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Background <p>Pancreatic adenocarcinoma (PAAD) has a poor prognosis due to late diagnosis and limited treatment options. While protein-coding genes are known to contribute to disease pathogenesis, their specific roles require further investigation.</p> Methods <p>We analyzed RNA-seq and clinical data from 179 PAAD patients in TCGA to examine TICRR (TOPBP1 Interacting Checkpoint And Replication Regulator). Prognostic analyses included survival and risk assessment. Complementary cell-based experiments explored TICRR and associated non-coding RNAs (ncRNAs). Multi-omics profiling examined potential relationships between TICRR expression and tumor microenvironment features.</p> Results <p>Higher TICRR expression showed association with poorer survival outcomes. Experimental modulation of MIR659 and AC074099.1 expression appeared to influence malignant phenotypes in vitro. Multi-omics data suggested potential links between TICRR-associated molecular changes and features of immune evasion and genomic instability.</p> Conclusion <p>Our findings suggest possible connections between TICRR expression and PAAD progression. The observed phenotypic changes following ncRNA modulation may indicate their involvement in related oncogenic processes. These preliminary observations warrant further investigation into potential regulatory relationships between TICRR and associated ncRNAs, which could inform future therapeutic strategies.</p>

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Deciphering TICRR's oncogenic landscape in pancreatic adenocarcinoma: molecular insights and clinical implications

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月17日

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  • Ke-Jie He,
  • Haitao Wang

摘要

Background

Pancreatic adenocarcinoma (PAAD) has a poor prognosis due to late diagnosis and limited treatment options. While protein-coding genes are known to contribute to disease pathogenesis, their specific roles require further investigation.

Methods

We analyzed RNA-seq and clinical data from 179 PAAD patients in TCGA to examine TICRR (TOPBP1 Interacting Checkpoint And Replication Regulator). Prognostic analyses included survival and risk assessment. Complementary cell-based experiments explored TICRR and associated non-coding RNAs (ncRNAs). Multi-omics profiling examined potential relationships between TICRR expression and tumor microenvironment features.

Results

Higher TICRR expression showed association with poorer survival outcomes. Experimental modulation of MIR659 and AC074099.1 expression appeared to influence malignant phenotypes in vitro. Multi-omics data suggested potential links between TICRR-associated molecular changes and features of immune evasion and genomic instability.

Conclusion

Our findings suggest possible connections between TICRR expression and PAAD progression. The observed phenotypic changes following ncRNA modulation may indicate their involvement in related oncogenic processes. These preliminary observations warrant further investigation into potential regulatory relationships between TICRR and associated ncRNAs, which could inform future therapeutic strategies.