Long non-coding RNA SNHG1 regulates NOB1 expression by sponging miR-326 and promotes tumorigenesis in osteosarcoma

Wang, Jiandong; Cao, Lei; Wu, Jianhong; Wang, Qiugen

doi:10.3892/ijo.2017.4187

Cited by 78 publications

(92 citation statements)

References 50 publications

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“…7 For example, lncRNA HOX transcript antisense RNA has been verified as an effective diagnostic marker in patients with liver, colon, breast, and pancreatic cancer. 12,13 However, the mechanism of it in PC still needs to be explored. A few studies have indicated that SNHG1 can promote the proliferation of tumor cells and decrease their apoptosis in cancers.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Downregulation of long noncoding RNA SNHG1 inhibits cell proliferation, metastasis, and invasion by suppressing the Notch‐1 signaling pathway in pancreatic cancer

Chen

Dong

Wang

et al. 2018

J of Cellular Biochemistry

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Background Pancreatic cancer (PC) has become the fourth most lethal among human cancers. Long noncoding RNAs (lncRNAs) have been reported to play a role in the progression of a variety of cancers. However, the role of lncRNA SNHG1 in PC is not clear. Methods Real‐time Quantitative PCR Detection System (qPCR) was used to detect the expression of SNHG1 in PC cells. Then, the SNHG1 knockdown cell was constructed with si‐SNHG1. AsPC‐1 and PANC1 cells were used to analyze the ability of cell proliferation, invasion, and migration. MTT assay was used to analyze the proliferation ability. Transwell experiments and wound healing experiments were used to detect the capacity of invasion and migration. Finally, Western blot analysis was used to explore the mechanism of SNHG1 in PC. Results SNHG1 was significantly upregulated in PC cells. Knockdown of SNHG1 could obviously suppress cell proliferation, invasion, and migration. Furthermore, SNHG1 knockdown inhibited the activation of the Notch‐1 signaling pathway and inhibited the expression of N‐cadherin, Hes1, Vimentin, Notch‐1. The inhabitation was reversed when Notch‐1 was overexpressed in si‐SNHG1 cells. Conclusion The lncRNA SNHG1 promotes cell growth and metastasis in PC through activation of the Notch‐1 signaling pathway in PC.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: Downregulation of long noncoding RNA SNHG1 inhibits cell proliferation, metastasis, and invasion by suppressing the Notch‐1 signaling pathway in pancreatic cancer

Chen

Dong

Wang

et al. 2018

J of Cellular Biochemistry

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“…Previous studies demonstrated that the basal expression of antioxidants and two-phase enzyme in Nrf2 knockout mice was markedly lower compared with wild-type mice, with sensitivity to ROS-induced cytotoxicity increased, indicating that antioxidant genes were vital to protecting against myocardial injury and the expression of Nrf2 was involved in the expression and induction of antioxidants. In addition, knockout of Nrf2 inhibited the ability of fibroblasts to fight against injury induced by ROS (33,34). Importantly, the present study demonstrated that dioscin significantly increased Nrf2 protein expression in the heart of CHD model pigs, and the results indicated that the effects of dioscin may be mediated by Sirt1/Nrf2 to protect against CHD in pigs.…”

Section: Discussionsupporting

confidence: 50%

Dioscin protects against coronary heart disease by reducing oxidative stress and inflammation via Sirt1/Nrf2 and p38 MAPK pathways

