SPP1 (Secreted Phosphoprotein 1)

Harnessing its therapeutic potential represents the cornerstone for developing future OPN-targeted therapies. This strategic approach will create new avenues for liver disease treatment, enabling precise interventions tailored to specific disease contexts.

Gemcitabine/Cisplatin (Gem/Cis) chemotherapy is a standard treatment for muscle-invasive bladder cancer (MIBC) but yields suboptimal response rates. Using TCGA bladder cancer data, the transcriptomic gene set was further validated revealing a prognostic signature associated with patients' outcome. These findings uncover a novel mechanism of chemotherapy resistance in bladder cancer driven by tumor-stromal interactions and macrophage recruitment and suggest that targeting macrophage infiltration may improve chemotherapy response in bladder cancer.

Macrophage depletion abrogates metastasis, while the FABP1 inhibitor orlistat reverses SPP1 upregulation in macrophages...Importantly, virtual screening identifies indole-3-acetic acid (IAA) as an RNF32 inhibitor that suppresses liver metastasis and reverses immunosuppression in vivo. This study establishes RNF32 as a dual-functional driver of metastasis and proposes IAA as a promising therapeutic agent, offering new hope for targeting both tumor-intrinsic EMT and the immune microenvironment in CRC liver metastasis.

This study successfully identified SPP1, LYZ, and MCM5 as key hub genes for the comorbidity of RA and cervical cancer. By regulating processes like inflammation, immune evasion, and cell proliferation, these genes not only have a high diagnostic potential but may also contribute to the occurrence and development of cervical cancer.

(4) In summary, a tumor-intrinsic TF network cooperates with SPP1+ macrophage signaling to promote a permissive microenvironment and HCC progression. This integrated axis highlights tractable vulnerabilities for therapeutic intervention.

When combined with the immune checkpoint inhibitors (ICIs) in vivo, siSPP1-mIFNγ@mLNPs significantly boost anti-tumor immune responses in both orthotopic lung cancer and pulmonary metastases. Overall, siSPP1-mIFNγ@mLNPs present innovative perspectives for precise cell-type targeting strategies and position SPP1+ macrophage reprogramming as a clinically actionable strategy to convert ICI non-responders into long-term survivors.

In addition, the gene expression profiles of the ADCs induced by the three fiber types indicate that both types of thin flexible DWCNTs used in the present study promoted a number of carcinogenic pathways in the rat lung that were also promoted by MWCNT-7, which is a class 2B carcinogen. These results support the conclusion that DWCNTs are carcinogenic in the rat lung and highlight the importance of further assessments of the potential lung carcinogenicity of inhaled thin flexible CNTs.

Overexpressed ESM1 may mediate a reduced level of immune cell infiltration in TME through immune signalling pathways. ESM1 can be used as a predictive biomarker for immune-related and clinical progression in BC.

Our synthesis provides an appraisal of reproducible communication architectures in glioma and outlines pragmatic reporting standards and trial-ready pharmacodynamic endpoints for myeloid-informed precision immuno-oncology. We hope these insights will assist researchers and clinicians as they design multi-omics pipelines and interventions to convert suppressive ecosystems into responsive ones.

The humanized anti-TM4SF4 antibody, Hz2B7-1.2, exhibits strong antitumor activity through multiple mechanisms, including inhibition of oncogenic signaling pathways, reduction of EMT-associated stemness, and modulation of immune responses. These findings support Hz2B7-1.2 as a promising therapeutic candidate for TM4SF4-positive cancers, warranting further clinical investigation.

Immunohistochemistry and Western blot analyses further validated their elevated protein expression in high-grade glioma tissues. Collectively, this spatial multi-omic framework delineates endocytosis-associated immune remodeling in glioma and identifies FCGR2B, CLEC7A, and LYAR as potential biomarkers and therapeutic targets for disrupting immunosuppressive niches.

We constructed an efferocytosis-related prognostic gene model for LUAD. Furthermore, LDHA may target M2 macrophages, highlighting its potential as a therapeutic target in LUAD.