PDLIM4 (PDZ and LIM domain 4)

Given the high mutation frequency of PDLIM4 recorded in the TCGA cancer database, our findings reveal a critical regulatory signaling pathway that suppresses LUAD progression and augments chemotherapy efficacy.

Focusing on TCP1, a chaperonin subunit upregulated in high-risk tumors, we demonstrate that TCP1 knockdown in breast cancer cell lines substantially impairs cell migration (~50% reduction in wound closure) and invasion (P < 0.01). These findings reveal functionally distinct malignant cell states within breast cancer and identify TCP1 as a promising therapeutic target to disrupt aggressive, stem-like tumor cell programs, ultimately guiding more personalized treatment strategies.

This study classified BC by mRNAsi-related genes and established corresponding risk models. The findings of the present study propose a novel classification tool based on stem cell characteristics, which has the potential to be employed for prognostic stratification in BC patients and to offer guidance for developing personalised treatment strategies.

Finally, clinical data validated the correlation between YAP, FHL3, and KRAS expression. In conclusion, we identified a new target of Hippo-YAP signaling, FHL3, which interacts with MAZ to promote KRAS transcription and downstream oncogenic signaling pathway activation, thereby promoting HCC progression.

Experiments further indicated that siPDLIM4 LNPs and DDP LNPs have an anti-tumor property, while siPDLIM4/DDP LNPs exhibit the most significant anti-tumor efficacy. In summary, our research identifies PDLIM4 as a facilitator of malignant progression and DDP resistance in GC cells, targeting PDLIM4 not only inhibits the malignant progression of GC, but also provides an effective strategy to enhance DDP sensitivity in GC treatment, emphasizing its potential as a therapeutic target.

Our research results indicate that ABLIM1 may be an independent prognostic factor for individuals diagnosed with osteosarcoma. By regulating the DCC/PI3K/AKT/mTOR axis, ABLIM1 promotes the growth, migration and invasion of osteosarcoma cells. Therefore, targeting ABLIM1 may serve as an effective therapeutic target for the treatment of osteosarcoma.

Additional layers of resistance arise when imatinib, a substrate for the P-glycoprotein (P-gp) efflux pump, is shunted out of the intracellular space and when leukemic cells engage alternative signaling pathways such as the SIRT1 and JAK2-STAT5...It is important to study the mechanisms of resistance responsible for treatment failure to develop therapeutic strategies to overcome this resistance. This paper aims to review the important mechanisms of resistance to TKIs, both in CML and AML.

Furthermore, PDLIM3 inhibited the transcriptional activity of Yes-associated protein (YAP), suggesting that YAP may be involved in the PDLIM3-mediated suppression of HNSCC metastatic ability. Our findings identify a potential signaling axis wherein PDLIM3 regulates YAP-EMT, thereby influencing tumor metastatic ability, and suggest the potential role of PDLIM3 as a tumor suppressor and prognostic biomarker for HNSCC.

Future studies are needed to more effectively illustrate the interplay between EBV infection and these epigenetic mechanisms. Notably, our study highlighted a correlation between EBV and epigenetic changes in laryngeal carcinoma.

A novel six-gene signature model including COL8A2, MET, FN1, MPZL2, PDLIM4 and CLDN10 was established based on a total of 52 DEGs from the intersection of LNM-related modules identified by WGNCA from TCGA, THCA and GSE60542 to predict the situation of lymph node metastasis in PTC. Those six hub genes were all more highly expressed in PTC tumors and played potential biological functions on the development of PTC in in vitro experiments, which had potential values as diagnostic and therapeutic targets.

Our findings demonstrate that Prickle1 loss in the myometrium results in a UL phenotype characterized by altered collagen expression, excessive extracellular matrix (ECM) deposition, aberrant smooth muscle cell organization, increased Esr1 and Pgr expression, and dysregulated Wnt/PCP signaling. This novel mouse model serves as a valuable preclinical tool for understanding UL pathogenesis and developing future pharmacotherapies.

PDLIM1 expression and function were negatively modulated by the upregulation of miR-3940-5p, consequently affecting the malignant phenotype of DLBCL cells. These findings suggest that the miR-3940-5p/PDLIM1 axis may play a crucial role in DLBCL pathogenesis and could potentially be exploited for therapeutic interventions.