Multi-Omics Analysis Identified TMED2 as a Shared Potential Biomarker in Six Subtypes of Human Cancer

TMED2/9/10 Serve as Biomarkers for Poor Prognosis in Head and Neck Squamous Carcinoma

“…The results of the single-cell analysis of TMED2/9/10 implied its relationship with specific immune responses. Recently, it has been shown that TMED2 overexpression was negatively correlated with CD8 + T immune cell levels in HNSC, suggesting that TMED2 might initiate tumor development by altering the levels of immune infiltration in the tumor microenvironment ( Sial et al, 2021 ). Also, Sun et al found that TMED2 was required for cellular interferon (IFN) responses to viral DNA.…”

“…According to previous studies, abnormal expression of TMED proteins with related pathways was closely associated with poor prognosis in many diseases, such as non-alcoholic fatty liver, multiple myeloma, diabetes, Alzheimer’s disease, strong chordoma, osteoarthritis ( Wang et al, 2012 ; Hou et al, 2017 ; Shin et al, 2019 ; Ge et al, 2020 ; Yang J. et al, 2021 ; Huang et al, 2021 ). For instance, TMED2 was expressed higher in sphere-shaped clones (SCs) and might play a role in cancer cell proliferation; the increased expression of TMED2 was significantly related to unfavorable outcomes in patients with breast cancer ( Sial et al, 2021 ). TMED3 played a role in promoting the progression and development of lung squamous cell carcinoma, liver cancer, and breast progression ( Zheng et al, 2016 ; Pei et al, 2019 ; Xie et al, 2021 ), and TMED8 methylation was a novel predictive and prognostic feature for patients with high-risk neuroblastoma ( Liu and Li, 2021 ).…”

“…Therefore, TMED proteins might serve as prognostic markers to predict tumor prognosis. Current studies have found that the expression level of TMED2 in HNSC was up-regulated and related to different cancer stages, races, genders, and ages ( Sial et al, 2021 ). Nevertheless, the potential prognosis value of the TMED family has not been fully elucidated in HNSC.…”

Prostate cancer in omics era

“…Three metabolic pathways, including fatty acid metabolism, TCA cycle, and glycerophospholipid metabolism, were upregulated in SPOP mutant tissues Oberhuber et al [ 130 ] Tissue M + P + T STAT3 low vs STAT3 high At the transcriptome level, OXPHOS is upregulated in PCa, as is the TCA cycle/OXPHOS at the proteome level. A promising independent prognostic marker in PCa is PDK4, a critical regulator of the TCA cycle Murphy et al [ 131 ] Tissue serum E + M + P + T BPH vs. PCa Higher accuracy in predicting PCa aggressiveness compared to clinical features alone or individual omics data with Ordinal C‐Index value of 0.94 and Multi AUC value of 0.91 Itkonen et al [ 132 ] Cell line M + P + T CDK9 inhibitor treated vs. untreated Inhibition of CDK9 causes acute metabolic stress in prostate cancer cells by consuming ATP and triggering rapid and sustained phosphorylation of AMPK, as well as dramatically downregulating oxidative phosphorylation in mitochondria and accumulation of acylcarnitines, metabolic intermediates in fatty acid oxidation Kamoun et al [ 133 ] Tissue E + G + T PCa vs. NAT A group of 36 transcriptomic biomarkers outperformed the most commonly used prognostic molecular signatures in identifying a subpopulation of patients without biochemical relapse Gómez et al [ 134 ] Urine serum M + T Low vs. high grade PCa Between the two groups of patients, there were significant changes in 36 metabolic pathways, including glycine, glucose, and 1-methlynicotinamide, metabolites important for energy metabolism and nucleotide synthesis Paez et al [ 135 ] Tissue P + T PRAD vs. NAT HO-1 is related with cellular cytoskeleton integrity, and its stimulation in PCa cells resulted in reduced cell trajectory and velocity, a lower frequency of migratory events, and a markedly increased proportion of filopodia-like protrusions that facilitate attachment between adjacent cells Sial et al [ 136 ] …”

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“…According to previous studies, abnormal expression of TMED proteins with related pathways was closely associated with poor prognosis in many diseases, such as non-alcoholic fatty liver, multiple myeloma, diabetes, Alzheimer's disease, strong chordoma, osteoarthritis (Wang et al, 2012;Hou et al, 2017;Shin et al, 2019;Ge et al, 2020;Yang J. et al, 2021;Huang et al, 2021). For instance, TMED2 was expressed higher in sphere-shaped clones (SCs) and might play a role in cancer cell proliferation; the increased expression of TMED2 was significantly related to unfavorable outcomes in patients with breast cancer (Sial et al, 2021). TMED3 played a role in promoting the progression and development of lung squamous cell carcinoma, liver cancer, and breast progression (Zheng et al, 2016;Pei et al, 2019;Xie et al, 2021), and TMED8 methylation was a novel predictive and prognostic feature for patients with high-risk neuroblastoma (Liu and Li, 2021).…”