An oncogenic gene, SNRPA1, regulates PIK3R1, VEGFC, MKI67, CDK1 and other genes in colorectal cancer

Zeng, Qingmin; Lei, Fang; Chang, Ying; Gao, Zhaoya; Wang, Yanzhao; Gao, Qingkun; Niu, Pei; Li, Qiang

doi:10.1016/j.biopha.2019.109076

Cited by 25 publications

(27 citation statements)

References 32 publications

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“…PIK3R1 has been identified to be differentially expressed in many human cancers. For example, PIK3R1 functions as a tumor suppressor in hepatocellular carcinomas and renal cancer [27,28], whereas acts as an oncogene in ovarian and colon tumors and plays a role in tumor progression and metastasis [29,30]. However, the relationship between PIK3R1 and LSCC cell development has not been fully elucidated.…”

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confidence: 99%

Silencing of miR-17-5p suppresses cell proliferation and promotes cell apoptosis by directly targeting PIK3R1 in laryngeal squamous cell carcinoma

et al. 2020

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Background: Increasing evidence has suggested that microRNAs (miRNAs) act as key post-transcriptional regulators in tumor progression. Previous studies have confirmed that miR-17-5p functions as an oncogene in multiple cancers and contributes to tumor progression. However, the role and biological functions of miR-17-5p in the development of laryngeal squamous cell carcinoma (LSCC) still remain unknown.Methods: qRT-PCR was used to detect miRNA and mRNA expression levels in LSCC tissues and cell lines. CCK-8 assay was used to measure cell viability and flow cytometry was performed to evaluate cell apoptosis. Western blot analysis was used to detect the protein levels of BAX, BCL-2, cleaved Caspase-3, PIK3R1 and AKT. Luciferase reporter assay was used to detect the effect of miR-17-5p on PIK3R1 expression. Xenograft animal model was used to test the effect of miR-17-5p on LSCC cell in vivo. Results:In the present study, we found that miR-17-5p expression level was upregulated in LSCC tissues and cell lines. Depletion of miR-17-5p in LSCC cells significantly reduced cell proliferation and promoted cell apoptosis in vitro and in vivo. Mechanically, knockdown of miR-17-5p in LSCC cells inhibited BCL-2 expression while enhanced BAX and cleaved Caspase-3 protein expression. Moreover, depletion of miR-17-5p in LSCC cells suppressed AKT phosphorylation but did not influence PTEN expression. Importantly, miR-17-5p positively regulated PIK3R1 expression by directly binding to its 3′-untranslated region (UTR). Additionally, PIK3R1, which expression was downregulated in LSCC tissues and cell lines, was involved in LSCC cell survival by modulating the activation of AKT signal pathway. Dysregulation of miR-17-5p/PIK3R1 axis was participated in LSCC cell proliferation and apoptosis by inhibiting the activation of the PI3K/AKT signaling pathway. Conclusions:In conclusion, our study indicates that the miR-17-5p/PIK3R1 axis plays an essential role in the development of LSCC and provides a potential therapeutic target for LSCC treatment. BackgroundLaryngeal squamous cell carcinoma (LSCC) is the most common head and neck malignancy accounting for more than 95% of head and neck squamous cell carcinoma (HNSCC), with 177,422 new cases and 94,771

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Silencing of miR-17-5p suppresses cell proliferation and promotes cell apoptosis by directly targeting PIK3R1 in laryngeal squamous cell carcinoma

et al. 2020

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“…The characterization of the currently identified leader genes, reported in Table 2 , revealed their involvement in several biological processes, such as cell signaling (i.e., CTNNB1, CBL, GRB2, PIK3CA, PIK3R1), transcriptional pathways (i.e., JUN, RELA), cell proliferation/differentiation (i.e., FOS) and immuno-inflammatory processes (i.e., IL1B, IL4, IL6, IL10; see Table 2 ) [ 22 ]. Evidence supporting the role exerted by leader genes in both CRC and periodontitis pathogenesis [ 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 ], reported in Table 2 , suggested that the pathogenic mechanisms underlying the association between periodontitis and CRC may be mainly related to the effect of the products of the leader genes on cell cycle dysregulation and on alteration of the immuno-inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

The Association between Periodontitis and Human Colorectal Cancer: Genetic and Pathogenic Linkage

