LncRNA INHBA-AS1 promotes colorectal cancer cell proliferation by sponging miR-422a to increase AKT1 axis.

OBJECTIVE: In recent years, long non-coding RNAs (lncRNAs) have emerged for regulating the development, as well as progression in colorectal cancer (CRC), which assists in finding new targets for CRC treatment. A previous study indicated that INHBA-AS1 promotes oral squamous cell progression by sponging miR-143-3p. However, the exact function possessed by lncRNA INHBA-AS1 in CRC development remains unclear. PATIENTS AND METHODS: The expression level of INHBA-AS1 in CRC tissues and cell lines was determined by qRT-PCR. The functional role of INHBA-AS1 in CRC was investigated by a series of in vitro assays. RNA immunoprecipitation (RIP), bioinformatics analysis was utilized to explore the potential mechanisms of INHBA-AS1. RESULTS: The present study identified INHBA-AS1 as a kind of lncRNA with high expression in CRC tissues and cells. Functionally, NHBA-AS1 downregulation in CRC cells suppressed CRC cell proliferation as well as colony formability. Mechanistically, INHBA-AS1/miR-422a/AKT1 established the ceRNA network to regulate MMP-2, -7, -9 expressions that participated the modulation of CRC progression. CONCLUSIONS: In summary, LncRNA INHBA-AS1 contributes to CRC progression through AKT1 pathway, and provides a new mechanism to regulate CRC development, as well as a potential target for treating CRC.

[Influence of hypothyroidism on pregnancy outcome and fetus during pregnancy].

OBJECTIVE: To investigate the influence of hypothyroidism on pregnancy outcome and fetus in pregnant women. METHODS: A total of 4 286 pregnant women, who received prenatal examination in our hospital from January 2013 to October 2015, were selected as study subjects. The incidence of hypothyroidism and the influence on pregnancy outcomes and fetus were investigated. RESULTS: In 4 286 pregnant women surveyed, 209 hypothyroidism cases were detected(4.9%), including 85 clinical hypothyroidism cases and 124 subclinical hypothyroidism cases. In health group, the premature delivery rate was 1.0%, significantly lower than that in clinical hypothyroidism group(10.6%)and in subclinical hypothyroidism group(6.5%), the differences were significant(χ(2)= 38.884, P<0.001; χ(2)=17.722, P<0.001). In healthy group, the incidence of anemia was 3.8%, significantly lower than that in clinical hypothyroidism group(18.8%)and in subclinical hypothyroidism group(9.7%), the differences were significant(χ(2)=30.949, P<0.001; χ(2)=23.275, P<0.001). In health group, the incidence of low birth weight was 1.1%, significantly lower than that in clinical hypothyroidism group(14.1%)and in subclinical hypothyroidism group(4.8%), the differences were significant(χ(2)=50.593, P<0.001; χ(2)=15.637, P<0.001). In health group, the fetal distress incidence was 1.9%, significantly lower than that in clinical hypothyroidism group(10.6%)and in subclinical hypothyroidism group(5.6%), the differences were significant(χ(2)=19.257, P< 0.001; χ(2)=12.357, P<0.001). In health group, the fetal Apgar score(9.69 ± 0.32)was significantly higher than those in clinical hypothyroidism group(9.25 ± 0.45)and in subclinical hypothyroidism group(9.28 ± 0.44), the differences were significant(t=8.823, P<0.001; t=15.175, P<0.001). CONCLUSION: Hypothyroidism during pregnancy has adverse influences on pregnancy outcome and fetus, and it is necessary to strengthen the hypothyroidism detection in pregnant women for the early treatment.

Gastric cancer exosomes promote tumour cell proliferation through PI3K/Akt and MAPK/ERK activation.

BACKGROUND: Exosomes are nanometer-sized vesicles that are released by normal and neoplastic cells. Previous studies have focused on the interaction between tumour-derived exosomes and the immune system, as a consequence of immune suppression or enhancement. However, the effects of tumour-derived exosomes on tumour cells themselves have not been well studied. AIMS: To investigate the effects of gastric cancer exosomes on tumour cell proliferation and the possible mechanisms. METHODS: By serial centrifugation and sucrose gradient ultracentrifugation, we isolated and purified the exosomes from gastric cancer SGC7901 cells, then viewed them by electron microscopy. Cell proliferation was measured by 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide assay. Protein expression was assayed by Western blotting. RESULTS: SGC7901-cell-derived exosomes promoted the proliferation of SGC7901 and BGC823 cells. The increase in proliferation induced by exosomes was accompanied by activation of Akt and extracellular-regulated protein kinase, and phosphoinositide 3-kinase or extracellular-regulated protein kinase inhibitor partially reversed the proliferative effect of exosomes. Moreover, the exosome-induced increase in activity of Akt and extracellular-regulated protein kinase coincided with decreased expression of the Casitas B-lineage lymphoma family of ubiquitin ligases. CONCLUSION: Gastric cancer exosomes promoted tumour cell proliferation, at least in part, by activation of PI3K/Akt and mitogen-activated protein kinase/extracellular-regulated protein kinase pathways. The decreased expression of Casitas B-lineage lymphoma proteins might have contributed to the activation of Akt and extracellular-regulated protein kinase.