Abstract
T-complex protein-1 ring complex (TRiC), also known as Chaperonin Containing T-complex protein-1 (CCT), is a multisubunit chaperonin required for the folding of nascent proteins. Mounting evidence suggests that TRiC also contributes to the development and progression of tumors, but there are limited studies on pathogenic functions in hepatocellular carcinoma (HCC). We comprehensively evaluated the expression pattern and biological functions of TRiC subunits using The Cancer Genome Atlas and The Human Protein Atlas. Expression levels of TRiC subunits TCP1, CCT2/3/4/5/6A/7/8 were significantly upregulated in HCC tissues at both transcript and protein levels, which predicted shorter overall survival (OS). Moreover, high mutation rates were found in several CCT subunits, and patients with altered CCT genes exhibited poorer clinical outcomes. Functional enrichment analysis showed that co-regulated genes were preferentially involved in ‘protein folding’ and ‘microtubule-based process’, while genes co-expressed with CCT subunits were primarily involved in ‘ribosome’ and ‘spliceosome’. Knockout of CCT5 in a HCC cell line reduced while overexpression enhanced proliferation rate, cycle transition, migration, and invasion. In conclusion, these findings suggest that subunits of the TRiC may be potential biomarkers for the diagnosis of HCC and play an important role in the occurrence and development of HCC.
Highlights
Hepatocellular carcinoma (HCC) is one of the most frequent malignant tumors throughout the world
Our results showed that CCT5 was significantly upregulated in hepatocellular carcinoma (HCC) and it seemed to be a good indicator of prognosis in HCC
Expression levels of T-complex protein-1 ring complex (TRiC) subunits were significantly upregulated in HCC compared to normal tissues except for subunit CCT6B
Summary
Hepatocellular carcinoma (HCC) is one of the most frequent malignant tumors throughout the world. HCC prognosis has improved greatly over the past 20 years, the five-year survival rate continues to be extremely low. Several targeted drugs are available that can prolong life, but again these have not markedly improved 5-year survival. The development of HCC is a complex process, and its occurrence, development, and metastasis are closely related to various gene mutations, the constantly activation of cell signal transduction pathways and abnormal neovascularization. A large number of studies have found the pathogenesis and therapeutic targets of HCC [2, 3], but there are currently no common therapeutic targets for broadspectrum treatment. It may be possible to identify prognostic biomarkers and more efficacious treatment targets by screening tumor-related gene networks
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