Yang

Zhao

et al. 2018

Mol Med Report

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Cardiovascular diseases are common diseases in Sweden as in most countries. In 2016, 25,700 persons suffered from coronary heart disease (CHD) and 25% of these died within 28 days. The present study investigated whether dioscin may exert protective effects against CHD‑induced heart apoptosis, oxidative stress and inflammation in a pig model and the potential underlying mechanisms. Adult pigs were used to establish a CHD model group and 80 mg/kg dioscin was administered for 4 weeks. Histological analysis and measurement of serum levels of heart injury markers demonstrated that 80 mg/kg dioscin markedly alleviated CHD, while left ventricular ejection fraction and left ventricular systolic internal diameter measurements indicated that 80 mg/kg dioscin also increased heart function in the CHD pig model. Furthermore, western blotting demonstrated that 80 mg/kg dioscin significantly reduced protein levels of apoptosis markers in the heart of CHD model pigs, including Bcl‑2‑associated X and caspase‑3, potentially via the suppression of poly (ADP‑ribose) polymerase 1 (PARP)/p53 expression. Additionally, the results of ELISA and western blotting demonstrated that 80 mg/kg dioscin may reduce oxidative stress and inflammation in CHD model pigs through the promotion of sirtuin 1 (Sirt1)/nuclear factor erythroid 2‑related factor 2 (Nrf2) protein expression and the suppression of PARP/p53 and p38 mitogen‑activated protein kinase (MAPK) expression. The results of the current study indicate that dioscin may protect against CHD by regulating oxidative stress and inflammation via Sirt1/Nrf2 and p38 MAPK pathways.

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“…However, the mechanism of SNHG1's effect on hepatocellular carcinoma has not been elucidated. Furthermore, it was demonstrated that SNHG1 acts as an important regulator of the regulation of progression of various cancers by sponging to miR-195 and miR-199a-3p [22]. Now, we investigated the influence of SNHG1 on cell migration and invasion in hepatocellular carcinoma and its relationship with miR-195.…”

Section: Introductionmentioning

confidence: 98%

Long non-coding RNA SNHG1 promotes cell proliferation and invasion of hepatocellular carcinoma by acting as a molecular sponge to modulate miR-195

Zhang¹,

Song²

2020

aoms

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Introduction: Although long non-coding RNA SNHG1 (lncRNA SNHG1) action on cell proliferation and invasion of hepatocellular carcinoma (HCC) cells has been reported, the effects of lncRNA SNHG1 on migration of HCC cells and the mechanisms are still unclear. The present study aimed to investigate the influence of lncRNA SNHG1 on metastasis in HCC cells and the possible mechanisms underlying this phenotype. Material and methods: Expression of lncRNA SNHG1 and miR-195 was determined using qRT-PCR in both HCC cell lines Huh7 and HepG2. Si-RNA was used to silence SNHG1 and miR-195 inhibitor was used to inhibit expression of miR-195. Luciferase reporter assay was conducted to confirm whether miR-195 was the direct binding target of SNHG1. Results: lncRNA SNHG1 was significantly up-regulated and miR-195 was significantly down-regulated in HCC cell lines. When transfected with si-SN-HG1, migration and invasion of HCC cells, as well as expression of astrocyte elevated gene 1 (AEG-1) protein, were significantly inhibited compared with the control cells. Results of dual luciferase reporter assay showed that lncRNA SNHG1 acted as an endogenous sponge of miR-195. On the other hand, the expression of miR-195 in tumor tissue was much lower than that of miR-195 in the corresponding normal tissue. Furthermore, the correlation analysis showed a strong negative relationship between lncRNA SNHG1 and miR-195 expression in HCC tissues. Conclusions: SNHG1 may promote cell invasion and migration in HCC cells by sponging miR-195. These results can provide deeper understanding of SNHG1 in hepatocellular cancer and give new potential targets for treatment of HCC.

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Long non-coding RNA SNHG1 regulates NOB1 expression by sponging miR-326 and promotes tumorigenesis in osteosarcoma

Cited by 78 publications

References 50 publications

RETRACTED: Downregulation of long noncoding RNA SNHG1 inhibits cell proliferation, metastasis, and invasion by suppressing the Notch‐1 signaling pathway in pancreatic cancer

RETRACTED: Downregulation of long noncoding RNA SNHG1 inhibits cell proliferation, metastasis, and invasion by suppressing the Notch‐1 signaling pathway in pancreatic cancer

Dioscin protects against coronary heart disease by reducing oxidative stress and inflammation via Sirt1/Nrf2 and p38 MAPK pathways

Long non-coding RNA SNHG1 promotes cell proliferation and invasion of hepatocellular carcinoma by acting as a molecular sponge to modulate miR-195

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