Background <p>Long non-coding RNAs (lncRNAs) regulate gene expression at different levels, and their abnormal expression is involved in tumor development and progression. Long intergenic non-coding RNA 1614 (LINC01614) has attracted increasing interest because it is aberrantly expressed in several cancer types.</p> Methods <p>This narrative review summarizes current evidence on LINC01614 in cancer biology, with a focus on cancer progression, therapy response, and its possible relevance to precision medicine. PubMed, Web of Science, and Google Scholar were searched from database inception to May 18, 2026. The search terms included “LINC01614,” “lncRNA,” “cancer,” “biomarker,” “therapy response,” and “therapy resistance.”</p> Results <p>LINC01614 is frequently dysregulated in solid tumors. Available studies have linked it to cancer cell growth, migration, invasion, apoptosis regulation, metabolic changes, and therapy response. The evidence is uneven across tumor types. Some mechanisms are supported by functional assays and rescue experiments, whereas others mainly rely on public datasets, risk models, or small tissue cohorts. LINC01614 should be viewed as an emerging cancer-related lncRNA, not as a fully validated driver across all cancers.</p> Conclusions <p>This review summarizes the reported roles of LINC01614 in cancer progression and therapy response. Current evidence suggests that LINC01614 may regulate cancer-related pathways in a tumor-dependent manner. Its clinical value needs to be further defined by larger cohorts, direct mechanistic studies, and models that better reflect human tumors.</p> Graphical Abstract <p></p>

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Emerging roles of LINC01614 in cancer progression and therapy response

  • Tongtong Li,
  • Zijian Hu,
  • Zhirui Liu,
  • Chenwei Zhou

摘要

Background

Long non-coding RNAs (lncRNAs) regulate gene expression at different levels, and their abnormal expression is involved in tumor development and progression. Long intergenic non-coding RNA 1614 (LINC01614) has attracted increasing interest because it is aberrantly expressed in several cancer types.

Methods

This narrative review summarizes current evidence on LINC01614 in cancer biology, with a focus on cancer progression, therapy response, and its possible relevance to precision medicine. PubMed, Web of Science, and Google Scholar were searched from database inception to May 18, 2026. The search terms included “LINC01614,” “lncRNA,” “cancer,” “biomarker,” “therapy response,” and “therapy resistance.”

Results

LINC01614 is frequently dysregulated in solid tumors. Available studies have linked it to cancer cell growth, migration, invasion, apoptosis regulation, metabolic changes, and therapy response. The evidence is uneven across tumor types. Some mechanisms are supported by functional assays and rescue experiments, whereas others mainly rely on public datasets, risk models, or small tissue cohorts. LINC01614 should be viewed as an emerging cancer-related lncRNA, not as a fully validated driver across all cancers.

Conclusions

This review summarizes the reported roles of LINC01614 in cancer progression and therapy response. Current evidence suggests that LINC01614 may regulate cancer-related pathways in a tumor-dependent manner. Its clinical value needs to be further defined by larger cohorts, direct mechanistic studies, and models that better reflect human tumors.

Graphical Abstract