ABSTRACT
ILF3 antisense RNA 1 (ILF3-AS1), the antisense RNA of interleukin enhancer binding factor 3 (ILF3), is a lncRNA located on chromosome 19p13. 2. ILF3-AS1 played a key role in the occurrence and development of a variety of tumors, but its role in cervical cancer had not been explored yet. Therefore, we first used TCGA and GTEx database to conduct bioinformatics analysis. The results suggested that ILF3-AS1 was down-regulated in cervical cancer tissues (P < 0. 001) and was associated with a good prognosis (P = 0. 045). The qRT-PCR experiment showed that expression of ILF3-AS1 in cervical cancer tissues and SiHa, HeLa, CaSki cervical cancer cell lines was lower than that in control groups. Subsequently, overexpressing of ILF3-AS1 can significantly inhibit the cancer cell viability and stimulate apoptosis (P<0. 001). Analysis using the Star Base v3. 0 database suggested that ILF3-AS1 can target miR-130a-3p; while miR-130a-3p may target PTEN. The qRT-PCR test showed that the expression of miR-130a-3p in cervical cancer was significantly higher than that in normal cervical tissues (P < 0. 01). The results of the luciferase reporter assay showed that ILF3-AS1 can specifically bind to miR-130a-3p (P<0. 01). After overexpression of ILF3-AS1 in HeLa cells, the expression of miR-130a-3p was significantly down-regulated (P < 0. 01). Co-transfection with pcDNA3. 1-ILF3-AS1 and miR-130a-3p mimics, the inhibitory effect of LF3-AS1 on cell proliferation can partially be reversed (P<0. 001). After HeLa cells overexpressed ILF3-AS1, the expression of phosphatase and tensin homolog deleted on chromosome ten (PTEN) mRNA (P < 0. 001) and proteins (P < 0. 001) significantly increased; when miR-130a-3p mimics was simultaneously used in HeLa cell, the increased expression of PTEN mRNA (P <0. 001) and proteins (P < 0. 001) was notably inhibited. In summary, ILF3-AS1 inhibited the proliferation of cervical cancer cells by sponging miR-130a-3p to regulate the expression of PTEN.
ABSTRACT
Objective To find out and clarify the causes and the pathogens of vulvovagmitis in childhood girls, to determine the clinical treatment. Methods There were 345 cases of childhood girls .ranged from 18 days to 12 years, with symptoms of vulvovagini tis, and their vaginal secretions were examined by routine smear for cleaning degree, trichomonas , Candida and clue cells, gram-stain for neisseria gonorrhoeae, culture for bacteria, mycoplasma urealytium, mycoplasma hominis and chlamydia trachomatis. Results One hundred and nine pathogens were detected(31.6% of the whole cases ), including specific pathogen 70 cases(20. 3% )and non-specif ic pathogen 32 cases(9.3%). Gardnerella was detected most frequently in specific pathogen while enteric bacilli was detected most frequently in non-specific pathogen. Conclusions Non-specific vulvovaginitis is the most frequent cause in childhood vulvovagimtis, and bacterial vaginosis is the mast frequent in specific infection. Symptomatic treatment is effective, but antibiotic treatment should be based on pathogenic findings of vaginal secretions.