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Background <p>Esophageal squamous cell carcinoma (ESCC) remains a significant part of the global health burden, increasing the need to make its molecular basis clear in regard to therapeutic development. This study focuses on the long non-coding RNA LMNTD2-AS1 and its regulatory network in ESCC.</p> Methods <p>The expression level of LMNTD2-AS1 in clinical specimens and selected cell lines was quantified using quantitative RT‑PCR (qRT‑PCR). To assess its impact on malignant phenotypes, functional experiments including CCK‑8, Transwell, and flow cytometry‑based apoptosis assays were conducted. Subsequently, bioinformatic analyses combined with dual‑luciferase reporter assays were employed to validate the existence of a regulatory axis involving LMNTD2‑AS1, miR‑449b‑5p, and MYCN.</p> Result <p>This study revealed that LMNTD2-AS1 was significantly upregulated in ESCC tissues and cellular models. Downregulation of LMNTD2-AS1 expression decreased the rates of cell vitality and invasion while increasing apoptosis. LMNTD2-AS1 acted as a ceRNA and directly interacted with miR-449b-5p, resulting in the derepression of MYCN. Rescue assays confirmed that miR-449b-5p inhibition rescues the anti-tumor effects caused by LMNTD2-AS1 reduction. Reducing MYCN expression negated the cancer-promoting effects of inhibitory miR-449b-5p.</p> Conclusion <p>In conclusion, this preliminary study demonstrates that LMNTD2-AS1 promotes ESCC progression via the miR-449b-5p/MYCN axis. By elucidating this network and its downstream signaling, we provide a mechanistic framework for ESCC pathogenesis. While broader clinical and in vivo validation is required, this axis represents a promising target for therapeutic intervention.</p>

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LMNTD2-AS1 promotes esophageal squamous cell carcinoma progression by sponging miR-449b-5p to upregulate MYCN

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月6日

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  • Rukeyeguli Wusiman,
  • Zhenhong Chang,
  • Feng Yang,
  • Dian Lin,
  • Jiangqi Xu

摘要

Background

Esophageal squamous cell carcinoma (ESCC) remains a significant part of the global health burden, increasing the need to make its molecular basis clear in regard to therapeutic development. This study focuses on the long non-coding RNA LMNTD2-AS1 and its regulatory network in ESCC.

Methods

The expression level of LMNTD2-AS1 in clinical specimens and selected cell lines was quantified using quantitative RT‑PCR (qRT‑PCR). To assess its impact on malignant phenotypes, functional experiments including CCK‑8, Transwell, and flow cytometry‑based apoptosis assays were conducted. Subsequently, bioinformatic analyses combined with dual‑luciferase reporter assays were employed to validate the existence of a regulatory axis involving LMNTD2‑AS1, miR‑449b‑5p, and MYCN.

Result

This study revealed that LMNTD2-AS1 was significantly upregulated in ESCC tissues and cellular models. Downregulation of LMNTD2-AS1 expression decreased the rates of cell vitality and invasion while increasing apoptosis. LMNTD2-AS1 acted as a ceRNA and directly interacted with miR-449b-5p, resulting in the derepression of MYCN. Rescue assays confirmed that miR-449b-5p inhibition rescues the anti-tumor effects caused by LMNTD2-AS1 reduction. Reducing MYCN expression negated the cancer-promoting effects of inhibitory miR-449b-5p.

Conclusion

In conclusion, this preliminary study demonstrates that LMNTD2-AS1 promotes ESCC progression via the miR-449b-5p/MYCN axis. By elucidating this network and its downstream signaling, we provide a mechanistic framework for ESCC pathogenesis. While broader clinical and in vivo validation is required, this axis represents a promising target for therapeutic intervention.