SNHG11 promotes cell proliferation in colorectal cancer by forming a positive regulatory loop with c-Myc

Huang, Weizhen; Dong, Shaoting; Cha, Yinlian; Yuan, Xianxian

doi:10.1016/j.bbrc.2020.05.002

Cited by 26 publications

(23 citation statements)

References 27 publications

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“…NR_003239.1) is a recently identified lncRNA; however, little is known with regard to its functional roles in cancer. It has been previously reported that SNHG11 expression is frequently upregulated in several types of cancer ( 9 - 11 ). In HCC, SNHG11 overexpression has been reported to facilitate cell proliferation and migration ( 19 ).…”

Section: Discussionmentioning

confidence: 97%

“…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 ). However, to the best of our knowledge, to date, limited information is available on the expression and function of SNHG11 in PCa.…”

Section: Introductionmentioning

confidence: 99%

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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: Discussionmentioning

confidence: 97%

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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“…In addition, we found another putative Xist regulator, Snhg1, which has not yet been implicated in XCI and which might function as an activator of Xist. This poorly-studied lncRNA, which has been suggested to function through binding to Igf2bp1 (Huang et al, 2020) , which in turn modulates protein stability of a series of target genes, including pluripotency factors (Bi et al, 2020) , warrants further investigation in the future.…”

Section: Discussionmentioning

confidence: 99%

“…It might be involved in inducing Xist expression, since it was positively associated with Xist in both our approaches. This poorly studied lncRNA, which has been implicated in cancer warrants further investigation in the future (Huang et al, 2020) .…”

Section: Identification Of Putative Xist Regulatorsmentioning

confidence: 99%

Integrated analysis of Xist upregulation and gene silencing at the onset of random X-chromosome inactivation at high temporal and allelic resolution

Pacini

Dunkel

Mages

et al. 2020

Preprint

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To ensure dosage compensation between the sexes, one randomly chosen X chromosome is silenced in each female cell in the process of X-chromosome inactivation (XCI). XCI is initiated during early development through upregulation of the long non-coding RNA Xist, which mediates chromosome-wide gene silencing. Cell differentiation, Xist upregulation and silencing are thought to be coupled at multiple levels to ensure inactivation of exactly one out of two X chromosomes. Here we perform an integrated analysis of all three processes through allele-specific single-cell RNA-sequencing. Specifically, we assess the onset of random XCI with high temporal resolution in differentiating mouse embryonic stem cells, and develop dedicated analysis approaches. By exploiting the inter-cellular heterogeneity of XCI onset, we identify Nanog downregulation as its main trigger and discover additional putative Xist regulators. Moreover, we confirm several predictions of the stochastic model of XCI where monoallelic silencing is thought to be ensured through negative feedback regulation. Finally, we show that genetic variation modulates the XCI process at multiple levels, providing a potential explanation for the long-known Xce effect, which leads to preferential inactivation of a specific X chromosome in inter-strain crosses. We thus draw a detailed picture of the different levels of regulation that govern the initiation of XCI. The experimental and computational strategies we have developed here will allow us to profile random XCI in more physiological contexts, including primary human cells in vivo.

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“…Consequently, SNHG11 facilitates hypoxia-induced migration and invasion in vitro and the lung metastasis of colorectal cancer cells in vivo [ 153 ] ( Figure 2 and Table 2 ). It is also acknowledged that SNHG11 upregulates MYC expression [ 176 ]. Since MYC can post-transcriptionally stabilize HIF-1α [ 177 ], SNHG11 may regulate the stability of HIF-1α, at least partly via VHL and MYC.…”

Section: Lncrnas Regulating Hif-1α Expressionmentioning

confidence: 99%

The Hypoxia–Long Noncoding RNA Interaction in Solid Cancers

Son

Yun

Song

et al. 2021

IJMS

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Hypoxia is one of the representative microenvironment features in cancer and is considered to be associated with the dismal prognosis of patients. Hypoxia-driven cellular pathways are largely regulated by hypoxia-inducible factors (HIFs) and notably exert influence on the hallmarks of cancer, such as stemness, angiogenesis, invasion, metastasis, and the resistance towards apoptotic cell death and therapeutic resistance; therefore, hypoxia has been considered as a potential hurdle for cancer therapy. Growing evidence has demonstrated that long noncoding RNAs (lncRNAs) are dysregulated in cancer and take part in gene regulatory networks owing to their various modes of action through interacting with proteins and microRNAs. In this review, we focus attention on the relationship between hypoxia/HIFs and lncRNAs, in company with the possibility of lncRNAs as candidate molecules for controlling cancer.

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SNHG11 promotes cell proliferation in colorectal cancer by forming a positive regulatory loop with c-Myc

Cited by 26 publications

References 27 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

Integrated analysis of Xist upregulation and gene silencing at the onset of random X-chromosome inactivation at high temporal and allelic resolution

The Hypoxia–Long Noncoding RNA Interaction in Solid Cancers

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