Additional file 1: Table S1-S3. of Comparison of different therapeutic strategies for complete hydatidiform mole in women at least 40Â years old: a retrospective cohort study

Comparisons were conducted among groups based on different therapeutic strategies and no significant differences were found. Comparison of clinical characteristics between prophylactic chemotherapy group and expectant group was presented in Table S1. Comparison of clinical characteristics between expectant group and hysterectomy group was presented in Table S2. Comparison of clinical characteristics between prophylactic chemotherapy group and hysterectomy group was presented in Table S3. (DOCX 20 kb

Additional file 2: Table S4-S5. of Comparison of different therapeutic strategies for complete hydatidiform mole in women at least 40Â years old: a retrospective cohort study

Comparisons were conducted between groups of patients with GTN based on therapeutic strategies and no significant differences were noted. Comparison of clinical characteristics between prophylactic chemotherapy group and expectant group was presented in Table S4. Comparison of clinical characteristics between hysterectomy group and expectant group was presented in Table S5. (DOCX 19 kb

miR-375 Mediated Acquired Chemo-Resistance in Cervical Cancer by Facilitating EMT

<div><p>Acquired chemo-resistance is one of the key causal factors in cancer death. Emerging evidences suggest that miRNA and epithelial–mesenchymal transition play critical roles in the chemo-resistance in cancers. Here, we showed the association of paclitaxel-resistance with miR-375 over-expression and epithelial–mesenchymal transition inducement in cervical cancer. Using different cervical cancer cell models, we found that paclitaxel transiently induced up-regulation of miR-375 expression, proliferation inhibition, transition from epithelial to mesenchymal phenotype, and consequently impaired paclitaxel sensitivity. Forced over-expression of miR-375 may suppress Ecadherin expression by a directly targeting pathway, which led to paclitaxel resistance. Contrarily, re-expression of Ecadherin partly reversed epithelial–mesenchymal transition phenotype and miR-375 induced paclitaxel-resistance. Our findings suggest that paclitaxel-induced miR-375 over-expression facilitates epithelial–mesenchymal transition process via directly targeting Ecadherin, proliferation inhibition, and consequently results in chemo-resistance in cervical cancer cells. A reversion of miR-375 or Ecadherin expression may be a novel therapeutic approach for overcoming chemo-resistance in cervical cancer.</p></div

Additional file 1: Table S1. of Autophagy maintains the stemness of ovarian cancer stem cells by FOXA2.

Sequences of primer and shRNA. (DOC 37 kb

Additional file 2: FigureS1. of Autophagy maintains the stemness of ovarian cancer stem cells by FOXA2.

The serum-free condition did not affect basal autophagic flux of spheres. (a) Protein level of LC3B was detected by Western Blotting in 3AO sphere cells. Cells were cultivated in medium for spheres (serum-free) or medium for parental cells (with 10% fetal bovine serum) for 24 h in the presence or absence of BafA1. GAPDH was analyzed as the loading control. (b) The LC3B II/GAPDH ratio was determined by the Quentity One software. (c)The autophagic flux was determined as the ratio between the LC3B II levels with BafA1 and without BafA1 in histograms. Three independent experiments were performed and the results were expressed as the means ± SD, and analyzed using Student’s t-test. (TIFF 402 kb

Paclitaxel inhibits proliferation, induces EMT, and up-regulates miR-375 expression simultaneously in cervical cancer cells.

<p>(<b>a</b>) Visible morphological changes from “cobblestone”-like to “fibroblast”-like cells was observed in SiHa after 72 h paclitaxel treatment. The representative cells with morphological changes were labeled (<b>b</b>) Immunoblotting measured the expression of Ecadherin and other EMT related proteins (vimentin, Ncadherin, and fibronectin) in cervical cancer cells (SiHa and CaSki) under different amounts (0, 5, 10, 20 nM) of paclitaxel treatment. The expression of Ecadherin protein was decreased and the expressions of vimentin, Ncadherin, and fibronectin protein were increased in cells treated with paclitaxel for 72 hours in a dose-responsive manner. All the expressions of the proteins were normalized to ß-actin and the data in bar graphs are presented as mean of triple samples from three independent experiments. All error bars indicated s.e.m. (**p≤0.01, *p≤0.05). (<b>c,</b><b>d</b>) The transient cell proliferation inhibition and morphological changes induced by paclitaxel were observed. The proliferation changes in SiHa and CaSki cells after paclitaxel administration were analyzed by CellTrace CFSE cell proliferation (<b>c</b>) and MTT assay (<b>d</b>) at 24 h, 72 h, 96 h, day 5, day 7, day 14, and day 21, respectively. The proliferation rate of paclitaxel treated SiHa and CaSki cells was significantly reduced at day 7 and restored at day 21 after paclitaxel administration. The survived CaSki cells were restored into normal morphology at day 21 after paclitaxel administration.</p

