CTTN (Cortactin)

In contrast, other zinc-dependent HDACs, including HDAC8, displayed negligible or very weak activity on full-length CTTN. These findings provide new mechanistic insight into KDAC substrate preferences and highlight the value of biochemical reconstitution for dissecting complex acetylation networks.

These data demonstrate that ADPH-dependent NF-κB activation and IL-8 secretion are enhanced by CagA. Together, we present here a novel CagA>cortactin>FAK>Src>IKKβ signaling cascade, contributing to proinflammatory responses by H. pylori.

This DANCR-mediated regulation promotes the interaction between ABL2 and the cytoskeletal regulator cortactin, which leads to activation of the SSH1-cofilin pathway and then facilitates the formation of lamellipodia, cytoskeletal reorganization and the metastatic ability of tumors. In summary, our findings delineate the DANCR/miR-125a-5p/ABL2/cofilin axis as a critical regulator of cytoskeletal dynamics in neuroblastoma metastasis, offering novel insights for the diagnosis and therapeutic targeting of high-risk neuroblastoma.

While several promising biomarker candidates have been identified, the evidence base remains limited due to small sample sizes, heterogeneous methodologies, and inadequate follow-up data. Cortactin/FAK protein expression and immune signatures are the most promising but require validation in larger, well-designed prospective cohorts.

We unveil MSN as a non-canonical GRK5/HDAC7 axis that promotes glioma malignancy by modulating the cortactin/MSN/CD44 pathway. Targeting this axis potentially represents a promising therapeutic strategy against gliomas.

Notably, one SRE located within the promoter region of the OBI1 gene is present in 45% of OSCC samples...Furthermore, we found that the frequently amplified region 11q13 in HNSCC is prone to large-scale somatic SVs, affecting the expression of ANO1, FADD, and CTTN, thereby confirming the association of SVs in this region with OSCC development. Our study provides novel insights into the role of somatic SVs in OSCC, especially with respect to SREs and large-scale SVs in critical genomic regions, thereby enhancing our comprehension of the molecular pathogenesis of OSCC.

A sequential strategy using cortactin depletion followed by an anti-Bcl-xL senolytic eliminated the persistent CTCs and suppressed blood-borne metastasis. Thus, this study uncovered a unique senescent CTC subpopulation regulated by a cortactin/mTOR/p53/mtROS axis that can be targeted to suppress metastatic progression of melanoma.

Finally, we demonstrate that the high expression of FILIP1L is associated with poor prognosis in breast cancer patients. In summary, FILIP1L is a novel invadopodia component which regulates breast cancer invasion and tumor progression in a cell cycle- and EMT-dependent manner by controlling invadopodia and motility of cancer cells.

This study provides a research basis for the identification of clinical biomarker of CTTN for predicting the prognosis of patients with HCC after surgery and offers potential targets for the blockade therapy of CTCs. The online version contains supplementary material available at 10.1007/s10616-025-00879-4.

Furthermore, dextran-based permeability measurements showed that the presence of HA of low Mw (i.e., 5 kDa) led to increased permeability of the BBB component, a feature that is characteristic of the blood-brain tumor barrier (BBTB). In summary, the developed 3D in vitro GBM model effectively recapitulates key features of the TME, highlighting the impact of the HA size on cancer cell invasion and BBB/BBTB permeability.

PLXDC2 is a potential biomarker of PDAC diagnosis. Targeting the PLXDC2-cortactin interaction may offer a novel therapeutic strategy.

Treatment of PDOs led to a dose-dependent reduction in viability and clonogenic capacity, accompanied by downregulation of stemness and proliferation markers. Overall, these findings demonstrate that selective HDAC6 inhibition by Mesinostat modulates key oncogenic pathways in TNBC, supporting its potential as a promising therapeutic approach for HDAC6-overexpressing breast cancers.