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<p>Gastric cancer (GC) is one of the most common malignancies with a poor prognosis. The development of novel biomarkers is of utmost importance to screen patients with GC. Molecular mechanism study of GC may provide a research basis for the development of targeted drugs. We identified tRF-29-79MP9P9NH525 (tRF-29) as a GC-associated tRNA-derived fragment (tRF). The specific hair-pin structure reverse primer and amplification primers were first designed and then applied for tRF-29 quantification. Receiver operator characteristic curve, Kaplan–Meier survival curve, and multivariate Cox analysis were applied to analyze the diagnostic and prognostic values of tRF-29 in GC. Ethynyl-2′-deoxyuridine, cell cloning, Transwell assay, and flow cytometry were used to detect the effects of tRF-29 on proliferation, migration, and cell cycle distribution of GC cells. Xenograft tumor formation in NOD-SCID mice was applied in determining tRF-29′s effects on tumor growth. Fluorescence in situ hybridization, dual luciferase reporter assay, Western blot, immunohistochemistry, and RNA-binding protein immunoprecipitation were conducted to explore the molecular mechanism underlying tRF-29 regulating GC development. It was found that tissue tRF-29 showed effective diagnostic efficiency in GC and could discriminate different gastric mucosa. Besides, plasma tRF-29 improved GC diagnostic values of common tumor markers and had prognostic values in GC. tRF-29 was found to suppress proliferation and cell cycle progression. tRF-29 inhibited the growth of xenograft tumors. Mechanically, tRF-29 exerted Kinesin family member 14 (KIF14) mRNA destabilization by combining with argonaute 2 (Ago2) and regulated AKT/P27 pathway. In conclusion, tRF-29 inhibited GC progression by combining with Ago2 and regulated AKT/P27 pathway by silencing KIF14 expression.</p><p></p>

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Identification of tRF-29-79MP9P9NH525 as a biomarker and tumor suppressor of gastric cancer via regulating KIF14/AKT pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月15日

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  • Jiaxin Ge,
  • Ji Dai,
  • Haoqiang Ji,
  • Jie Guo,
  • Xiaoban Shen,
  • Desen Sun,
  • Qiang Chen,
  • Pan Chen,
  • Guoliang Ye,
  • Junming Guo,
  • Shuangshuang Zhang

摘要

Gastric cancer (GC) is one of the most common malignancies with a poor prognosis. The development of novel biomarkers is of utmost importance to screen patients with GC. Molecular mechanism study of GC may provide a research basis for the development of targeted drugs. We identified tRF-29-79MP9P9NH525 (tRF-29) as a GC-associated tRNA-derived fragment (tRF). The specific hair-pin structure reverse primer and amplification primers were first designed and then applied for tRF-29 quantification. Receiver operator characteristic curve, Kaplan–Meier survival curve, and multivariate Cox analysis were applied to analyze the diagnostic and prognostic values of tRF-29 in GC. Ethynyl-2′-deoxyuridine, cell cloning, Transwell assay, and flow cytometry were used to detect the effects of tRF-29 on proliferation, migration, and cell cycle distribution of GC cells. Xenograft tumor formation in NOD-SCID mice was applied in determining tRF-29′s effects on tumor growth. Fluorescence in situ hybridization, dual luciferase reporter assay, Western blot, immunohistochemistry, and RNA-binding protein immunoprecipitation were conducted to explore the molecular mechanism underlying tRF-29 regulating GC development. It was found that tissue tRF-29 showed effective diagnostic efficiency in GC and could discriminate different gastric mucosa. Besides, plasma tRF-29 improved GC diagnostic values of common tumor markers and had prognostic values in GC. tRF-29 was found to suppress proliferation and cell cycle progression. tRF-29 inhibited the growth of xenograft tumors. Mechanically, tRF-29 exerted Kinesin family member 14 (KIF14) mRNA destabilization by combining with argonaute 2 (Ago2) and regulated AKT/P27 pathway. In conclusion, tRF-29 inhibited GC progression by combining with Ago2 and regulated AKT/P27 pathway by silencing KIF14 expression.