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Background <p>Several signaling pathways and related transcripts have been found to be dysregulated in breast cancer. Methods and Results: In this study, we used an in silico step aiming to find the most relevant biological pathways and related long non-coding RNAs (lncRNAs) in the pathoetiology of breast cancer. This step led to identification of EGFR and its related lncRNAs as contributors to the pathology of this type of cancer. Then, we assessed expression of these transcripts in breast cancer samples and their adjacent non-cancerous tissues (ANCTs). Among the assessed transcripts, LINC00265 was markedly upregulated in tumor tissues, exhibiting a mean fold-change of 3.26 (95% CI 1.28–8.23; <i>P</i> = 0.017). The results of correlation analyses revealed that in ANCTs, LINC00265 expression aligned with EGFR and two lncRNAs (ZEB1-AS1 and PITPNA-AS1), whereas in carcinoma the regulatory network shifted—LINC00265 decoupled from the other genes, and EGFR, ZEB1-AS1 and PITPNA-AS1 formed a tightly co-regulated module. ROC curve analyses indicated that among the transcripts tested, LINC00265 exhibited the most promising sensitivity for tumor detection, whereas ZEB1-AS1 provided greater specificity. Conclusions: Taken together, our data demonstrated up-regulation of LINC00265 in breast cancer tissues independent of standard clinicopathologic parameters and co-expressed transcripts in this cohort of patients. Further studies are needed to confirm these results in larger cohorts of patients.</p>

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LINC00265 is significantly upregulated in breast carcinoma: expression, correlation networks, and potential prognostic value

  • 期刊论文

  • 发表日期：

    2026年1月28日

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  • Zahra Tajik,
  • Zahra Fazeli,
  • Farkhondeh Pouresmaeili,
  • Solat Eslami,
  • Lobat Geranpayeh,
  • Fatemeh Ghadyani,
  • Soudeh Ghafouri-Fard

摘要

Background

Several signaling pathways and related transcripts have been found to be dysregulated in breast cancer. Methods and Results: In this study, we used an in silico step aiming to find the most relevant biological pathways and related long non-coding RNAs (lncRNAs) in the pathoetiology of breast cancer. This step led to identification of EGFR and its related lncRNAs as contributors to the pathology of this type of cancer. Then, we assessed expression of these transcripts in breast cancer samples and their adjacent non-cancerous tissues (ANCTs). Among the assessed transcripts, LINC00265 was markedly upregulated in tumor tissues, exhibiting a mean fold-change of 3.26 (95% CI 1.28–8.23; P = 0.017). The results of correlation analyses revealed that in ANCTs, LINC00265 expression aligned with EGFR and two lncRNAs (ZEB1-AS1 and PITPNA-AS1), whereas in carcinoma the regulatory network shifted—LINC00265 decoupled from the other genes, and EGFR, ZEB1-AS1 and PITPNA-AS1 formed a tightly co-regulated module. ROC curve analyses indicated that among the transcripts tested, LINC00265 exhibited the most promising sensitivity for tumor detection, whereas ZEB1-AS1 provided greater specificity. Conclusions: Taken together, our data demonstrated up-regulation of LINC00265 in breast cancer tissues independent of standard clinicopathologic parameters and co-expressed transcripts in this cohort of patients. Further studies are needed to confirm these results in larger cohorts of patients.