CCT2 (Chaperonin Containing TCP1 Subunit 2)

This study integrates clinical samples with single-cell transcriptomic sequencing, proteomics, and RNA sequencing and reveals that FOLFIRINOX (a combination regimen of 5-fluorouracil, oxaliplatin, irinotecan, and leucovorin) treatment induces a higher proportion of senescent tumor cells (senTCs). When combined with SenExo-cCCT2, the FOLFIRINOX regimen enhances the capacity of pancreatic cancer cells to induce senescence. Subsequently, anti-PD-L1 therapy facilitates the immune-mediated clearance of senTCs, markedly improving the therapeutic efficacy of combined chemotherapy and immunotherapy for pancreatic cancer.

CircCCT2 promotes HNSCC development through the miR-146a-5p/IRAK1 axis, revealing that circCCT2 is a potential biomarker and target for HNSCC.

In addition, Tat-CCT2 treatment significantly ameliorated ischemia-induced microglial activation in the ventral horn of spinal cord 24 h after reperfusion. These results suggest that Tat-CCT2 mitigates ischemia-induced neuronal damage in the spinal cord.

This study first revealed the high expression of CCT2 in PTC and its essential role in the migration, invasion, proliferation, and anti-apoptosis of tumor cells. CCT2 promotes the metastasis and tumorigenesis of PTC by regulating ZEB1 and EMT-related genes. These findings provide new potential targets for molecular targeted therapy of PTC and explore new directions for future clinical treatment strategies.

These findings highlight CCT2 upregulation as a potential driver of breast cancer progression and immune evasion. Our study provides new insights into the molecular mechanisms underlying breast cancer progression, suggesting that CCT2 is a promising therapeutic target and prognostic predictor for breast cancer.

Additionally, dihydroartemisinin inhibits glioblastoma by targeting the CCT2 and the following KRAS signaling. Our findings overcome the challenge posed by the undruggable nature of KRAS and offer potential therapeutic strategies for glioblastoma treatment.

This efficient PEG signature prognostic model can predict the outcomes of TPBC. Furthermore, ACTL6A expression level was associated with the response to NACT, and could serve as an important factor in predicting prognosis and drug sensitivity of patients with TPBC.

Enhanced MDA5 degradation occurs in PRRSV infection via two autophagic pathways, including the binding of MDA5 with the autophagy receptor P62 and the aggrephagy receptor CCT2, triggering intense innate immune suppression. The research reveals a novel mechanism of immune evasion in PRRSV infection and provides fundamental insights for the development of new vaccines or therapeutic strategies.

CCT2 was a novel promotor for EOC progression and a crucial sustainer for CSC traits mainly by preventing β-catenin degradation. Targeting CCT2 may represent a promising therapeutic strategy for EOC.

The feasibility of using CCT2 as a biomarker to detect cancer progression was confirmed using antibodies to detect CCT2 in the identification of circulating tumor cells using the CellSearch System. These results provide validation to further develop the use of CCT2 as a diagnostic marker for cancer progression and metastasis and as a promising therapeutic target for new drug development.