Ovarian cancer

Jayson, Gordon C; Kohn, Elise C.; Kitchener, Henry C; Ledermann, Jonathan A.

doi:10.1016/s0140-6736(13)62146-7

Cited by 1,626 publications

(1,483 citation statements)

References 121 publications

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“…Despite many advances in surgical techniques and chemotherapy during the past decades, the 5-year survival rates remain as low as 35% and 20% for stages III and IV, respectively (5-7). Similar to other malignancies, ovarian cancer is characterized by rapid proliferation, invasion, and the formation of regional/distant metastasis (8). Thus, a deeper understanding of the mechanisms underlying the initiation and progression of ovarian cancer is urgently needed.…”

Section: Introductionmentioning

confidence: 99%

Frequent Loss of NISCH Promotes Tumor Proliferation and Invasion in Ovarian Cancer via Inhibiting the FAK Signal Pathway

Dong

et al. 2015

Molecular Cancer Therapeutics

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NISCH encodes the imidazoline receptor Nischarin and is a known tumor suppressor in many human malignancies; however, its roles in ovarian cancer are still largely unknown. Here, we aim to investigate the biologic functions of NISCH in ovarian cancer. We found that NISCH was significantly downregulated, which correlated considerably with advanced tumor stage, poor differentiation, lymph node metastasis, and the serous/mucinous subtypes in a panel of ovarian cancer tissues. Moreover, NISCH gene silencing was mainly the product of promoter hypermethylation, which could be reversed by treatment with 5-aza-dC. In vitro, NISCH overexpression suppressed cell proliferation and colony formation by hindering cell-cycle progression, whereas the opposite was observed in NISCH knockdown counterparts. In vivo, abundant NISCH expression hindered the growth of HO8910 xenografts, whereas NISCH knockdown accelerated the growth of SKOV3 xenografts. In addition, NISCH significantly attenuated cell invasion by inhibiting the phosphorylation of FAK and ERK, which could be neutralized by PF-562271 (a FAK/Pyk2 inhibitor). Accordingly, NISCH knockdown xenografts exhibited increased peritoneal/pelvic metastases that were not present in counterparts treated with PF-562271. Furthermore, NISCH expression in primary ovarian cancer cells predicted a cellular resistance to PF-562271. In conclusion, we showed that NISCH was frequently silenced by promoter hypermethylation in human ovarian cancer. NISCH manipulated cellular proliferation and invasion by arresting cell cycle and inhibiting the FAK signal. Our findings revealed the biologic functions of NISCH in ovarian cancer, and might be useful for treating patients with aberrant expression of NISCH.

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Section: Introductionmentioning

confidence: 99%

Frequent Loss of NISCH Promotes Tumor Proliferation and Invasion in Ovarian Cancer via Inhibiting the FAK Signal Pathway

Dong

et al. 2015

Molecular Cancer Therapeutics

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“…Ovarian cancer is the most lethal type of gynecological cancer (21). Although the international standard of care is surgery supplemented with paclitaxel and platinum based chemotherapy, the majority of patients will relapse in one to two years due to chemoresistance (22).…”

Section: Discussionmentioning

confidence: 99%

“…Ovarian cancer is the fifth most common type of disease in females, and in the United States in 2014 there were an estimated 21,290 new cases and 14,180 mortalities due to ovarian cancer (1). Although the 5-year survival rate of females with ovarian cancer has improved, it is only ~20% (2).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-20a contributes to cisplatin-resistance and migration of OVCAR3 ovarian cancer cell line

Liu

Han

et al. 2017

Oncology Letters

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Abstract. MicroRNAs (miRs) have been reported to be associated with the development of numerous types of cancer. However, the function of miRs in human ovarian carcinoma chemoresistance remains largely undefined. In the present study, cell chemotherapy combined with a Cell Counting Kit-8 assay demonstrated that miR-20a performed important roles in ovarian cancer cells chemoresistance. Flow cytometry, cellular proliferation assays and Transwell assays results revealed that the proliferation and migration rates of OVCAR3/DDP cells were increased in comparison with parental cells. Western blot analysis results suggested that epithelial-mesenchymal transition (EMT) activated by miR-20a contributed to OVCAR3/DDP cell migration. The present study highlighted the importance of miR-20a in regulating the chemoresistant properties of OVCAR3 cells and promoting cisplatin-resistant cell migration by activating EMT. The results of present study may therefore provide novel insights into reversing the chemoresistance of ovarian cancer and improving its treatment.

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“…Due to late presentation, in many parts of the world it remains the most lethal gynecological cancer [2]. In 2004, a new model description of this disease was proposed that combined both histopathological and molecular features and which classified epithelial ovarian cancers into two broad categories designated Type I and Type II tumors [3].…”

Section: Editorialmentioning

confidence: 99%

“…These genetic abnormalities can help define the response of cancers to specific treatments, hence the widespread use of platinum containing drugs which have useful efficacy particularly in type II disease. Platinum containing regimens are the standard of care in first line treatment of this disease [2]. However, resistance frequently develops and there is an ongoing need for improved second line options.…”

Section: Editorialmentioning

confidence: 99%