TACC3 expression

Contrast-enhanced CT-based radiomics can non-invasively predict TACC3 expression and provide valuable prognostic information, contributing to personalized treatment strategies.

The regulatory effects of gene, variant, and DNA methylation were explored through dual-luciferase and 5-azacytidine treatment experiments, complemented by multiple database analyses...In addition, subjects with high-TACC3 expression presented an immunosuppressive microenvironment. These findings provide insights into the involvement of genetic variants of cellular senescence genes in the development and progression of colorectal cancer.

Finally, TACC3 inhibition in vivo elicited ICD in a vaccination assay and potentiated the anti-tumor efficacy of T-DM1 by inducing dendritic cell maturation and enhancing intratumoral infiltration of cytotoxic T cells. Together, these results illustrate that ICD is a key mechanism of action of T-DM1 that is lost in resistance and that targeting TACC3 can restore T-DM1-mediated ICD and overcome resistance.

A detailed understanding of the regulation of TACC3 expression, its key partners, and molecular functions in cancer cells is vital for uncovering the most vulnerable tumors and maximizing the therapeutic potential of targeting this highly oncogenic protein. In this review, we summarize the established and emerging interactors and spatiotemporal functions of TACC3 in cancer cells, discuss the potential of TACC3 as a biomarker in cancer, and therapeutic potential of its inhibition.

Our studies further demonstrated that high expression of TACC3 and KIF11 mediated the resistance of PDAC to gemcitabine, and deficiency of TACC3 or KIF11 increased the sensitivity of PDAC cells to chemotherapy. In conclusion, our study reveals the fundamental role of TACC3 expression in PDAC cell proliferation and chemoresistance, suggesting that TACC3 can be used as a molecular marker to evaluate the prognosis of PDAC.

In vivo, FAM111B inhibition hampered tumor growth and metastasis of HCC. This study highlighted a key player of FAM111B in modulating the malignant biological progression of HCC via TACC3/PI3K/AKT signaling pathway, displaying a potential therapeutic target for HCC.

Targeting TACC3 by guide RNAs or small molecule inhibitors strongly inhibits growth of organoids and breast cancer cell line- and patient-derived xenografts with CA by induction of multipolar spindles, mitotic and G1 arrest. Altogether, our results show that TACC3 is a multifunctional driver of highly aggressive breast tumors with CA and that targeting TACC3 is a promising approach to tackle this disease.

Notably, we demonstrated that high CA tumors express much higher levels of TACC3, and high TACC3 expression leads to drastically worse clinical outcome in cancer patients with CA. Altogether, our results show, for the first time, that TACC3 is a multifunctional driver of the growth of the highly aggressive breast tumors with CA and that targeting TACC3 is a promising approach to tackle this aggressive disease.

The results of this study revealed TACC3 as a target of WHSC1 in CRC that is positively correlated with PI3K/Akt pathway activation and tumor development.

Notably, we demonstrated that high CA tumors express much higher levels of TACC3, and high TACC3 expression, in association with its downstream effectors, KIFC1, HDAC2 and MBD2, leads to drastically worse clinical outcome in cancer patients with CA. Altogether, our results show, for the first time, that TACC3 is a multifunctional driver of the growth of the highly aggressive breast tumors with CA and that targeting TACC3 is a promising approach to tackle this aggressive disease.

Disease-free survival and overall survival of patients with high TACC3 expression were significantly shorter (p < 0.01 and p < 0.05, respectively). These results suggest that elevated expression of TACC3 could reflects aggressiveness of primary central nervous system lymphomas.