Upregulated expression of MNX1-AS1 long noncoding RNA predicts poor prognosis in gastric cancer

Zhang, Wei; Huang, Lunhua; Lu, Xinyang; Wang, Kecheng; Ning, Xiaofei; Liu, Zhiqiang

doi:10.17305/bjbms.2019.3713

Cited by 17 publications

(19 citation statements)

References 33 publications

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“…Currently, the expression pattern and functional role of lncRNA MNX1-AS1 in diverse tumours have been gradually identified [22,24,44,45] Yang et al found that overexpression of MNX1-AS1 exerted tumourpromoting roles in lung adenocarcinoma [45]. A current study by Ji et al showed that enrichment of MNX1-AS1 is strongly linked to TNM stage in hepatocellular carcinoma (HCC) patients [46].…”

Section: Discussionmentioning

confidence: 99%

TEAD4 modulated LncRNA MNX1-AS1 contributes to gastric cancer progression partly through suppressing BTG2 and activating BCL2

et al. 2020

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Background: Gastric cancer (GC) is the third leading cause of cancer-related mortality globally. Long noncoding RNAs (lncRNAs) are dysregulated in obvious malignancies including GC and exploring the regulatory mechanisms underlying their expression is an attractive research area. However, these molecular mechanisms require further clarification, especially upstream mechanisms. Methods: LncRNA MNX1-AS1 expression in GC tissue samples was investigated via microarray analysis and further determined in a cohort of GC tissues via quantitative reverse transcription polymerase chain reaction (qRT-PCR) assays. Cell proliferation and flow cytometry assays were performed to confirm the roles of MNX1-AS1 in GC proliferation, cell cycle regulation, and apoptosis. The influence of MNX1-AS1 on GC cell migration and invasion was explored with Transwell assays. A xenograft tumour model was established to verify the effects of MNX1-AS1 on in vivo tumourigenesis. The TEAD4-involved upstream regulatory mechanism of MNX1-AS1 was explored through ChIP and luciferase reporter assays. The mechanistic model of MNX1-AS1 in regulating gene expression was further detected by subcellular fractionation, FISH, RIP, ChIP and luciferase reporter assays. Results: It was found that MNX1-AS1 displayed obvious upregulation in GC tissue samples and cell lines, and ectopic expression of MNX1-AS1 predicted poor clinical outcomes for patients with GC. Overexpressed MNX1-AS1 expression promoted proliferation, migration and invasion of GC cells markedly, whereas decreased MNX1-AS1 expression elicited the opposite effects. Consistent with the in vitro results, MNX1-AS1 depletion effectively inhibited the growth of xenograft tumour in vivo. Mechanistically, TEAD4 directly bound the promoter region of MNX1-AS1 and stimulated the transcription of MNX1-AS1. Furthermore, MNX1-AS1 can sponge miR-6785-5p to upregulate the expression of BCL2 in GC cells. Meanwhile, MNX1-AS1 suppressed the transcription of BTG2 by recruiting polycomb repressive complex 2 to BTG2 promoter regions. Conclusions: Our findings demonstrate that MNX1-AS1 may be able to serve as a prognostic indicator in GC patients and that TEAD4-activatd MNX1-AS1 can promote GC progression through EZH2/BTG2 and miR-6785-5p/ BCL2 axes, implicating it as a novel and potent target for the treatment of GC.

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Section: Discussionmentioning

confidence: 99%

TEAD4 modulated LncRNA MNX1-AS1 contributes to gastric cancer progression partly through suppressing BTG2 and activating BCL2

et al. 2020

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“…A total of 882 patients from the all eligible articles were included to evaluate prognostic value of MNX1-AS1 (presented in Table 1). All articles covered gastric cancer(GC) (n = 3) [8][9][10], lung cancer (LC) (n = 3) [6,20,21], other cancer(n = 3) including: esophageal squamous cell carcinoma (ESCC), cervical cancer (CC), epithelial ovarian cancer (EOC) [14,18,22].…”

Section: Search Results Of Eligible Studiesmentioning

confidence: 99%

“…Discussion MNX1-AS1, also known as MAYA and CCAT5, is located at chromosome 7q36.3 [6]. Upregulation of MNX1-AS1 expression has been found in a variety of cancers, including gastric cancer [8][9][10], lung cancer [6,20,21], esophageal squamous cell carcinoma [14,15], and estrogen-dependent cancer [7,18,22], etc. MNX1-AS1 play a role of functional oncogene in addition to activating AKT/mTOR pathway and its natural sense transcript MNX1 in breast cancer cells, it also promotes the process of EMT [7].…”

