Journal of cellular biochemistry
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Like other tumors, lung cancer must induce angiogenesis as it grows. Hypoxia-inducible factor 1α (HIF-1α) is the inducible subunit of the HIF-1 transcription factor that regulates genes involved in the response to hypoxia, some of which contributes to angiogenesis. Vascular endothelial growth factor (VEGF) is one of the genes upregulated by HIF-1 and is the primary cytokine in relation to angiogenesis. ⋯ The treatment with anti-HIF-1α siRNA prior to hypoxia exposure was shown to decrease HIF-1α and VEGF-A expressions and reduce hypoxia-induced angiogenesis, suggesting that HIF-1α expression resulted in increased VEGF-A expression and activation of HIF-1α/VEGF pathway was responsible for hypoxia-induced angiogenesis. In conclusion, we identified the relationship between HIF-1α/VEGF pathway and response to radiotherapy and its role in angiogenesis in lung cancer in vitro. HIF-1α/VEGF pathway as a target for antiangiogenic treatment strategies for this tumor requires further investigation.
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Retracted Publication
microRNA-383 suppresses the PI3K-AKT-MTOR signaling pathway to inhibit development of cervical cancer via down-regulating PARP2.
This study aims to evaluate the effect of the regulatory relationship between microRNA-383 (miR-383) and PARP2 in the cell migration and invasion in human with cervical cancer (CC) via the PI3K-AKT-MTOR signaling pathway. Cancerous tissues and corresponding paracancerous tissues were collected from 115 patients with CC. The positive expression rate of PARP2 was detected by immunohistochemistry. ⋯ In the miR-383 mimic and si-PARP2 groups, the cell viability, migration, and invasion were descended, in comparison to the blank and NC groups. All above parameters showed an opposite trend in the miR-383 inhibitor group when compared with the blank and NC groups. This study demonstrates that miR-383 could down-regulate PARP2 to protect against CC by inhibiting PI3K-AKT-MTOR signaling pathway.
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Exosomes are required for the regenerative effects of human cardiosphere-derived cells (CDCs). Studies show that they mimic the cardioprotective benefits of CDCs in rodents and porcine myocardial infarction (MI) models. Hypoxic preconditioning of stem cells increases the cardioprotective effects of exosomes in MI models by enhancing angiogenesis. ⋯ In this study, we have demonstrated that human CDCs secreted exosomes under hypoxic conditions (1% O2 for 2 days) enhanced tube formation by human umbilical vein endothelial cells (HUVECs) at a concentration of 25 µg/mL. Pro-angiogenic exosomal miRNAs including miR-126, miR-130a, and miR-210 showed a substantial increase (>2-, >2-, and >4-fold, respectively) in the hypoxic exosomes compared to normoxic CDC-derived exosomes. Our study suggested a significant benefit of hypoxic CDC exosomes for the treatment of cardiac diseases by induction of angiogenesis via enrichment of pro-angiogenic exosomal miRNAs.
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This network meta-analysis was conducted to compare effects of different placebo-controlled insulin-sensitizing drugs, including metformin, pioglitazone, rosiglitazone, and troglitazone on hormonal parameters in polycystic ovary syndrome (PCOS) patients. We searched PubMed, EMBASE, and Cochrane Library databases from their inception to July 2017. Randomized controlled trials (RCTs) met our inclusion criteria were included. ⋯ However, there were no statistical significance among the placebo-controlled insulin-sensitizing drugs in follicle stimulating hormone (FSH) (IU/L), luteinizing hormone (LH) (IU/L), dehydroepiandrostrone-sulphate (DHEAS) (µg/dL), free testosterone (FT) (pg/mL) and androstenedione (ng/mL). The results of cluster analysis showed that rosiglitazone may be the best drug for PCOS patients regarding to DHEAS, TT, FSH, and LH, metformin may be the best drug for PCOS patients as for E2 , FT, and androstenedione. Rosiglitazone had the best effect on PCOS patients in terms of DHEAS, TT, FSH, and LH, metformin had the best effect on PCOS patients for E2 , FT, and androstenedione.
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Spinal cord injury (SCI) is lead to locomotor impairment because of neurological damage after following trauma. Quercetin (Que) has been confirmed to have a neuro-protective effect during nerve damage processes. The purpose of this study was to determine the roles of Que in functional recovery, cavity formation, astrocyte activation, and nerve regeneration following SCI. ⋯ Que promoted locomotor function and electrophysiological recovery, reduced cavity formation, contributed to astrocyte activation and axonal regeneration after acute SCI. Moreover, Que up-regulated the expression of BDNF, but reduced p-JNK2 and p-STAT3 expression after acute SCI. Taken together, Que promoted locomotor and electrophysiological functional recovery, astrocyte activation and axonal regeneration after acute SCI, possibly through BDNF and JAK2/STAT3 signaling pathways.