&lt;p&gt;Long Non-Coding RNA NCK1-AS1 Serves an Oncogenic Role in Gastric Cancer by Regulating miR-137/NUP43 Axis&lt;/p&gt;

Li, Weihua; Duan, Jiming; Shi, Wenbin; Lei, Liqiang; Lv, Pin

doi:10.2147/ott.s259336

Cited by 14 publications

(8 citation statements)

References 23 publications

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“…MiR-137-3p (i.e., miR-137) plays a tumor-suppressive role in a variety of cancers [37][38][39], including GC [40,41]. Studies have also reported that long non-coding RNAs (lncRNAs) or circular RNAs (circRNAs) sponge miR-137-3p through a ceRNA mechanism in GC [42,43]. However, no studies have reported that mRNA can regulate miR-137-3p through a ceRNA mechanism, nor has it been reported that miR-137-3p can target COL5A1 or FSTL1.…”

Section: Discussionmentioning

confidence: 99%

COL5A1 Promotes the Progression of Gastric Cancer by Acting as a ceRNA of miR-137-3p to Upregulate FSTL1 Expression

Yang

et al. 2022

Cancers

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MicroRNAs (miRNAs) and their target genes have been shown to play an important role in gastric cancer but have not been fully clarified. Therefore, our goal was to identify the key miRNA–mRNA regulatory network in gastric cancer by utilizing a variety of bioinformatics analyses and experiments. A total of 242 miRNAs and 1080 genes were screened from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), respectively. Then, survival-related differentially expressed miRNAs and their differentially expressed target genes were screened. Twenty hub genes were identified from their protein–protein interaction network. After weighted gene co-expression network analysis was conducted, we selected miR-137-3p and its target gene, COL5A1, for further research. We found that miR-137-3p was significantly downregulated and that overexpression of miR-137-3p suppressed the proliferation, invasion, and migration of gastric cancer cells. Furthermore, we found that its target gene, COL5A1, could regulate the expression of another hub gene, FSTL1, by sponging miR-137-3p, which was confirmed by dual-luciferase reporter assays. Knockdown of COL5A1 inhibited the proliferation, invasion, and migration of gastric cancer cells, which could be rescued by the miR-137-3p inhibitor or overexpression of FSTL1. Ultimately, bioinformatics analyses showed that the expression of FSTL1 was highly correlated with immune infiltration.

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Section: Discussionmentioning

confidence: 99%

COL5A1 Promotes the Progression of Gastric Cancer by Acting as a ceRNA of miR-137-3p to Upregulate FSTL1 Expression

Yang

et al. 2022

Cancers

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“…miR-137 is targeted by lncRNA NCK1-AS1. Low NCK1-AS1 expression augments the profile of miR-137, reduces that of NUP 43, and represses GC cell proliferation, migration, and invasion [ 51 ]. The inhibitory impact of miR-137 on GC has been substantiated by the above findings.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA p53 upregulated regulator of p53 levels (PURPL) promotes the development of gastric cancer

et al. 2022

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Gastric cancer (GC), one of the most prevalent malignancies across the world, has an increasing incidence rate. Long non-coding RNA (lncRNA) PURPL (also referred to as LINC01021) has been demonstrated to influence malignant GC behaviors and partake in other cancers. Notwithstanding, reports pertaining to the underlying mechanism of PURPL in GC haven’t been rarely seen. Presently, in-vivo and ex-vivo experiments were implemented to examine the PURPL-miR-137-ZBTB7A-PI3K-AKT-NF-κB regulatory axis in GC. Our statistics revealed that PURPL presented a high expression in GC tissues and cell lines. PURPL overexpression remarkably exacerbated colony formation, migration, and invasion and repressed apoptosis in GC cells (AGS and MNK-45). In-vivo experiments also corroborated that cell growth was boosted by PURPL up-regulation. Mechanistic investigations verified that PURPL interacted with miR-137 and lowered its profile in GC cell lines. miR-137 overexpression or ZBTB7A knockdown upended the oncogenic function mediated by PURPL. PURPL initiated the PI3K/AKT/NF-κB pathway. PI3K and NF-κB inhibition impaired the promoting impact on GC cells elicited by PURPL overexpression and contributed to PURPL down-regulation. These findings disclosed that PURPL serves as an oncogene in the context of GC via miR-137-ZBTB7A-PI3K-AKT-NF-κB axis modulation.

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“…Studies have also reported that long non-coding RNAs (lncRNAs) or circular RNAs (circRNAs) sponge miR-137-3p through a ceRNA mechanism in GC [45][46]. However, no one has reported that mRNA can regulate miR-137-3p through a ceRNA mechanism, nor has it been reported that miR-137-3p can target COL5A1 or FSTL1.…”

Section: Discussionmentioning

confidence: 99%

Identification of a Key Competing Endogenous RNA Axis, “COL5A1/miR-137-3p/FSTL1”, Associated With Gastric Cancer Progression by Integrated Bioinformatics Analyses and Experimental Verification

Yang

et al. 2021

Preprint

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Background MicroRNAs (miRNAs) and their target genes have been shown to play an important role in gastric cancer (GC), but this role has not been fully clarified. Therefore, our goal was to find the key miRNA-mRNA regulatory network in GC by combining a variety of bioinformatics and experimental analyses. Methods Differentially expressed miRNAs (DEMs) and genes (DEGs) were screened from TCGA and GEO, respectively. Survival-related differentially expressed miRNAs (SRDEMs) were determined by Cox proportional hazards regression and lasso regression analyses. Differentially expressed target genes (DETGs) of SRDEMs were predicted by TargetScan and miRDB and overlapped with DEGs. We constructed a protein–protein interaction (PPI) network of DETGs and conducted weighted gene coexpression network analysis (WGCNA) to screen the hub genes. Then, qRT–PCR and western blotting were performed to detect the expression level, and a dual-luciferase reporter assay was conducted to verify the binding of miRNA and mRNAs. CCK-8, EdU, wound healing and Transwell assays were conducted to compare the proliferation, migration and invasion abilities of GC cells in the different groups. Results We identified 11 SRDEMs and 233 DETGs, from which we selected miR-137-3p and its target gene COL5A1 for further research because of their key roles in the results of the bioinformatics analyses. Then, we showed that miR-137-3p was significantly downregulated in GC and that overexpression of miR-137-3p suppressed the proliferation, invasion and migration of GC cells by targeting COL5A1. Furthermore, we found that COL5A1 could regulate the expression of FSTL1 and GC progression by sponging miR-137-3p. Finally, bioinformatics analyses showed that FSTL1 might promote GC progression by regulating the immune infiltration of GC. Conclusions miR-137-3p played a tumor-suppressive role in GC, and its target gene COL5A1 could competitively bind miR-137-3p to upregulate the expression of FSTL1, which affects immune infiltration.

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<p>Long Non-Coding RNA NCK1-AS1 Serves an Oncogenic Role in Gastric Cancer by Regulating miR-137/NUP43 Axis</p>

Cited by 14 publications

References 23 publications

COL5A1 Promotes the Progression of Gastric Cancer by Acting as a ceRNA of miR-137-3p to Upregulate FSTL1 Expression

COL5A1 Promotes the Progression of Gastric Cancer by Acting as a ceRNA of miR-137-3p to Upregulate FSTL1 Expression

Long non-coding RNA p53 upregulated regulator of p53 levels (PURPL) promotes the development of gastric cancer

Identification of a Key Competing Endogenous RNA Axis, “COL5A1/miR-137-3p/FSTL1”, Associated With Gastric Cancer Progression by Integrated Bioinformatics Analyses and Experimental Verification

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