Previous studies have revealed that dysregulation of long non-coding RNAs (lncRNAs) can facilitate carcinogenesis. This study aims to investigate the biological role of a certain lncRNA in cutaneous squamous cell carcinoma (CSCC). According to the data of TCGA database, high expression of long intergenic non-protein coding RNA 1048 (LINC01048) is an unfavorable prognostic factor for patients with CSCC. Therefore, we further detected the expression pattern of LINC01048 in CSCC tissues. Obviously, LINC01048 was expressed higher in the CSCC tissues and recurrence tissues compared with that in adjacent normal tissues and non-recurrence tissues. Furthermore, Kaplan–Meier analysis revealed the negative correlation between LINC01048 expression and the overall survival and disease-free survival of CSCC patients. Subsequently, functional assays were conducted to prove the inhibitory effect of silenced LINC01048 on the proliferation and apoptosis of CSCC cells. Mechanistically, LINC01048 was proved to be transcriptionally activated by USF1. Pathway analysis and western blot assay showed that knockdown of LINC01048 led to the activation of Hippo pathway. Moreover, YAP1, a Hippo pathway factor, was positively regulated by LINC01048. Further mechanism investigation revealed that LINC01048 increased the binding of TAF15 to YAP1 promoter to transcriptionally activate YAP1 in CSCC cells. Finally, rescue assays demonstrated that YAP1 involved in LINC01048-mediated CSCC cell proliferation and apoptosis. In conclusion, USF1-induced upregulation of LINC01048 promoted CSCC by interacting with TAF15 to upregulate YAP1.

BackgroundThe recent emergence of azithromycin-resistant (AZM-R) N. gonorrhoeae isolates that have coevolved decreased susceptibility to extended-spectrum cephalosporins has caused great concern. Here we investigated the prevalence of decreased susceptibility to ceftriaxone (CROD) in AZM-R isolates and genetically characterized AZM-R isolates in Guangzhou, China from 2009 to 2013.MethodsThe minimum inhibitory concentration (MIC) of AZM and ceftriaxone was determined using an agar-dilution method. All AZM-R isolates were screened for mutations in 23S rRNA, mtrR and penA genes and genotyped using N. gonorrhoeae multi-antigen sequence typing (NG-MAST).ResultsOf the 485 identified N. gonorrhoeae isolates, 445 (91.8 %) were isolated from male urethritis subjects, and 77 (15.9 %) were AZM-R (MIC ≥ 1 mg/L), including 33 (6.8 %) with AZM low-level resistant (AZM-LLR, MIC = 1 mg/L) and 44 (9.1 %) with AZM middle-level resistant (AZM-MLR, MIC ≥ 2 mg/L). Significantly more CROD (MIC ≥ 0.125 mg/L) showed in AZM-MLR isolates (43.2 %, 19/44) as compared with that in AZM-LLR isolates (18.2 %, 6/33) (p < 0.05). For the 23S rRNA, mtrR, penA or combined 23S rRNA/MtrR/penA mutations, no significant difference was found between AZM-LLR isolates and AZM-MLR isolates (P > 0.05); similar results were detected between combined AZM-LLR/CROD isolates and combined AZM-MLR/CROD isolates (P > 0.05). No mutation A2059G or AZM high-level resistant (AZM-HLR, MIC ≥ 256 mg/L) isolate was detected. Among 77 AZM-R isolates, 67 sequence types (STs) were identified by NG-MAST, of which 30 were novel. Most STs were represented by a single isolate.ConclusionsThe AZM-R together CROD isolates are now present in Guangzhou, China, which deserve continuous surveillance and the mechanism of concurrent resistance needs further study.Electronic supplementary materialThe online version of this article (doi:10.1186/s12879-016-1469-3) contains supplementary material, which is available to authorized users.

Background Maternal infection during pregnancy is known to adversely affect foetal development, but previous studies have rarely investigated the impact of gynaecological diseases during pregnancy on offspring during adulthood. Vaginitis is one of the most prevalent gynaecological diseases during pregnancy. Methods The effect of maternal vaginal inflammation on offspring was simulated by inducing maternal vaginal infection. We performed a transvaginal injection of lipopolysaccharide (LPS) in pregnant mice to induce vaginitis and investigated their offspring by means of behavioural tests and molecular and cellular measurements. Results Behavioural tests revealed that the offspring of mothers transvaginally injected with LPS exhibited sex‐dependent differences. Male offspring showed increased anxiety‐related behaviours, including reduced time exploring the open arm in the elevated plus maze test and light chamber in the light‐dark box test. Serum levels of corticosterone were increased in LPS male offspring, indicating activation of the hypothalamic‐pituitary‐adrenal (HPA) axis. Corticotropin‐releasing hormone (CRH) protein expression and c‐Fos positive cells were increased in the hypothalamic paraventricular nucleus (PVN) in LPS male offspring, which presented with an increased number of microglia. Conclusion This study suggests that prenatal vaginal infection increases anxiety‐like behaviour in male offspring, possibly via activation of the HPA axis.