PDLIM5 (PDZ And LIM Domain 5)

Pdlim5 knockout not only reduces tumor growth but also normalizes tumor vasculature, alleviates hypoxia, and enhances immunotherapy and chemotherapy responses. These findings highlight the PDLIM5's role in facilitating tumor angiogenesis via ACTN1/ACTN4-mediated F-actin bundling and tip cell filopodia formation, providing mechanistic insights that may inform future therapeutic strategies targeting this pathway.

As XML continues to unravel the complexities within prostate cancer datasets, the identification of severity-specific biomarkers is poised at the forefront of precision oncology. This integration paves the way for targeted interventions, improving patient outcomes, and heralding a new era of individualized care in the fight against prostate cancer.

The p97-Npl4 complex bridges Stat3 with E3 ligases PDLIM2 and PDLIM5, thereby promoting Stat3 degradation and enabling TI-Treg cell development. Collectively, this work shows an important role for the p97-Npl4 complex in controlling Treg-TH17 cell balance in tumors and identifies possible targets for immunotherapy.

Immunoprecipitation and immunostaining results showed that by binding to the LIM domain of Id2, a scaffold protein PDZ and LIM 5 (PDLIM5) involved in the Id2 cytoplasmic relocation, which inactivated Id2 and resulted in higher TNFα expression in LPS-treated microglia. Collectively, our data delineate a novel effect of Id2 on TNFα regulation in microglia, which may shed a light on the proinflammatory cytokines regulating in microglia associated neuroimmune disorders.

A weighted genetic risk score (GRS) was developed using the 40 validated SNPs and the area under the receiver-operating characteristic curve for the GRS to predict PCa was 0.67 (95% CI, 0.63-0.71). These identified SNPs provide valuable insights into the molecular mechanisms of prostate carcinogenesis in Taiwan and underscore the significant role of genetic susceptibility in regional differences in PCa incidence.

The prognostic indicators reported here could be considered as a resource for identifying tumorigenesis and chemoresistance to farnesyltransferase inhibitor. They could help identify important research directions for the development of new prognostic and therapeutic techniques for AML.

In conclusion, HAGLR seemed to play a tumor suppressive role in ccRCC. HAGLR and associated gene signature may have implementation in improving existing prognostic measure and developing effective immunotherapeutic strategies for ccRCC.

9.5% of our tumors have oncogenic fusions that may be clinically relevant, which suggests patients with advanced cancers should have comprehensive molecular profiling that includes RNA sequencing. Additional studies are needed to determine the function of the identified unclassified gene fusions to assess potential clinical significance. Table- Unclassified Fusions (number per total unclassified fusions)Tumor Type (Total Number of Samples Profiled)Fusion Positive samplesUnclassified FusionsProstate adenocarcinoma (89)8 (32%)BMPR1B-PDLIM5 (2 patients), CDC13-SUGCT, NIPBL-RAI14, TTC6-MIPOL1, NFIB-UBE3B, GALNT7-SPOCK3, TBCA-AP3B1Breast cancer (224)8 (32%)NIPBL-PIEZO1, ETV6-RINT1, PAK1-TEX14, PAK1-MMP20, PAK1-LOC101928896, TTC6-MIPOL1, BMPR1B-PDLIM5, CMTM8-OSBPL10Non-small cell lung cancer (751)4 (16%)PANX1-PRPF19 (2 patients), TTC6-MIPOL1, GALNT7-SMIM8Head and neck cancer (177)2 (8%)ETV6-DNAH14, TP53BP1-SND1Salivary gland tumor (22)1 (4%)NFIB-CHCHD7Pancreatic adenocarcinoma (186)1 (4%)CMTM8-GPD1LOvarian cancer (362)1 (4%)NIPBL-SLC1A3Total Number of Fusions25

The gold-based nanoparticle is loaded with the EGFR-TKI (gefitinib) and IR780, and the surface-modified gold nanoshell layer has a photothermal effect for thermally triggered drug release...The low-temperature PTT combined with sonodynamic therapy (SDT) by cRGD-GIPG thus shows potent anticancer activity against EGFR-TKI-resistant NSCLC cells in vitro and in vivo. The present work provides a valuable strategy for highly targeted and EGFR-TKI-resistant reversal therapy in NSCLC.

LINC02027/miR-625-3p/PDLIM5 axis inhibits the development of HCC.

When PDLIM5 siRNA entered PC-9/GR cells, the sensitivity of drug-resistant cells to gefitinib could be restored through the transforming growth factor-β (TGF-β)/EMT pathway. Therefore, PDLIM5 may be an important reason for the resistance of NSCLC cells to gefitinib, and this nanoplatform may become a novel treatment for EGFR TKIs resistance in NSCLC patients.