ArticleMolecular cancer2025
Loss of TACC2 impairs chemokine CCL3 and CCL4 expression and reduces response to anti-PD-1 therapy in soft tissue sarcoma.
Article in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- CCL3+ Neutrophil Signature Predicts Response to Neoadjuvant Toripalimab plus Chemotherapy in Patients with Hypopharyngeal Squamous Cell Carcinoma: A Phase II Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Trial
- Serum cytokines predict response and survival in esophageal squamous cell carcinoma receiving chemoradiotherapy combined with anti-PD-1 antibody: analyses of two phase II clinical trials.Journal for immunotherapy of cancer · 2026Trial
- Exhausted CD8⁺ T cells promote ovarian cancer immunosuppression via CCL3-Driven M2 macrophage polarization.Cell death & disease · 2026Article
- The Immunological Landscape of the Tumor Microenvironment: Implications for Immunotherapy of Unresectable and Metastatic Soft Tissue Sarcomas.Current treatment options in oncology · 2026Review
- USP21 drives immune evasion in colorectal cancer via deubiquitination and stabilization of β-catenin.Cellular & molecular immunology · 2026Article
- Semaphorins: from CD8⁺ T cells to cancer immunotherapy.Biomarker research · 2026Review
- Prognostic Significance and Immune Correlation of CCL3 Expression in Colon Adenocarcinoma: Insights From Multidatabase Analysis.Biochemistry research international · 2026Article
- MAVS/CMTM6 axis couples mitochondrial homeostasis to immunogenic senescence via CCL3-driven T-cell recruitment in renal carcinoma.Journal for immunotherapy of cancer · 2025Article
- Review
- Unveiling the Role of CCL3: A Driver of CIPN in Colon Cancer Patients?Biomedicines · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
backgroundSoft tissue sarcoma (STS) is a rare, heterogeneous malignancy with limited treatment options for metastatic disease. Despite advances in immunotherapy, including PD-1 inhibitors, clinical outcomes remain suboptimal, highlighting the need for novel biomarkers and therapeutic strategies. This study investigated the role of TACC2 in STS, focusing on its impact on the immune microenvironment and immunotherapy response.
methodsWhole-exome sequencing was performed to characterize TACC2-related genomic alterations in STS cohorts, complemented by immunohistochemistry for protein-level validation. Mechanistic insights were obtained through chromatin immunoprecipitation (ChIP) and co-immunoprecipitation assays, focusing on TACC2's interaction with the NuRD/CoREST complex. The efficacy of anti-PD-1 therapy was evaluated in TACC2-overexpressing mouse models, and clinical relevance was analyzed using patient survival and treatment response data.
resultsTACC2 acted as a tumor suppressor in STS, with low expression associated with poor overall survival. Mechanistically, TACC2 enhanced CCL3 and CCL4 transcription, promoting CD8 + T cell infiltration by inhibiting NuRD/CoREST nuclear translocation. In vivo, TACC2 overexpression synergized with PD-1 blockade therapy, leading to a significant reduction in tumor volume and prolonged survival. Clinically, high TACC2 expression was associated with improved responses to immunotherapy.
conclusionsIn conclusion, TACC2 is an important regulator of the immune response in STS, functioning as a tumor suppressor and a modulator of response to PD-1 blockade. Its role in modulating chemokine expression and CD8 + T cell infiltration highlights its potential as a therapeutic target and predictive biomarker for STS immunotherapy.
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