Calycosin inhibits nasopharyngeal carcinoma cells by influencing EWSAT1 expression to regulate the TRAF6-related pathways

Kong, Lingping; Li, Xin; Wang, Hong; He, Guobin; Tang, Anzhou

doi:10.1016/j.biopha.2018.06.143

Cited by 27 publications

(25 citation statements)

References 31 publications

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“…As an E3 ubiquitin ligase, TRAF6 may rely on ubiquitin to regulate tumorigenesis [ 4 ]. TRAF6 is a significant oncogene in pancreatic cancer [ 5 ], prostate cancer [ 6 ], and nasopharyngeal carcinoma [ 7 ]. In addition, TRAF6 activates NF- κ B signaling in RAS-driven lung cancers [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

TRAF6 Promotes Gastric Cancer Cell Self-Renewal, Proliferation, and Migration

Yang

Jin

et al. 2020

Stem Cells International

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Gastric cancer is the third most common type of tumor associated with death. TRAF6 belongs to the tumor necrosis factor receptor-associated factor family and has been demonstrated to be involved in tumor progression in various cancers. However, the exact effect of TRAF6 on gastric cancer stem cells has not been extensively studied. In this study, abnormal expression of TRAF6 was found in gastric cancer tissues. Overexpression of TRAF6 enhanced proliferation and migration, and TRAF6 knockdown reversed this phenomenon in gastric cancer cells. Moreover, TRAF6 may inhibit differentiation and promote stemness and epithelial-mesenchymal transition (EMT). Transcriptome profiles revealed 701 differentially expressed genes in the wild-type group and the TRAF6 knockout group. Potential molecules associated with cell proliferation and migration were identified, including MAPK, FOXO, and IL-17. In conclusion, TRAF6 is a significant factor promoting proliferation and migration in gastric cancer cells and may provide a new target for the accurate treatment of gastric cancer.

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Section: Introductionmentioning

confidence: 99%

TRAF6 Promotes Gastric Cancer Cell Self-Renewal, Proliferation, and Migration

Yang

Jin

et al. 2020

Stem Cells International

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“…lncRNA Ewing sarcoma associated transcript 1 (EWSAT1) is a novel cancer-associated lncRNA that serves critical roles in the occurrence and progression of tumors, including nasopharyngeal carcinoma ( 13 , 14 ), osteosarcoma ( 15 ), colorectal ( 16 ) and ovarian cancer ( 17 ), and Ewing sarcoma ( 18 ). However, the biological role and mechanism of EWSAT1 in gliomas remain to be identified.…”

Section: Introductionmentioning

confidence: 99%

Long non‑coding RNA EWSAT1 contributes to the proliferation and invasion of glioma by sponging miR‑152‑3p

et al. 2020

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Long non-coding RNAs (lncRNA) are a type of ncRNA with a length ranging from 200-1,000 nucleotides. Previous studies have confirmed that the lncRNA Ewing sarcoma associated transcript 1 (EWSAT1) exerts regulatory roles in cancer development and progression. However, its clinical significance in glioma remains unknown. In the present study, RNA-sequencing data from the Gene Expression Omnibus database and The Cancer Genome Atlas was explored to investigate the association between EWSAT1 expression and prognosis in patients with glioma. Increased EWSAT1 was associated with the presence of necrosis on magnetic resonance imaging scans in patients with glioma. Furthermore, knockdown of EWSAT1 was indicated to suppress the proliferative and invasive abilities of glioblastoma cell lines using Cell Counting Kit-8 and Transwell assays. Additionally, microRNA (miR)-152-3p was identified as a potential target of EWSAT1. The present study demonstrated that EWSAT1 interacted directly with miR-152-3p, and rescue experiments confirmed that EWSAT1 participated in glioma development by suppressing miR-152-3p. These results indicated that EWSAT1 is involved in the occurrence and progression of glioma, and may serve as a novel target and potential prognostic biomarker of glioma treatment.

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“…Interestingly, a functional phytoestrogen of calycosin is found with potent anti-cancer activities, such as liver cancer, breast cancer, colorectal cancer [24]. Recently, an attractive study in vitro shows calycosin inhibits proliferation of NPC cells through affecting lncRNA ewing sarcomaassociated transcript 1 (EWSAT1) expression [25]. However, the current evidence has not been revealed for detailed molecular mechanisms of calycosin against NPC.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatic and experimental findings to indicate anti-cancer targets and mechanisms of calycosin against nasopharyngeal carcinoma

Liu

Pan

Wang

et al. 2020

Preprint

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Background: Calycosin is a naturally-occurring phytoestrogen that reportedly exerts anti- nasopharyngeal carcinoma (NPC) effects. Nevertheless, the molecular mechanisms for anti-NPC using calycosin remain unrevealed. Methods: Thus, a network pharmacology was used to uncover anti-NPC pharmacological targets and mechanisms of calycosin. Additionally, validated experiments were conducted to validate the bioinformatic findings of calycosin for treating NPC. Results: As results, bioinformatic assays showed that the predictive pharmacological targets of calycosin against NPC were TP53, MAPK14, CASP8, MAPK3, CASP3, RIPK1, JUN, ESR1, respectively. And the top 20 biological processes and pharmacological mechanisms of calycosin against NPC were identified accordingly. In clinical data, NPC samples showed positive expression of MAPK14, reduced TP53, CASP8 expressions. In studies in vitro and in vivo, calycosin-dosed NPC cells resulted in reduced cell proliferation, promoted cell apoptosis. In TUNEL staining, calycosin exhibited elevated apoptotic cell number. And immunostaining assays resulted in increased TP53, CASP8 positive cells, and reduced MAPK14 expressions in calycosin-dosed NPC cells and tumor-bearing nude mice. Conclusion: Altogether, these bioinformatic findings reveal optimal pharmacological targets and mechanisms of calycosin against NPC, following with representative identification of human and preclinical experiments. Notably, some of original biotargets may be potentially used to treat NPC.

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Calycosin inhibits nasopharyngeal carcinoma cells by influencing EWSAT1 expression to regulate the TRAF6-related pathways

Cited by 27 publications

References 31 publications

TRAF6 Promotes Gastric Cancer Cell Self-Renewal, Proliferation, and Migration

TRAF6 Promotes Gastric Cancer Cell Self-Renewal, Proliferation, and Migration

Long non‑coding RNA EWSAT1 contributes to the proliferation and invasion of glioma by sponging miR‑152‑3p

Bioinformatic and experimental findings to indicate anti-cancer targets and mechanisms of calycosin against nasopharyngeal carcinoma

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