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<p>The initial manifestations of nasopharyngeal carcinoma (NPC) are subtle and imperceptible, leading to unfavorable clinical outcomes and limited therapeutic alternatives among Southeast Asian populations. Deletion of chromosome 3p is a commonly observed genetic alteration in NPC. In our endeavor to elucidate the key genes and pathways driving NPC growth, we have discovered that Villin like (VILL), located at 3p22.2, functions as a novel tumor suppressor gene (TSG) with significantly diminished expression levels in NPC. This finding underscores the tremendous potential of VILL as an unexplored molecule warranting further investigation. Overexpressing VILL effectively inhibits proliferation by inducing G1 phase arrest in NPC cells while its knockdown yields contrasting effects on cell growth regulation. Furthermore, our study demonstrates that VILL targets MYC. Knockdown of VILL and overexpression of MYC significantly enhance proliferation in an immortal nasopharyngeal epithelial cell line NP69. Moreover, we are the first to report that VILL plays a tumor suppressive role in NPC. Consequently, VILL emerges as a novel prognostic biomarker and a potential therapeutic candidate for NPC.</p>

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Villin like suppresses nasopharyngeal carcinoma proliferation by downregulating MYC

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年10月28日

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  • Yueting Wen,
  • Ziying Zhou,
  • Yibo Zhou,
  • Zhongxi Huang

摘要

The initial manifestations of nasopharyngeal carcinoma (NPC) are subtle and imperceptible, leading to unfavorable clinical outcomes and limited therapeutic alternatives among Southeast Asian populations. Deletion of chromosome 3p is a commonly observed genetic alteration in NPC. In our endeavor to elucidate the key genes and pathways driving NPC growth, we have discovered that Villin like (VILL), located at 3p22.2, functions as a novel tumor suppressor gene (TSG) with significantly diminished expression levels in NPC. This finding underscores the tremendous potential of VILL as an unexplored molecule warranting further investigation. Overexpressing VILL effectively inhibits proliferation by inducing G1 phase arrest in NPC cells while its knockdown yields contrasting effects on cell growth regulation. Furthermore, our study demonstrates that VILL targets MYC. Knockdown of VILL and overexpression of MYC significantly enhance proliferation in an immortal nasopharyngeal epithelial cell line NP69. Moreover, we are the first to report that VILL plays a tumor suppressive role in NPC. Consequently, VILL emerges as a novel prognostic biomarker and a potential therapeutic candidate for NPC.