SNHG5 enhances Paclitaxel sensitivity of ovarian cancer cells through sponging miR-23a.

BACKGROUND: Ovarian cancer is one of the most lethal gynecological malignancies throughout the world. Long non-coding RNA (lncRNA) small nucleolar RNA host gene 5 (SNHG5) has been reported to play an important role in several human cancers, but the role of SNHG5 in the chemoresistance of ovarian cancer cells is yet elusive. METHOD: The expression of SNHG5 and miR-23a were determined by quantitative reverse transcriptase polymerase chain reaction. The effects of SNHG5 and miR-23a on the sensitivity of ovarian cancer cells to paclitaxel (PTX) were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and flow cytometry. The subcellular location of SNHG5 was detected by a subcellular fraction assay. The interaction between SNHG5 and miR-23a was determined by luciferase reporter assay and RNA immunoprecipitation assay. RESULTS: The expression of SNHG5 was downregulated in the cancer genome atlas cohort. Similarly, decreased expression of SNHG5 was observed in ovarian cancer tissues. Moreover, lower expression of SNHG5 was found in PTX-resistant ovarian cancer patients as well as PTX-resistant ovarian cancer cell lines. Downregulation of SNHG5 expression was indicative of poor prognosis in patients with ovarian cancer. Overexpression of SNHG5 enhanced the sensitivity of SKOV3/PTX and HeyA-8/PTX cells to PTX in vitro and enhanced PTX sensitivity in tumors in vivo. Interestingly, an inverse correlation between SNHG5 and miR-23a expression was found in ovarian cancer tissues and SNHG5 functioned as a decoy for miR-23a. Silencing of miR-23a overcame the resistance of SKOV3/PTX and HeyA-8/PTX cells to PTX. More importantly, miR-23a overexpression could reverse the inductive effect of SNHG5 overexpression on PTX sensitivity of ovarian cancer cells. CONCLUSION: SNHG5 enhanced the sensitivity of ovarian cancer cells to PTX through sponging miR-23a, providing a new mechanism of chemoresistance in ovarian cancer.

Analyzing the clinical significance of postoperative methotrexate in the management of early abdominal pregnancy: analysis of 10 cases.

OBJECTIVES: To assess the clinical value and treatment outcomes of postoperative methotrexate (MTX) therapy in themanagement of early abdominal pregnancy. MATERIAL AND METHODS: We retrospectively analyzed ten (10) cases of early abdominal pregnancy at our hospital between7th August, 2006 and 20th April, 2017. RESULTS: Out of the ten (10) cases identified, six (6) patients and four (4) patients underwent surgery (laparotomy or laparoscopy)only and surgery (laparotomy or laparoscopy) plus IM 50 mg/m2 methotrexate (MTX) within 24 hours of surgeryrespectively. The gestation age and serum ß-HcG levels were significantly lower (p < 0.05, 6.0 ± 1.82 and 8073.2 ± 9561.0)in the surgery plus MTX group in comparison to (7.33 ± 3.61 and 15625 ± 21275.2) for the surgery only group. Ultrasoundimaging findings reported extra uterine pregnancy in all cases and diagnostic surgery was necessary to locate precise siteof implantation to plan further treatment. Days of hospitalization were shorter in the surgery + MTX group than in thesurgery only group (3.00 ± 0.816 versus 5.66 ± 2.80). CONCLUSIONS: Earliness in diagnosis coupled with the appropriate (methotrexate) MTX regime could help prevent unwantedcomplications that could arise from delayed or misdiagnosis.

Maternal high-fat diet impairs follicular development of offspring through intraovarian kisspeptin/GPR54 system.

BACKGROUND: Excessive gestational weight gain (GWG), which is associated with adverse long-term effects on the health of the offspring, has become a major clinical problem. Accumulating evidence indicates that the ovary kisspeptin/GPR54 system directly participates in a series of physiological activities. We used a model of high-fat diet (HFD) during gestational to investigate offspring's ovarian function and whether kisspeptin/GPR54 system is involved. METHODS: After introducing the male and confirmation of mating by checking a vaginal sperm plug, female rats were randomized into two groups: control diet called NCD group and high-fat diet called HFD group. After birth, all rats were changed into a control diet and litter size was adjusted to 12 pups per litter. Ovaries were collected for assessment at postnatal day (PND) 4 and PND 30. The timing of vaginal opening was recorded, and the estrous cyclicity was monitored for 2 consecutive weeks immediately. Primary granulosa cells and ovaries which were taken from PND 4 were collected for determination of the direct effect of kisspeptin-10 (kp-10) in vitro. RESULTS: Neonatal rats exposed to HFD during gestation had a lower number of secondary follicles in the ovary. The expression of follicle-stimulating hormone receptor (FSHR) and kisspeptin was not altered. At prepuberty, the number of antral follicles and preovulatory follicles was elevated with decreased type III follicles in the HFD group. While the expression of ovulation-related genes was decreased, the expression levels of follicular growth-related genes and steroidogenesis synthesis related genes were elevated. A significant increase in kiss1 mRNA and kisspeptin protein was detected without changes in kiss1r mRNA and GPR54. Maternal high-fat diet during gestation resulted in a significant advanced puberty onset and an irregular estrous cycle in offspring rats. In addition, the administration of kp-10 produced an increase in viability of primary granulosa cells and enlarged the size of oocytes. CONCLUSIONS: HFD exposure during maternal gestation had a long-term effect on reproductive function in the offspring and the increased ovarian kisspeptin/GPR54 system might be involved.