FAT10 promotes the progression of bladder cancer by upregulating HK2 through the EGFR/AKT pathway

Zou, Yan; Du, Yunyan; Cheng, Cheng; Deng, Xueqiang; Shi, Zimin; Lu, Xiongbing; Hu, Honglin; Qiu, Jun; Jiang, Weifan

doi:10.1016/j.yexcr.2020.112401

Cited by 17 publications

(14 citation statements)

References 24 publications

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“…FAT10 oncogenic effects were shown to be dependent of AKT signaling pathway activation in HCC [104]. Indeed, FAT10 overexpression induced phosphorylation of AKT in both HCC and bladder cancer cells [104,105]. Remarkably, TRIB3 has been previously listed has one of the genes involved in cell death and survival, modulated by exogenous FAT10 expression [103].…”

Section: Discussionmentioning

confidence: 98%

Tribbles Gene Expression Profiles in Colorectal Cancer

Fernandes

Yassuda

Bragança

et al. 2021

Gastrointestinal Disorders

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Colorectal cancer (CRC) is the third most common cancer and the second leading cause of death due to cancer in the world. Therefore, the identification of novel druggable targets is urgently needed. Tribbles proteins belong to a pseudokinase family, previously recognized in CRC as oncogenes and potential therapeutic targets. Here, we analyzed the expression of TRIB1, TRIB2, and TRIB3 simultaneously in 33 data sets from CRC based on available GEO profiles. We show that all three Tribbles genes are overrepresented in CRC cell lines and primary tumors, though depending on specific features of the CRC samples. Higher expression of TRIB2 in the tumor microenvironment and TRIB3 overexpression in an early stage of CRC development, unveil a potential and unexplored role for these proteins in the context of CRC. Differential Tribbles expression was also explored in diverse cellular experimental conditions where either genetic or pharmacological approaches were used, providing novel hints for future research. This comprehensive bioinformatic analysis provides new insights into Tribbles gene expression and transcript regulation in CRC.

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Section: Discussionmentioning

confidence: 98%

Tribbles Gene Expression Profiles in Colorectal Cancer

Fernandes

Yassuda

Bragança

et al. 2021

Gastrointestinal Disorders

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“…Furthermore, UBD knockdown significantly promoted EGFR ubiquitination, while overexpression of UBD reduced EGFR ubiquitination. Another study has shown that UBD stabilizes the expression of EGFR by regulating its degradation and ubiquitination effects, and positively regulates HK2 via the EGFR/AKT pathway to promote the development of bladder cancer ( Zou et al, 2021 ). UBD also stabilizes the expression of Nav1.5 by antagonizing the ubiquitination and degradation of Nav1.5, thereby preventing the degradation of Nav1.5 protein.…”

Section: Discussionmentioning

confidence: 99%

Ubiquitin D Promotes Progression of Oral Squamous Cell Carcinoma via NF-Kappa B Signaling

Wang

Feng

et al. 2021

Molecules and Cells

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Ubiquitin D (UBD) is highly upregulated in many cancers, and plays a pivotal role in the pathophysiological processes of cancers. However, its roles and underlying mechanisms in oral squamous cell carcinoma (OSCC) are still unclear. In the present study, we investigated the role of UBD in patients with OSCC. Quantitative real-time polymerase chain reaction and Western blot were used to measure the expression of UBD in OSCC tissues. Immunohistochemistry assay was used to detect the differential expressions of UBD in 244 OSCC patients and 32 cases of normal oral mucosae. In addition, CCK-8, colony formation, wound healing and Transwell assays were performed to evaluate the effect of UBD on the cell proliferation, migration, and invasion in OSCC. Furthermore, a xenograft tumor model was established to verify the role of UBD on tumor formation in vivo. We found that UBD was upregulated in human OSCC tissues and cell lines and was associated with clinical and pathological features of patients. Moreover, the overexpression of UBD promoted the proliferation, migration and invasion of OSCC cells; however, the knockdown of UBD exerted the opposite effects. In this study, our results also suggested that UBD promoted OSCC progression through NF-κB signaling. Our findings indicated that UBD played a critical role in OSCC and may serve as a prognostic biomarker and potential therapeutic target for OSCC treatment.

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“…In addition, HLA-F locus adjacent transcript 10 (FAT10) promotes cell growth and mediates HK2 expression through the EGFR/AKT pathway in BC cells. It was also shown that the upregulated expression of HK2 correlated with FAT10 in BC patients [ 65 ]. On the other hand, PKM2 modulated the expression of SREBP-1c via the AKT/mTOR signaling pathway, which suppressed the transcription of fatty acid synthase (FASN, a major lipogenic gene), leading to reduced tumor growth.…”

Section: Potential Signaling Pathways and Key Drivers Of Glycolytic Enzymesmentioning

confidence: 99%

Current Development and Application of Anaerobic Glycolytic Enzymes in Urothelial Cancer

Yang

Chuang

Kuo

et al. 2021

IJMS

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Urothelial cancer is a malignant tumor with metastatic ability and high mortality. Malignant tumors of the urinary system include upper tract urothelial cancer and bladder cancer. In addition to typical genetic alterations and epigenetic modifications, metabolism-related events also occur in urothelial cancer. This metabolic reprogramming includes aberrant expression levels of genes, metabolites, and associated networks and pathways. In this review, we summarize the dysfunctions of glycolytic enzymes in urothelial cancer and discuss the relevant phenotype and signal transduction. Moreover, we describe potential prognostic factors and risks to the survival of clinical cancer patients. More importantly, based on several available databases, we explore relationships between glycolytic enzymes and genetic changes or drug responses in urothelial cancer cells. Current advances in glycolysis-based inhibitors and their combinations are also discussed. Combining all of the evidence, we indicate their potential value for further research in basic science and clinical applications.

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FAT10 promotes the progression of bladder cancer by upregulating HK2 through the EGFR/AKT pathway

Cited by 17 publications

References 24 publications

Tribbles Gene Expression Profiles in Colorectal Cancer

Tribbles Gene Expression Profiles in Colorectal Cancer

Ubiquitin D Promotes Progression of Oral Squamous Cell Carcinoma via NF-Kappa B Signaling

Current Development and Application of Anaerobic Glycolytic Enzymes in Urothelial Cancer

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