TRIM28 (Tripartite Motif Containing 28)

These results provide novel insights into the molecular mechanisms underlying CRC progression and underscore the potential of CBX8 as a therapeutic target for developing targeted therapies and senolytic-based anticancer strategies. This study advances our understanding of CRC pathogenesis and offers promising directions for precision medicine in CRC treatment.

A TRIM28 variant defective in orphan-NR interaction fails to localize to telomeres and is unable to promote H3K9me3 and ALT phenotypes. These findings indicate that telomeric orphan NRs recruit TRIM28 for telomeric H3K9me3 and ALT activation, emphasizing the role of chromatin structure in ALT activation.

In trophoblast cells, TRIM28 alleviated H2O2-induced apoptosis by promoting p53 ubiquitination and thereby reducing its pro-apoptotic activity. TRIM28 attenuates oxidative stress-induced trophoblast apoptosis and may help protect against the development of EOPE.

In this group, each tumour has its own genetics, whose molecular mechanisms are increasingly well understood, with fusions, tandem duplications or gene mutations which can help the pathologist to achieve to an accurate diagnosis in each morphological context. In some situations, the identification of these molecular alterations may lead to a targeted treatment.

These findings support the existence of distinct cancer stem cell subtypes exhibiting multipotent and pluripotent properties. Secretome profiling provides valuable insights into tumor heterogeneity and highlights novel biomarker candidates, offering potential avenues for improved diagnosis and targeted therapeutic strategies in lung cancer.

Patient-derived organoid studies further confirm PMM2's role in promoting CRC progression through the PMM2-KIFC3 axis. Collectively, these findings establish PMM2 as a prognostic biomarker and potential therapeutic target in CRC, highlighting its critical role in metabolic reprogramming and tumorigenesis.

Moreover, this axis contributes to acquired resistance to osimertinib, an epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI); combined inhibition of USP5 and osimertinib synergistically induces apoptosis and suppresses tumor growth in vitro and in vivo. These findings establish USP5-mediated stabilization of CD73 as a central mechanism underlying glycolytic metabolism and osimertinib resistance in LUAD, highlighting the USP5/CD73 pathway as a promising prognostic indicator and therapeutic target for LUAD treatment.

Western blot analysis demonstrated that TRIM28 mediates CLDN3 SUMOylation and degradation. CLDN3 influences the growth and chemotherapy resistance of CRC cells, its interaction with TRIM28 makes the TRIM28/CLDN3 axis as a promising therapeutic target for CRC.

TRIM28 is critical in promoting BTZ resistance in GC cells. Targeting TRIM28 could potentiate BTZ treatment outcomes and offer a promising therapeutic strategy for overcoming drug resistance in GC treatment.

pneumoniae suppressed S-nitrosylation of tripartite motif containing protein 28 (TRIM28) by diminishing Mn2+ levels, allowing TRIM28 to physically interact with the transcription factor SP1 to promote the transcription of solute carrier family 27 member 1 (SLC27A1) and lipid deposition. Taken together, these findings indicate that tumor-resident S. pneumoniae plays an important role in conferring pazopanib resistance, suggesting that S. pneumoniae could serve as a potential biomarker of pazopanib response in ccRCC.

Both cytosolic RNA and DNA sensors were required for the ensuing interferon response and for the heightened sensitivity to PD-1 blockade elicited by ARID1A deficiency. These findings thus reveal an unanticipated heterochromatin gatekeeper function of ARID1A that operates outside the SWI/SNF complex and can be exploited to potentiate immune checkpoint therapy activity.

In OC mice, TRIM28 overexpression promotes angiogenesis and Bev resistance via ESM1-mediated ITGB1/FAK activation. This work unveils a new molecular pathway underlying Bev resistance in OC and proposes TRIM28 and ESM1 as potential therapeutic targets.