CircHACE1 functions as a competitive endogenous RNA to curb differentiated thyroid cancer progression by upregulating Tfcp2L1 through adsorbing miR-346.

Circular RNAs (circRNAs) are correlated with the occurrence and progression of differentiated thyroid cancer (THCA). However, the regulatory mechanism of circRNAs in differentiated THCA is unclear. In the present study, we analyzed the circRNA microarray dataset (GSE93522) of thyroid tumors and discovered that circRNA HACE1 (circHACE1) was downregulated in differentiated THCA. We detected circHACE1 expression by quantitative real-time polymerase chain reaction (qRT-PCR). Gain-of-function experiments were performed to analyze the biological function of circHACE1 in differentiated THCA cells in vitro. The regulatory mechanism of circHACE1 in differentiated THCA was explored through bioinformatics analysis, dual-luciferase reporter, RIP (RNA immunoprecipitation), and/or RNA pull-down assays. The biological function of circHACE1 in THCA was confirmed by xenograft assay. We verified that circHACE1 was downregulated in differentiated THCA. Also, differentiated THCA patients with low circHACE1 expression were associated with TNM grade, lymphoid node metastasis, tumor size, and poor prognosis. CircHACE1 overexpression decreased xenograft tumor growth in vivo and induced cell cycle arrest, apoptosis, impeded proliferation, migration, and invasion in differentiated THCA cells in vitro. CircHACE1 could function as a microRNA (miR)-346 sponge and regulated Tfcp2L1 (transcription factor CP2 like 1) expression. MiR-346 overexpression offset circHACE1 elevation-mediated effects on malignant behaviors of differentiated THCA cells. Furthermore, Tfcp2L1 silencing counteracted the suppressive impact of miR-346 inhibitor on the malignancy of differentiated THCA cells. In conclusion, circHACE1 adsorbed miR-346 and elevated Tfcp2L1 expression, thus curbing cell malignancy in differentiated THCA, manifesting that circHACE1 might be a target for differentiated THCA treatment.

Long non-coding RNA HEIH contributes to diabetic retinopathy by regulating miR-939/VEGF axis.

Diabetes is one of the most prevalent metabolic diseases in the world. This study explored the role of long non-coding RNA HEIH in regulating the development of diabetic retinopathy (DR). The expression of HEIH gene was detected in the serum of patients with DR. Subsequently, high concentrations of D-glucose (HG) were used to stimulate ARPE-19 cells to construct a cell model of DR. HEIH was overexpressed and suppressed to further investigate the effects of HEIH on HG-induced ARPE-19 cell injury. Moreover, the regulatory relationship between HEIH and miR-939 was investigated, and a target relationship between miR-939 and VEGF in ARPE-19 cells was explored. We elucidated an association between HEIH/miR-939/VEGF axis and the PI3K/AKT pathway. HEIH was highly expressed in the serum of patients with DR. Moreover, HG-induced ARPE-19 cell injury and expression of HEIH. The overexpression of HEIE aggravated HG-induced ARPE-19 cell injury by significantly inhibiting cell viability, inducing apoptosis, promoting cytochrome C release from mitochondria to cytoplasm, and enhancing the caspase-3 activity, whereas suppression of HEIE had the opposite effects. In addition, the effects of the suppression of HEIH on HG-induced ARPE-19 cell injury were markedly reversed by inhibiting miR-939. miR-939 regulated HG-induced ARPE-19 cell injury by targeting VEGF. The suppression of HEIH reversed HG-induced activation of the PI3K/AKT signaling pathway. Our findings revealed that HEIH may contribute to DR by sponging miR-939 to target VEGF expression and by regulating the activation of the PI3K/AKT pathway. Inhibition of epidermal growth factor receptor and PI3K/Akt signaling suppresses cell proliferation and survival through regulation of Stat3 activation in human cutaneous squamous cell carcinoma. HEIH/miR-939/VEGF axis may provide a novel perspective for DR therapy.

Effects of removal of necrotic blastomeres from human cryopreserved embryos on pregnancy outcome.

This study assessed whether the implantation potential of embryos that were partially damaged after freezing and thawing can be improved by removal of necrotic blastomeres. We retrospectively analyzed the pregnancy rate and implantation rate of 170 human frozen embryo transfer cycles. Laser-assisted hatching and micromanipulation were performed to remove the necrotic blastomeres. A higher clinical pregnancy rate (22.22%) and embryo implantation rate (10.17%) were observed when transferred embryos comprised fully intact and partially damaged embryos compared with partially damaged embryos alone (5.88% and 2.82%, respectively). When transferred embryos were fully intact and partially damaged embryos, removal of necrotic blastomeres from partially damaged embryos significantly increased the clinical pregnancy rate (43.90% versus 24.00%, P<0.05) and the implantation rate (19.44% versus 10.29%, P<0.05). The results indicated that the implantation potential of partially damaged cryopreserved embryos can be improved by removal of necrotic blastomeres with laser-assisted hatching and micromanipulation.