Identification of the complex regulatory relationships related to gastric cancer from lncRNA‐miRNA‐mRNA network

Wang, Jie; Ding, Yanrui; Wu, Yanyan; Wang, Xiaoxia

doi:10.1002/jcb.29332

Cited by 33 publications

(27 citation statements)

References 43 publications

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“…The lncRNA NKX2‐1‐AS1 was identified to be highly expressed in primary lung adenocarcinomas and found to be associated with lung carcinoma cell migration [13]. Furthermore, bioinformatics studies have revealed that NKX2‐1‐AS1 may act as a competing endogenous RNA (ceRNA) in GC [14]. However, the contribution of aberrant expression of NKX2‐1‐AS1 in GC tumorigenesis and its prognostic relevance in GC remains elusive.…”

Section: Introductionmentioning

confidence: 99%

LncRNA NKX2‐1‐AS1 promotes tumor progression and angiogenesis via upregulation of SERPINE1 expression and activation of the VEGFR‐2 signaling pathway in gastric cancer

et al. 2021

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Long noncoding RNAs (lncRNAs) can compete with endogenous RNAs to modulate the gene expression and contribute to oncogenesis and tumor metastasis. lncRNA NKX2‐1‐AS1 (NKX2‐1 antisense RNA 1) plays a pivotal role in cancer progression and metastasis; however, the contribution of aberrant expression of NKX2‐1‐AS1 and the mechanism by which it functions as a competing endogenous RNA (ceRNA) in gastric cancer (GC) remains elusive. NKX2‐1‐AS1 expression was detected in paired tumor and nontumor tissues of 178 GC patients by quantitative reverse transcription PCR (qRT‐PCR). Using loss‐of‐function and gain‐of‐function experiments, the biological functions of NKX2‐1‐AS1 were evaluated both in vitro and in vivo. Further, to assess that NKX2‐1‐AS1 regulates angiogenic processes, tube formation and co‐culture assays were performed. RNA binding protein immunoprecipitation (RIP) assay, a dual‐luciferase reporter assay, quantitative PCR, Western blot, and fluorescence in situ hybridization (FISH) assays were performed to determine the potential molecular mechanism underlying this ceRNA. The results indicated that NKX2‐1‐AS1 expression was upregulated in GC cell lines and tumor tissues. Overexpression of NKX2‐1‐AS1 was significantly associated with tumor progression and enhanced angiogenesis. Functionally, NKX2‐1‐AS1 overexpression promoted GC cell proliferation, metastasis, invasion, and angiogenesis, while NKX2‐1‐AS1 knockdown restored these effects, both in vitro and in vivo. RIP and dual‐luciferase assays revealed that the microRNA miR‐145‐5p is a direct target of NKX2‐1‐AS1 and that NKX2‐1‐AS1 serves as a ceRNA to sponge miRNA and regulate angiogenesis in GC. Moreover, serpin family E member 1 (SERPINE1) is an explicit target for miR‐145‐5p; besides, the NKX2‐1‐AS1/miR‐145‐5p axis induces the translation of SERPINE1, thus activating the VEGFR‐2 signaling pathway to promote tumor progression and angiogenesis. NKX2‐1‐AS1 overexpression is associated with enhanced tumor cell proliferation, angiogenesis, and poor prognosis in GC. Collectively, NKX2‐1‐AS1 functions as a ceRNA to miR‐145‐5p and promotes tumor progression and angiogenesis by activating the VEGFR‐2 signaling pathway via SERPINE1.

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Section: Introductionmentioning

confidence: 99%

LncRNA NKX2‐1‐AS1 promotes tumor progression and angiogenesis via upregulation of SERPINE1 expression and activation of the VEGFR‐2 signaling pathway in gastric cancer

et al. 2021

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“…However, the mechanism of how GRM3 takes impact on TMB is still unclear at present. As for THSD7B and FLNC , it has been reported that they are associated with tumor progression and/or prognosis of multiple tumors, such as NSCLC, 51 gastric cancer, 52 and hepatocellular carcinoma, 53 where the mechanism is still a mystery. It is worth exploring other potential mechanisms of how these genes impact immunotherapy.…”

Section: Discussionmentioning

confidence: 99%

“…and Liu cohort 17 consisted of 110, 64, and 144 patients, respectively. In the Allen cohort,52.7% (58/110) was at the normal level of LDH, whereas 43.6% (48/110) was elevated. Overall the median TMB was 6.9 mutations per Mb.…”

mentioning

confidence: 90%

Integrated genomic analysis identifies a genetic mutation model predicting response to immune checkpoint inhibitors in melanoma

Jiang

Ding

et al. 2020

Cancer Medicine

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“…Mounting evidence demonstrates that lncRNA acts as a sponge for miRNA to regulate the level of target miRNA in human cancers. 31 For example, LncRNA PTCSC3 targeted miR-574-5p to decrease the level of miR-574-5p in cervical cancer. 32 We next used the bioinformatics analysis tool starBase to predict the potential targets of TMPO-AS1, and found that TMPO-AS1 was able to bind to miR-498.…”

Section: Discussionmentioning

confidence: 99%

Propofol suppresses hypoxia‐induced esophageal cancer cell migration, invasion, and EMT through regulating lncRNA TMPO‐AS1/miR‐498 axis

Gao

Guo

et al. 2020

Thoracic Cancer

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Background Propofol has been reported to be related to the migration, invasion, and epithelial‐mesenchymal transition (EMT) of esophageal cancer (EC) cells. However, the detailed mechanism has not yet been fully reported. The purpose of this research was to elucidate the function of long non‐coding RNA TMPO antisense RNA 1 (lncRNA TMPO‐AS1) and microRNA‐498 (miR‐498) in propofol‐regulated EC. Methods Transwell assay was performed to assess cell migratory and invasive abilities. Western blot assay was employed to determine the levels of EMT markers and hypoxia inducible factor‐1 (HIF‐1α). Quantitative real‐time polymerase chain reaction (qRT‐PCR) was carried out to detect the levels of TMPO‐AS1 and miR‐498. Moreover, the interaction between TMPO‐AS1 and miR‐498 was predicted by starBase, and then confirmed by the dual‐luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Results Propofol suppressed hypoxia‐induced EC cell migration, invasion, and EMT. Both TMPO‐AS1 overexpression and miR‐498 knockdown weakened the effect of propofol on hypoxia‐induced EC cell progression. Interestingly, TMPO‐AS1 targeted miR‐498 and suppressed miR‐498 expression. TMPO‐AS1 regulated EC cell progression via downregulating miR‐498 expression. Conclusions Collectively, our findings demonstrated that propofol inhibited hypoxia‐induced EC cell mobility through modulation of the TMPO‐AS1/miR‐498 axis, providing a theoretical basis for the treatment of EC.

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Identification of the complex regulatory relationships related to gastric cancer from lncRNA‐miRNA‐mRNA network

Cited by 33 publications

References 43 publications

LncRNA NKX2‐1‐AS1 promotes tumor progression and angiogenesis via upregulation of SERPINE1 expression and activation of the VEGFR‐2 signaling pathway in gastric cancer

LncRNA NKX2‐1‐AS1 promotes tumor progression and angiogenesis via upregulation of SERPINE1 expression and activation of the VEGFR‐2 signaling pathway in gastric cancer

Integrated genomic analysis identifies a genetic mutation model predicting response to immune checkpoint inhibitors in melanoma

Propofol suppresses hypoxia‐induced esophageal cancer cell migration, invasion, and EMT through regulating lncRNA TMPO‐AS1/miR‐498 axis

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