Spirito

Toti

Pilone

et al. 2020

Life

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Periodontitis has been associated with an increased risk of and mortality associated with human colorectal cancer (CRC). Current evidence attributes such an association to the direct and indirect effects of virulence factors belonging to periodontal pathogens, to inflammatory mediators and to genetic factors. The aims of the study were to assess the existence of a genetic linkage between periodontitis and human CRC, to identify genes considered predominant in such a linkage, thus named leader genes, and to determine pathogenic mechanisms related to the products of leader genes. Genes linking periodontitis and CRC were identified and classified in order of predominance, through an experimental investigation, performed via computer simulation, employing the leader gene approach. Pathogenic mechanisms relating to leader genes were determined through cross-search databases. Of the 83 genes linking periodontitis and CRC, 12 were classified as leader genes and were pathogenically implicated in cell cycle regulation and in the immune-inflammatory response. The current results, obtained via computer simulation and requiring further validation, support the existence of a genetic linkage between periodontitis and CRC. Cell cycle dysregulation and the alteration of the immuno-inflammatory response constitute the pathogenic mechanisms related to the products of leader genes.

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“…Further functional analysis revealed that MKI67 might take part in the occurrence of apoptosis by regulating the p53 signaling pathway (Xiong, Zeng, Jiang, Luo, & Chen, 2019). Furthermore, Zeng demonstrated that SNRPA1 (OMIM: 603521) can regulate PIK3R1 (OMIM:171833) , VEGFC (OMIM:601528) , and MKI67 molecules in colorectal cancer through gene overexpression and gene knockout experiments, and then be involved in tumorigenesis and development, suggesting that MKI67 may serve as a molecular target for cell cycle and apoptosis (Zeng et al, 2019). Consistent with the above studies, we found that MKI67 is highly expressed in TS tissues.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, Wang found multiple genes differentially expressed in scar tissues and normal tissues through bioinformatics analysis. And through further analysis, Wang found that CCNB2 may be involved in the development of scar by regulating the TP53 signaling pathway, providing ideas for the study of the mechanisms of scar (Zeng et al, 2019). Consistent with the above studies, we found that CCNB2 was highly expressed in TS.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics analysis and verification of gene targets for benign tracheal stenosis

Wang

Qiu

et al. 2020

Molec Gen & Gen Med

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Background Tracheal injury could cause intratracheal scar hyperplasia which in turn causes benign tracheal stenosis (TS). With the increasing use of mechanical ventilation and ventilator, the incidence of TS is increasing. However, the molecular mechanisms of TS have not been elucidated. It is significant to further explore the molecular mechanisms of TS. Methods The repeatability of public data was verified. Differently expressed genes (DEGs) and most significant genes were identified between TS and normal samples. Enrichment analysis of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were analyzed. The comparative toxicogenomics database were analyzed. TS patients were recruited and RT‐qPCR were performed to verify the most significant genes. Results There exist strong correlations among samples of TS and normal group. There was a total of 194 DEGs, including 61 downregulated DEGs and 133 upregulated DEGs. GO were significantly enriched in mitotic nuclear division, cell cycle, and cell division. Analysis of KEGG indicated that the top pathways were cell cycle, and p53 pathway. MKI67(OMIM:176741), CCNB1(OMIM:123836), and CCNB2(OMIM:602755) were identified as the most significant genes of TS, and validated by the clinical samples. Conclusion Bioinformatics methods might be useful method to explore the mechanisms of TS. In addition, MKI67, CCNB1, and CCNB2 might be the most significant genes of TS.

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An oncogenic gene, SNRPA1, regulates PIK3R1, VEGFC, MKI67, CDK1 and other genes in colorectal cancer

Cited by 25 publications

References 32 publications

Silencing of miR-17-5p suppresses cell proliferation and promotes cell apoptosis by directly targeting PIK3R1 in laryngeal squamous cell carcinoma

Silencing of miR-17-5p suppresses cell proliferation and promotes cell apoptosis by directly targeting PIK3R1 in laryngeal squamous cell carcinoma

The Association between Periodontitis and Human Colorectal Cancer: Genetic and Pathogenic Linkage

Bioinformatics analysis and verification of gene targets for benign tracheal stenosis

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