lncRNA SNHG11 Promotes Gastric Cancer Progression by Activating the Wnt/β-Catenin Pathway and Oncogenic Autophagy

Wu, Qiong; Ma, Jun; Wei, Jue; Wu, Meng; Wang, Yugang; Shi, Min

doi:10.1016/j.ymthe.2020.10.011

Cited by 141 publications

(113 citation statements)

References 82 publications

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“…For example, Liu et al ( 9 ) demonstrated that the upregulated expression of SNHG11 predicted a poor prognosis of patients with lung cancer and that the overexpression of SNHG11 facilitated the development of lung cancer. In gastric cancer, SNHG11 has been reported to promote gastric cancer cell proliferation and metastasis ( 10 ). In addition, SNHG11 expression has been discovered to be upregulated in colorectal cancer cells and to be associated with increased levels of cell proliferation ( 11 ).…”

Section: Introductionmentioning

confidence: 99%

lncRNA SNHG11 facilitates prostate cancer progression through the upregulation of IGF‑1R expression and by sponging miR‑184

et al. 2021

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Long non-coding RNA (lncRNA) small nucleolar RNA host gene 11 (SNHG11) has been shown to play an important role in the development and progression of numerous types of cancer. However, to the best of our knowledge, the role of SNHG11 in prostate cancer (PCa) development and metastasis remains unclear. Thus, the aim of the present study was to investigate the functional role and molecular mechanisms of SNHG11 in PCa progression. It was revealed that the SNHG11 expression levels were significantly upregulated in PCa tissues, in comparison with those in adjacent normal tissues. Functionally, SNHG11 knockdown significantly suppressed PCa cell proliferation, migration, invasion and metastasis in vitro and in vivo . Furthermore, SNHG11 was found to positively regulate insulin-like growth factor 1 receptor (IGF-1R) expression by sponging microRNA (miRNA/miR)-184 in PCa cells. The results of rescue experiments demonstrated that IGF-1R overexpression reversed the suppressive effects of SNHG11 knockdown on the proliferation, migration and invasion of PCa cells. On the whole, the findings of the present study suggest that SNHG11 expression is upregulated in PCa and that it facilitates PCa progression, at least in part, via the modulation of the miR-184/IGF-1R signaling axis.

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Section: Introductionmentioning

confidence: 99%

lncRNA SNHG11 facilitates prostate cancer progression through the upregulation of IGF‑1R expression and by sponging miR‑184

et al. 2021

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“…Our findings confirmed that Dex significantly improved neuronal injury. Previous studies indicated SNHG11 participated in the pathogenesis of various diseases [34][35][36], but its role in IS progression is undefined. In our work, we found that SNHG11 was highly expressed in OGD/ R-treated SH-SY5Y cells.…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine improves oxygen-glucose deprivation/reoxygenation (OGD/R) -induced neurological injury through regulating SNHG11/miR-324-3p/VEGFA axis

Chen

Fan

2021

Bioengineered

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Dexmedetomidine (Dex) has been reported to exhibit neuroprotective effects through various regulatory mechanisms. This study aims to investigate the role and molecular mechanism of SNHG11 in Dex-mediated neuroprotection. The ischemic stroke (IS) model was established in vivo by middle cerebral artery occlusion (MCAO) and in vitro by oxygen-glucose deprivation and reperfusion (OGD/R)-treated SH-SY5Y. SNHG11 was highly expressed after OGD/R, and Dex improved OGD/R-induced neurological injury. Additionally, Dex reversed the effects of SNHG11 on OGD/R-induced neurological injury. Furthermore, we found that SNHG11 upregulated vascular endothelial growth factor A (VEGFA) expression by targeting miR-324-3p. Through rescue assays, it was confirmed that SNHG11 regulated OGD/R-induced neurological injury through increasing VEGFA expression. At last, Dex was also discovered to improve neurological injury through regulating SNHG11 in the rat model. In conclusion, our work demonstrated that Dex improved OGD/R-induced neurological injury via SNHG11/miR-324-3p/VEGFA axis. These findings may offer a novel therapeutic strategy for IS treatment.

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“…Furthermore, we found that GC cell proliferation and migration were altered after applying the autophagy inhibitor 3-MA. Although autophagy was reported to regulate cell proliferation, migration and apoptosis [43][44][45][46] , the speci c mechanism remains to be explored and con rmed in vivo.…”

Section: Discussionmentioning

confidence: 99%

The Novel Role of Circular RNA ST3GAL6 on Blocking GC Malignant Behaviors Through Autophagy Regulated by the FOXP2/MET/Mtor Axis

Zhang

Cao

et al. 2021

Preprint

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Gastric cancer (GC) ranks third in motality among all cancers worldwide. Circular RNAs (circRNAs) play essential roles in the malignant progression and metastasis of gastric cancer. As a transcription factor, FOXP2 is involved in the progression of many tumours. However, the regulation and association between circRNAs and FOXP2 remain to be discovered. In our study, CircST3GAL6 was significantly depressed in GC tissues and cells. circST3GAL6 overexpression inhibited the proliferation, invasion and metastasis of GC cells in vitro and in vivo. Importantly, circST3GAL6 overexpression induced apoptosis and promote autophagy in GC cells. Furthermore, we found that circST3GAL6 sponged miR-300 and subsequently regulated FOXP2. We further revealed that FOXP2 suppressed the activation of the Met/AKT/mTOR axis, a classic pathway that regulates autophagy-mediated proliferation and migration. In summary, our ﬁndings revealed that circST3GAL6 functions as a tumour suppressor through the miR-300/FOXP2 axis in GC, regulates apoptosis and autophagy through FOXP2-mediated transcriptional inhibition of the MET axis and may be a biomarker for GC treatment.

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lncRNA SNHG11 Promotes Gastric Cancer Progression by Activating the Wnt/β-Catenin Pathway and Oncogenic Autophagy

Cited by 141 publications

References 82 publications

lncRNA SNHG11 facilitates prostate cancer progression through the upregulation of IGF‑1R expression and by sponging miR‑184

lncRNA SNHG11 facilitates prostate cancer progression through the upregulation of IGF‑1R expression and by sponging miR‑184

Dexmedetomidine improves oxygen-glucose deprivation/reoxygenation (OGD/R) -induced neurological injury through regulating SNHG11/miR-324-3p/VEGFA axis

The Novel Role of Circular RNA ST3GAL6 on Blocking GC Malignant Behaviors Through Autophagy Regulated by the FOXP2/MET/Mtor Axis

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