Metabolic reprogramming, which is considered a hallmark of cancer, can maintain the homeostasis of the tumor environment and promote the proliferation, survival, and metastasis of cancer cells. For instance, increased glucose uptake and high glucose consumption, known as the “Warburg effect,” play an essential part in tumor metabolic reprogramming. In addition, fatty acids are harnessed to satisfy the increased requirement for the phospholipid components of biological membranes and energy. Moreover, the anabolism/catabolism of amino acids, such as glutamine, cystine, and serine, provides nitrogen donors for biosynthesis processes, development of the tumor inflammatory environment, and signal transduction. The ubiquitin–proteasome system (UPS) has been widely reported to be involved in various cellular biological activities. A potential role of UPS in the metabolic regulation of tumor cells has also been reported, but the specific regulatory mechanism has not been elucidated. Here, we review the role of ubiquitination and deubiquitination modification on major metabolic enzymes and important signaling pathways in tumor metabolism to inspire new strategies for the clinical treatment of cancer.

Objective Esophageal cancer (EC), a common gastrointestinal malignancy, ranks as the sixth leading cause of cancer death worldwide. Esophageal squamous cell carcinoma (ESCC) is the predominant histological subtype of EC. Lack of potential biomarkers for treatment and prognosis is a limitation for early diagnosis and treatment of ESCC. Methods Based on The Cancer Genome Atlas (TCGA) database, the weighted gene co-expression network analysis (WGCNA) was constructed to identify gene modules associated with the metastasis in ESCC. The LASSO algorithm was used to construct a prognosis genes model. After the collinearity test, all independent prognostic parameters and important clinical parameters were included in the prognostic nomogram constructed by the Cox regression model. The nomogram was used to evaluate the prognostic significance of these parameters in ESCC. Finally, we used biological experiments to preliminary investigate the impact of ENO1 on the metastasis risk of ESCC. Results A total of 16 genetic modules were identified, and the brown module is considered the most relevant to tumor metastasis. (P = 0.02, R2 = 0.30). Protein-protein interaction (PPI) network was performed to identify the hub nodes in the brown module. The univariate and multivariate Cox regression analysis indicated that ENO1 and SUPT5H were independent prognostic factors. Expression data of ENO1 was pipelined along with patients’ clinic pathological data for nomogram construction 1-, and 2-OS forecasting. ENO1 gene was regarded as "real" hub genes for cancer metastasis risk. Low-expressed ENO1 inhibited migration and invasion of human ESCC cells in vitro. The mechanism may involve the Wnt signaling pathway and the influence of EMT. Conclusion ENO1 might be a novel metastasis risk biomarker for ESCC.

The most frequent malignant tumor of the head and neck is head and neck squamous cell carcinoma (HNSCC), which has a high frequency, a poor prognosis in the late stages, and subpar therapeutic results. As a result, early HNSCC diagnosis and treatment are urgently needed; however, there are no good diagnostic biomarkers or efficient therapeutic targets at this time. The long-stranded non-coding RNA HOTAIR may be important in the pathogenesis of cancer, according to recent research. By interactions with DNA, RNA, and proteins, it has been demonstrated that HOTAIR, a >200 nucleotide RNA transcript, plays a role in the biological processes of many types of tumor cells, including proliferation, metastasis, and prognosis of HNSCC. Hence, this review discusses HOTAIR’s function and molecular mechanisms in HNSCC.

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