Forced expression of Ecadherin attenuates the ability miR-375 to mediate EMT and paclitaxel-resistance.

<p>Immunoblotting (a) and MTS (b) analysis of Ecadherin and other EMT related proteins in SiHa with and without miR-375 overexpression after the Ecadherin-expressing or negative lentivirus vector transfection. Data in (a) and (b) were presented as the mean of triplets samples from independent experiments. All error bars indicated s.e.m. (**p≤0.01, *p≤0∶05). (c) Morphological changes in SiHa with and without miR-375 over-expression after the Ecadherin-expressing or negative lentivirus vector transfection. The representative cells with morphological changes had been labeled.</p

TGF-β1 or EGF-β induces EMT and paclitaxel resistance in cervical cells.

<p>(a) Visible morphological changes in SiHa and CaSki under TGF-β1 or EGF-β inducement. (b) MTS analysis of paclitaxel-sensitivity in cervical cancer cells. (c) Immunoblotting analysis of Ecadherin and other EMT related proteins after TGF-β1 or EGF-β induction. (d) miR-375 expression in SiHa and CaSki under TGF-β1 or EGF-β inducement. Data in b–d were presented as mean of triplets samples from independent experiments. All error bars indicated s.e.m. (**p≤0.01, *p≤0.05).</p

A Well-Circumscribed Border with Peripheral Doppler Signal in Sonographic Image Distinguishes Epithelioid Trophoblastic Tumor from Other Gestational Trophoblastic Neoplasms

<div><p>As epithelioid trophoblastic tumor (ETT) shares similar clinical features with other gestational trophoblastic neoplasms (GTNs), it is likely to be clinically misdiagnosed and subsequently treated in an improper way. This study aimed to identify the sonographic features of ETT that are distinct from other GTNs, including placental site trophoblastic tumor (PSTT) and invasive mole/choriocarcinoma (IM/CC). Here, we retrospectively analyzed ultrasound images of 12 patients with ETT in comparison with those of 21 patients with PSTT and 24 patients with IM/CC. The results showed that maximal diameter and hemodynamic parameters were not significantly different among ETT, PSTT and IM/CC (P>0.05). However, a well-circumscribed border with hypoechogenic halo was identified in the gray-scale sonogram in all 12 cases of ETT, while only in 1 out of 21 cases of PSTT and 1 out of 16 cases of IM/CC (P<0.001 for ETT vs. PSTT or IM/CC). Moreover, a peripheral pattern of Doppler signals was observed in 11 out of 12 ETT lesions, showing relatively more Doppler signal spots around the tumor border than within the boundary, while a non-peripheral pattern of Doppler signals in all 21 PSTT cases and 14 out of 16 IM/CC cases: with minimal, moderate or remarkable signal spots within the tumor, but not along the tumor (P<0.001 for ETT vs. PSTT or IM/CC). These distinct sonographic features of ETT correlated with histopathologic observations, such as expansive growth pattern and vascular morphology. Thus, we draw the conclusions that the well-circumscribed border with peripheral Doppler signal may serve as a reliable sonographic feature to discriminate ETT from other types of GTNs. With further validation in a larger patient set in our ongoing multi-center study, this finding will be potentially developed into a non-invasive pre-operative GTN subtyping method for ETT.</p></div

Additional file 3: Figure S2 . of Autophagy maintains the stemness of ovarian cancer stem cells by FOXA2.

Autophagic vesicles were visualized by transmission electron microscopy. Autophagosome and autolysosome vesicles were visualized by transmission electron microcopy in 3AO and sphere cells treated with BafA1 (50 nM, 4 h) or not. The typical images of autophagic vesicles (red arrows) were shown at high magnification. (TIFF 6804 kb