Ovarian cancer presents therapeutic challenges due to its typically late detection, aggressive metastasis, and therapeutic resistance. The transcription factor Krüppel-like factor 4 (KLF4) has been implicated in human cancers as a tumor suppressor or oncogene, although its role depends greatly on the cellular context. The role of KLF4 in ovarian cancer has not been elucidated in mechanistic detail. In this study, we investigated the role of KLF4 in ovarian cancer cells by transducing the ovarian cancer cell lines SKOV3 and OVCAR3 with a doxycycline-inducible KLF4 lentiviral vector. Overexpression of KLF4 reduced cell proliferation, migration, and invasion. The epithelial cell marker gene E-cadherin was significantly upregulated, whereas the mesenchymal cell marker genes vimentin, twist1and snail2 (slug) were downregulated in both KLF4-expressing SKOV3 and OVCAR3 cells. KLF4 inhibited the transforming growth factor β (TGFβ)-induced epithelial to mesenchymal transition (EMT) in ovarian cancer cells. Taken together, our data demonstrate that KLF4 functions as a tumor suppressor gene in ovarian cancer cells by inhibiting TGFβ-induced EMT.

Choline chloride-based deep eutectic solvents (DESs), composed of alcohols, organic acids and saccharides, were used as green solvents for extraction of major catechins inCamellia sinensisleaves.

We investigated the effects of two strains (SUO-1 and FUK) of the dinoflagellate Karenia mikimotoi on the rotifer Brachionus plicatilis. The SUO-1 strain was highly toxic to rotifers, whereas the FUK strain was less toxic. After 10-hour incubations, the survivorship of rotifers exposed to SUO-1 and FUK was 20% and 95%, respectively.Both the cell-free culture supernatant and the ruptured cell suspension prepared from these strains were not toxic to rotifers. Furthermore, when direct contact between K. mikimotoi and rotifers was interrupted with a cell-impermeable membrane (3-m pores), the toxicity of both the SUO-1 and FUK strains of K. mikimotoi to rotifers were completely inhibited even after a 24-h exposure. Cell suspensions of SUO-1 showed hemolytic activity toward horse erythrocytes, but the FUK strain did not. The cell-free supernatant and the ruptured cell suspension of SUO-1 showed no significant hemolytic activity. These results suggest that this highly toxic strain of K. mikimotoi causes lethality in rotifers by direct contact in which live cell-mediated hemolytic activity might be a contributing factor.

Objective Ovarian cancer is a gynecological malignancy that has a high mortality rate in women due to metastatic progression and recurrence. miRNAs are small, endogenous, noncoding RNAs that function as tumor suppressors or oncogenes in various human cancers by selectively suppressing the expression of target genes. The objective of this study is to investigate the role of miR-203 in ovarian cancer. Methods miR-203 was expressed in ovarian cancer SKOV3 and OVCAR3 cells using lentiviral vector and cell proliferation, migration, invasion were examined using MTT, transwell and Matrigel assays, respectively. Tumor growth was examined using Xenograft mouse model. Results miR-203 expression was downregulated, whereas expression of its target gene Snai2 was upregulated in human ovarian serous carcinoma tissue as compared to normal ovaries. In addition, high miR-203 expression was associated with long-term survival rate of ovarian cancer patients. miR-203 overexpression inhibited cell proliferation, migration, and invasion of SKOV3 and OVCAR3 ovarian cancer cells. Furthermore, miR-203 overexpression inhibited the epithelial to mesenchymal transition (EMT) in ovarian cancer cells. Silencing Snai2 with lentiviral short hairpin (sh) RNA mimics miR-203-mediated inhibition of EMT and tumor cell invasion. Xenografts of miR-203-overexpressing ovarian cancer cells in immunodeficient mice exhibited a significantly reduced tumor growth. Conclusion miR-203 functions as a tumor suppressor by down regulating Snai2 in ovarian cancer.

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