microRNAs (miRNAs) play crucial roles in cancer development and progression by targeting mRNAs for degradation and/or translational repression. micro-RNA-802 (miR-802) has been reported as a tumor suppressor and its deregulation is observed in various human cancers. However, the prognostic value of miR-802 and its underlying mechanisms involved in human cervical cancer are poorly investigated. The purposes of this study were to explore the role of miR-802 in cervical cancer and to clarify the regulation of serine/ arginine-rich splicing factor 9 (SRSF9) by miR-802. Here, we found that miR-802 was downregulated in both cervical cancer tissues and cell lines.Transfection of a miR-802 mimic into cervical cancer cells inhibited their proliferation and colony formation, and promoted cell cycle arrest at the G0/G1 phase and cell apoptosis. In addition, we found that miR-802 could directly target the 3′-untranslated region of SRSF9 and suppress SRSF9 expression. Rescue experiments revealed that overexpression of SRSF9 partially reversed the inhibition effect of miR-802 in cervical cancer cells. Overall, these findings demonstrate that miR-802 functions as a tumor suppressor in cervical cancer by targeting SRSF9, suggesting that miR-802 might serve as a potential therapeutic target in cervical cancer. K E Y W O R D S apoptosis, cervical cancer, microRNA-802, proliferation, serine/arginine-rich splicing factor 9How to cite this article: Zhang Q, Lv R, Guo W, Li X. microRNA-802 inhibits cell proliferation and induces apoptosis in human cervical cancer by targeting serine/arginine-rich splicing factor 9.

Interleukin (IL)-17 has been regarded as a significant factor in inflammation. In addition, IL-17 is known to be involved in the progression of cancers; however, the function of IL-17 in cervical cancer remains unclear. In the present study, cell viability was detected by Cell Counting Kit-8 assay. Quantitative PCR and western blotting were performed to detect gene and protein expression levels, respectively, in cancer cells or tissues. Ki-67 staining was used to evaluate cell proliferation. Wound-healing assay was used to detect cell migration. Moreover, Transwell assay was performed to investigate the invasion of cervical cancer cells. The results revealed that IL-17 significantly promoted the proliferation of cervical cancer cells. Additionally, IL-17 notably enhanced the migration and invasion of cervical cancer cells in vitro . IL-17 promoted the progression of cervical cancer via the activation of JAK2/STAT3 and PI3K/Akt/NF-κB signaling. In conclusion, IL-17 was a key regulator during the progression of cervical cancer through the JAK2/STAT3 and PI3K/Akt/nuclear factor-κB signaling pathway, which may serve as a novel target for the treatment of cervical cancer.

No abstract

Emerging evidence has revealed that long noncoding RNAs (lncRNAs) play crucial roles in the development and progression of tumors. The present study aimed to examine the roles and illustrate the underlying mechanisms of lncRNA ferritin heavy chain 1 pseudogene 3 (FTH1P3) in cervical cancer. The expression of lncRNA FTH1P3 and microRNA-145 (miRNA-145 or miR-145) in human cervical cancer samples and cervical cancer cell lines was detected by qRT-PCR (reverse transcription-quantitative polymerase chain reaction). FTH1P3 overexpression, siRNA plasmid, hsa-miR-145 mimic or hsa-miR-145 inhibitor were transfected. The target of FTH1P3 was predicted by bioinformatics analysis and validated by luciferase assay. Statistical significance analysis was performed by SPSS software. The results revealed that FTH1P3 was significantly upregulated in cervical cancer tissues compared with normal tissues. Increased expression of FTH1P3 was revealed in human cervical cancer cell lines compared with cervical normal epithelial cells. Downregulation of FTH1P3 inhibited cell proliferation, invasion and migration, and promoted apoptosis in cervical cancer cells. miR-145 was predicted and validated as a direct target of FTH1P3. Moreover, FTH1P3 siRNA partially attenuated the effects of the miR-145 inhibitor on cell viability and mobility in cervical cancer cells. The present results demonstrated that lncRNA FTH1P3 functioned as a promoting factor in cervical cancer by targeting miR-145.

In the pathogenic fungus Candida albicans, phosphoregulation of the checkpoint kinase Rad53 plays a crucial role in the filamentous growth response to genotoxic stresses. The protein phosphatase 4 (PP4) complex, containing Pph3 and either Psy2 or Psy4, is proved to play a critical role in Rad53 dephosphorylation. In previous studies, we characterized CaPtc2 (the ortholog of both Ptc2 and Ptc3 in Saccharomyces cerevisiae) as a potential DNA-damage-related protein phosphatase. In this study, we checked the genetic interaction of PTC2 with the PP4 complex in the DNA damage response pathway. The results suggest that Ptc2 shows a negative genetic interaction with Pph3, but positive genetic interaction with either Psy2 or Psy4 in response to genotoxic stress. Deletion of PTC2 alone resulted in no significant change in cell virulence, but double deletion of PTC2 PPH3 significantly decreased virulence, while double deletions of either PTC2 PSY2 or PTC2 PSY4 caused virulence levels similar to that shown by PSY2 or PSY4 single-gene deletion cells. Taken together, we propose that Ptc2 in C. albicans plays a compensatory role for Pph3 but is dependent on Psy2 and Psy4 in regulation of DNA damage and cell virulence.