Proliferation Potential-Related Protein Promotes the Esophageal Cancer Cell Proliferation, Migration and Suppresses Apoptosis by Mediating the Expression of p53 and Interleukin-17

Ye, Fei; Song, Jizhong; Wang, Yetao; Xu, Xuemei; Zhang, Kaiguang

doi:10.1159/000492393

Cited by 10 publications

(5 citation statements)

References 26 publications

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“…In the present study, it was found that DIM, a natural phytochemical Through KEGG analysis, it was found that DIM may be involved in the apoptosis, IL-17 and PI3K-Akt signaling pathways. A study has shown that TP53 and IL-17 can affect the proliferation and migration of esophageal cancer cells (22). Furthermore, PI3K-Akt can affect the proliferation, invasion and metastasis of a variety of tumor cells.…”

Section: Discussionmentioning

confidence: 99%

3,3'-Diindolylmethane inhibits the proliferation of esophageal squamous cell carcinoma cells via downregulation of STIM1

Xiong,

Tang,

et al. 2024

Oncol Lett

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3,3'-Diindolylmethane (DIM) is a natural phytochemical derived from cruciferous plants that has inhibitory effects on a wide range of tumor cells; however, its relevant effects on esophageal cancer cells have been poorly studied. Therefore, in the present study, a pharmacology network approach was used to predict the possible core targets of DIM acting on esophageal cancer. Subsequently, using in vitro experiments, TE-1 human esophageal cancer cells were treated with different concentrations of DIM (0, 40, 60 and 80 µM) for 24 h. Changes in cell activity were detected by Cell Counting Kit-8 assay, and changes in the expression levels of stromal interaction molecule 1 (STIM1) and apoptosis-related proteins, B-cell lymphoma-2 (Bcl-2) and Bax, were assessed by western blotting, followed by the upregulation of STIM1 by thapsigargin (Tg). Network pharmacology analysis showed that there were 39 potential core targets of DIM in esophageal cancer. The results of the in vitro experiments showed that DIM could inhibit the viability of esophageal cancer cells, downregulate the expression of STIM1 and Bcl-2 proteins and upregulate the expression of Bax protein, all in a concentration-dependent manner. The results also demonstrated that toxic carotenoids were agonist against STIM1 protein and upregulated STIM1 and Bax protein expression. After agonizing STIM1 protein expression using Tg, DIM was able to counteract the expression trend of STIM1, Bcl-2 and Bax protein in TE-1 cells. In summary, DIM induced apoptosis and inhibited the viability of esophageal cancer cells by downregulating the expression of STIM1 protein; therefore, the natural phytochemical, DIM, may be a potential substance for the early prevention and treatment of esophageal cancer cells.

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Section: Discussionmentioning

confidence: 99%

3,3'-Diindolylmethane inhibits the proliferation of esophageal squamous cell carcinoma cells via downregulation of STIM1

Xiong,

Tang,

et al. 2024

Oncol Lett

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“…These alterations in levels may be explained by the overexpression of the protein, the mislocalization of unassembled or misassembled protein [37]. Various studies have corroborated that SNRPG may contribute signi cantly to the initiation and progression of cancers [38][39][40][41][42].…”

Section: Discussionmentioning

confidence: 99%

The immunomodulation effects of small nuclear ribonucleoprotein polypeptide G (SNRPG) in human brain tumors

Zhao,

Guo,

Jiang

et al. 2023

Preprint

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Small nuclear ribonucleoprotein polypeptide G (SNRPG) or Smith protein G (SmG) is vitally involved in the biogenesis of the major and minor spliceosome precursors that are spliceosomaluridyl-rich small nuclear ribonucleoprotein particles (U snRNPs; U1, U2, U4 and U5). The plausible involvement of SNRPG in tumor formation and oncogenesis has made it the center of studies. In this study, for the first time, this tumorigenic and immune-modulating functioning of SNRPG employing TCGA and GEO dataset-derived brain tumors has been scrutinized by us. Most tumors demonstrate higher SNRPG expression compared with normal ones, including various human brain tumors. The TCGA cohorts also displayed variation in SNRPG genetic status in different tumor samples. Experimental validations supported the oncogenic effect of SNRPG, and furthermore, the mechanism might be associated with the regulation of immune response. Further bioinformatics analysis revealed that some malignancies demonstrated a link between the SNRPG expression and CD8 + T-cell while others were linked with fibroblast infiltration. Moreover, the mechanistic aspects of SNRPG entailed spliceosome-associated functions among others. More in-depth research indicated that SNRPG may impact tumorigenesis of human brain tumors via exerting post-transcriptional modulation of TP53 through the mechanism of alternative polyadenylation (APA) at the region of 3’ untranslated regions (UTRs). However, more research should be done to further confirm the preliminary results in our current study. Overall, current research presents the first detailed scrutiny of the oncogenic and immune-modulating functioning of SNRPG in several malignancies of human brain.

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“…The expression of SNRPG in different cancers can be explained by high levels of protein, the mis-localization of unassembled or misassembled proteins [29] . Thus, SNRPG might contribute to the initiation and progression of different cancers [30][31][32][33][34] . We found that SNRPE was highly expressed in tumor tissues by using ONCOMINE [16] , but the results of SNRPF and SNRPG groups were not similar in this study.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive analysis of the expression and prognostic value for SNRP members in hepatocellular carcinoma

Guo

Liang

2022

Preprint

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Background Heterogeneity and epigenetic modifications lead to differences among treatment strategies, management and prognosis in hepatocellular carcinomas. The family of small nuclear ribonucleoprotein polypeptides (SNRPs) plays a crucial role in tumorigenesis and progression. However, the expression profile and prognostic impact of these family members are not clear. Here, we discuss the expression levels and prognosis of SNRPs. family members Methods We compared the transcript levels of each SNRPs member in pan-cancerous tissues by ONCOMINE and further analyzed the expression levels and tumor staging of these markers in hepatocellular carcinoma using UALCAN and GEPIA online databases, while assessing the prognostic value of their mRNA expression and performing functional enrichment analysis by Metascape software using Kaplan–Meier plotter database. Results These results showed that mRNA levels of each member of SNRP (B, D1, D2, D3, E, F, G) were significantly upregulated in hepatocellular carcinoma compared to normal tissue and were more highly expressed in patients with advanced hepatocellular carcinoma. mRNA expression of SNRPB, SNRPD1 and SNRPG was associated with poorer overall survival (OS), recurrence-free survival (RFS) and progression-free survival (PFS), which was considered to be statistically significant. Conclusion We systematically analyzed the mRNA expression and prognostic significance of each member of SNRPs in HCC and demonstrated the correlation, interaction network, gene alteration and functional enrichment among SNRPs members. Our data suggest that SNRPs members as oncogenes may be a potential indicator of HCC.

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Proliferation Potential-Related Protein Promotes the Esophageal Cancer Cell Proliferation, Migration and Suppresses Apoptosis by Mediating the Expression of p53 and Interleukin-17

Cited by 10 publications

References 26 publications

3,3'-Diindolylmethane inhibits the proliferation of esophageal squamous cell carcinoma cells via downregulation of STIM1

3,3'-Diindolylmethane inhibits the proliferation of esophageal squamous cell carcinoma cells via downregulation of STIM1

The immunomodulation effects of small nuclear ribonucleoprotein polypeptide G (SNRPG) in human brain tumors

Comprehensive analysis of the expression and prognostic value for SNRP members in hepatocellular carcinoma

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