Section: Involvement Of Mnx1-as1 In Carcinogenesismentioning

confidence: 99%

“…Motor neuron and pancreas homeobox 1-antisense RNA1 (MNX1-AS1), is the antisense strand of MNX1 (7q36.6), also known as MAYA and CCAT5, which maps to chromosome 7q36.3 [6,7]. Several studies for the first time provided that MNX1-AS1 has a sponge adsorption effect on miR-6785-5p, thereby up-regulating the expression of BCL2, and overexpression of MNX1-AS1 might facilitate the proliferation, migration and invasion of gastric cancer cells [8][9][10]. Knockdown of MNX1-AS1 might affect the expression of CDK4, cyclin D, Bax, and Bcl-2, which may inhibit proliferation and migration capabilities, and promote apoptosis of ovarian cancer cells [11].…”

Section: Introductionmentioning

confidence: 99%

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The prognostic utility and clinical outcomes of MNX1-AS1 expression in cancers: a systematic review and meta-analysis

Li¹,

Wen²,

Zhang³

et al. 2020

Preprint

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Background: Recently, emerging studies have identified that MNX1-AS1 highly expressed among variety of cancers and related with worse prognosis of cancer patients. The purpose of this study was to evaluate the relationship between MNX1-AS1 expression with clinical features and prognosis in different cancers. Methods: In this study, we searched the Web of Science, PubMed, CNKI, and Wanfang databases to find relevant studies of MNX1-AS1. Pooled hazard ratios (HRs) and odds ratios (ORs) with 95% confidence intervals (CIs) were applied to explore the prognostic and clinical significance of MNX1-AS1. Results: A total of 9 literatures were included in this study, including 882 cancer patients. The results showed that patients with increased MNX-AS1 expression were more likely to develop lymph node metastasis (OR = 5.616, 95%CI: 3.093 - 10.199, P = 0.000) and advanced TNM stage (OR = 4.625, 95%CI: 2.366-9.040, P = 0.000). Moreover, we demonstrated that patients with high expression of MNX1-AS1 had poor OS in different cancers (HR = 1.976, 95%CI: 1.653 - 2.361, P=0.000). In addition, patients with high expression of MNX1-AS1 suffer from worse prognosis in gastric cancer (HR = 2.385, 95% CI: 1.838 - 3.094, P = 0.000) and lung cancer (HR= 1.959, 95%CI: 1.353 - 2.835, P = 0.000). Conclusions: High MNX1-AS1 expression is significantly associated with unfavorable clinical outcomes and it has the potential to serve as a prognostic biomarker in cancer patients.

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“…In this way, AGAP2-AS1 could participate as an epigenetic repressor of E-cadherin expression. As shown in Figure 3 , several other lncRNAs (Lnc01614, LOC554202, TUG1, AFAP1-AS1, NEAT, MNX1-AS1, AOC4P, SNHG20, CCAT1, TPT1-AS1, and LINC00941) have been found to be upregulated and associated with poor prognosis in clinical samples of GC [ 91 , 92 , 93 , 94 , 95 , 96 , 97 , 98 , 99 , 100 ]. The knockdown of these lncRNAs was associated with the re-expression of E-cadherin.…”

Section: Noncoding Rnas: Classification and Functionsmentioning

confidence: 99%

Competing Endogenous RNA Networks in the Epithelial to Mesenchymal Transition in Diffuse-Type of Gastric Cancer

Landeros

Santoro

Carrasco-Aviño

et al. 2020

Cancers

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The diffuse-type of gastric cancer (DGC), molecularly associated with epithelial to mesenchymal transition (EMT), is increasing in incidence. Loss of E-cadherin expression is the hallmark of the EMT process and is largely due to the upregulation of the EMT-inducing transcription factors ZEB1/2, Snail, Slug, and Twist1/2. However, ncRNA, such as miRNA and lncRNAs, can also participate in the EMT process through the direct targeting of E-cadherin and other EMT-inducing transcription factors. Additionally, lncRNA can sponge the miRNA pool that targets these transcripts through competing endogenous RNA (ceRNA) networks. In this review, we focus on the role of ncRNA in the direct deregulation of E-cadherin, as well as EMT-inducing transcription factors. Based on the relevance of the ceRNA network hypothesis, and the lack of said networks in EMT, we performed a prediction analysis for all miRNAs and lncRNAs that target E-cadherin, as well as EMT-inducing transcription factors. This analysis resulted in novel predicted ceRNA networks for E-cadherin and EMT-inducing transcription factors (EMT-TFs), as well as the expansion of the molecular basis of the DGC.

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Upregulated expression of MNX1-AS1 long noncoding RNA predicts poor prognosis in gastric cancer

Cited by 17 publications

References 33 publications

TEAD4 modulated LncRNA MNX1-AS1 contributes to gastric cancer progression partly through suppressing BTG2 and activating BCL2

TEAD4 modulated LncRNA MNX1-AS1 contributes to gastric cancer progression partly through suppressing BTG2 and activating BCL2

The prognostic utility and clinical outcomes of MNX1-AS1 expression in cancers: a systematic review and meta-analysis

Competing Endogenous RNA Networks in the Epithelial to Mesenchymal Transition in Diffuse-Type of Gastric Cancer

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