽  
Soft Agar ◽  
Tumor Formation ◽  
Cancer Development ◽  
Epithelial Cell Line ◽  
Ovarian Cancer Cell Lines ◽  
Gynaecological Malignancy ◽  
Tumor Tissues ◽  
Ovarian Epithelial Cell

Ovarian cancer is the second most common gynaecological malignancy, and microRNAs (miRNAs) play important role in the cancer development. Here, we found that the level of miR-200b/200a/429 was significantly increased in serum and tumor tissues of patients with stage-I ovarian cancer. Consistent with these results, we detected increased expression levels of miR-200b/200a/429 in ovarian cancer cell lines compared with the human nontumorigenic ovarian epithelial cell line T80. The overexpression of miR-200b/200a/429 in T80 cells stimulated proliferation and caused their growth in soft agar and tumor formation in nude mice. Furthermore, we determined that miR-200b/200a/429 targets inhibitor of growth family 5 (ING5) and that the overexpression of ING5 can block miR-200b/200a/429-induced T80 cell transformation and tumorigenesis. Our findings suggest that miR-200b/200a/429 may be a useful biomarker for the early detection of ovarian cancer and that miR-200b/200a/429 significantly contributes to ovarian cancer development through ING5.

scholarly journals The Formation and Control of Ice Crystal and Its Impact on the Quality of Frozen Aquatic Products: A Review

Crystals ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 68
Author(s):  
Mingtang Tan ◽  
Jun Mei ◽  
Jing Xie
Keyword(s):  
Product Quality ◽  
Freezing Point ◽  
Ice Crystals ◽  
Affecting Factors ◽  
Frozen Food ◽  
Aquatic Products ◽  
Size Number ◽  
Underlying Mechanisms ◽  
And Control ◽  
Ice Crystallization

Although freezing has been used to delay the deterioration of product quality and extend its shelf life, the formation of ice crystals inevitably destroys product quality. This comprehensive review describes detailed information on the effects of ice crystals on aquatic products during freezing storage. The affecting factors (including nucleation temperature, freezing point, freezing rate, and temperature fluctuation) on the size, number, distribution, and shape of ice crystals are also elaborated in detail. Meanwhile, the corresponding technologies to control ice crystals have been developed based on these affecting factors to control the formation of ice crystals by inhibiting or inducing ice crystallization. In addition, the effects of ice crystals on the water, texture, and protein of aquatic products are comprehensively discussed, and the paper tries to describe their underlying mechanisms. This review can provide an understanding of ice crystallization in the aquatic products during freezing and contribute more clues for maintaining frozen food quality.

Telomere Length and Arsenic: Improving Animal Models of Toxicity by Choosing Mice With Shorter Telomeres

2021 ◽  
Vol 40 (3) ◽  
pp. 211-217
Author(s):  
Brayden Whitlock
Keyword(s):  
Animal Models ◽  
Telomere Length ◽  
Mouse Models ◽  
Arsenic Exposure ◽  
Tumor Formation ◽  
The Body ◽  
Cancer Resistance ◽  
Selective Pressures ◽  
Toxicity Monitoring ◽  
In Captivity

Arsenic is both a chemotherapeutic drug and an environmental toxicant that affects hundreds of millions of people each year. Arsenic exposure in drinking water has been called the worst poisoning in human history. How arsenic is handled in the body is frequently studied using rodent models to investigate how arsenic both causes and treats disease. These models, used in a variety of arsenic-related testing, from tumor formation to drug toxicity monitoring, have virtually always been developed from animals with telomeres that are unnaturally long, likely because of accidental artificial selective pressures. Mice that have been bred in captivity in laboratory conditions, often for over 100 years, are the standard in creating animal models for this research. Using these mice introduces challenges to any work that can be affected by the length of telomeres and the related capacities for tissue repair and cancer resistance. However, arsenic research is particularly susceptible to the misuse of such animal models due to the multiple and various interactions between arsenic and telomeres. Researchers in the field commonly find mouse models and humans behaving very differently upon exposure to acute and chronic arsenic, including drug therapies which seem safe in mice but are toxic in humans. Here, some complexities and apparent contradictions of the arsenic carcinogenicity and toxicity research are reconciled by an explanatory model that involves telomere length explained by the evolutionary pressures in laboratory mice. A low-risk hypothesis is proposed which has the power to determine whether researchers can easily develop more powerful and accurate mouse models by simply avoiding mouse lineages that are very old and have strangely long telomeres. Swapping in newer mouse lineages for the older, long-telomere mice may vastly improve our ability to research arsenic toxicity with virtually no increase in cost or difficulty of research.

scholarly journals Gene therapy for ovarian cancer using carbonyl reductase 1 DNA with a polyamidoamine dendrimer in mouse models

2015 ◽  
Vol 23 (1) ◽  
pp. 24-28 ◽  
Author(s):  
A Kobayashi ◽  
Y Yokoyama ◽  
Y Osawa ◽  
R Miura ◽  
H Mizunuma
Keyword(s):  
Ovarian Cancer ◽  
Gene Therapy ◽  
Mouse Models ◽  
Carbonyl Reductase ◽  
Polyamidoamine Dendrimer
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