Background: Members of the ankyrin repeat and SOCS box (Asb) family are expressed abundantly in testes. Some Asb genes/proteins are required for spermatogenesis, but the function of Asb12 during spermatogenesis is not clear. We investigated the physiological role of Asb12 in murine testes. Methods:The clustered regularly interspaced short palindromic repeats/CRISPR-associated protein 9 system was used to generate Asb12-knockout (KO) mice. Histology and immunostaining were done to assess the effects of Asb12 KO on mouse testes and epididymides. Semen quality was analyzed using a computerassisted sperm analyzer. The terminal deoxynucleotidyl transferase-dUTP nick-end labeling assay was employed to examine testicular apoptosis. Real-time reverse transcription-quantitative polymerase chain reaction (PCR) was conducted to calculate gene transcription levels.Results: Asb12 was expressed predominantly in murine testes. Immunostaining of Asb12 protein revealed that Asb12 was located specifically in the acrosome of elongated spermatids, which suggested a potential role of Asb12 during spermatogenesis. However, Asb12-KO mice had normal fertility, and no overt difference was detected in testicular morphology, semen quality, or apoptosis when comparing Asb12-KO and Asb12-wild type (WT) mice. Gene expression of several Asb family members was increased significantly in the testes of Asb12-KO mice when compared with that in Asb12-WT mice, which suggested functional compensation from paralogs for Asb12 loss. Conclusions:We demonstrated that Asb12 is not essential for the spermatogenesis and fertility of mice.Our findings will assist researchers in avoiding redundant efforts, and provide a baseline resource for genetic studies on human fertility.

Competing endogenous RNA (ceRNA) appears to be an important post-transcriptional manner that regulates gene expression through a miRNA-mediated mechanism. Mutations in exon-19 of EGFR were frequently observed in lung cancer genes, which were associated with EGFR activity and EGFR-targeted therapies. Methods: We explored the transcriptome regulated by mutation in EGFR exon-19 E746-A750 fragment via using a network modeling strategy. We applied transcriptome sequencing to detect the deletion process of EGFR exon-19 E746-A750 fragment. Bioinformatics analyses were used to predict the gene target pairs and explain their potential roles in tumorigenesis and progression of lung cancer. Results:We conducted an explorative lncRNA/miRNA/circRNA and mRNA expression study with two groups of lung adenocarcinoma tissues, including EGFR exon-19 E746-A750 deletion group and EGFR exon-19 wild-type group. Meanwhile, we screen out the hub genes related to the EGFR-19-D patient. Significant pathways and biological functions potentially regulated by the deregulated 128 non-coding genes were enriched. Conclusion:Our work provides an important theoretical, experimental and clinical foundation for further research on more effective targets for the diagnosis, therapy and prognosis of lung cancer.