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  11. Expression And Functional Implications Of Yme1l In Nasopharyngeal Carcinoma

Expression and functional implications of YME1L in nasopharyngeal carcinoma

Fuwei Cheng1, Haiping Huang1, Shiyao Yin1

  • 1Department of Otolaryngology, The First Affiliated Hospital of Soochow University, Suzhou, China.

Cell Death & Disease
|June 18, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

Yeast mitochondrial amidase 1-like (YME1L) is upregulated in nasopharyngeal carcinoma (NPC), driving tumor growth by disrupting mitochondrial function and activating the Akt-mTOR pathway. Inhibiting YME1L shows anti-tumor effects in NPC.

Area of Science:

  • Mitochondrial biology
  • Oncology
  • Molecular mechanisms of cancer

Background:

  • Mitochondria are critical in nasopharyngeal carcinoma (NPC) progression.
  • Yeast mitochondrial amidase 1-like (YME1L), an AAA ATPase, regulates mitochondrial function and is linked to diseases.

Purpose of the Study:

  • To investigate the expression and functional role of YME1L in NPC.
  • To elucidate the molecular mechanisms underlying YME1L's involvement in NPC tumorigenesis.

Main Methods:

  • Analyzed YME1L expression in NPC tissues and cells versus normal controls.
  • Utilized genetic silencing (shRNA) and knockout (CRISPR-sgRNA) to assess YME1L's function in NPC cells.
  • Investigated YME1L's impact on mitochondrial function, cell viability, proliferation, migration, and apoptosis.

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  • Examined the role of YME1L in the Akt-mTOR signaling pathway.
  • Conducted in vivo studies using YME1L-shRNA-expressing adeno-associated virus (AAV) in NPC xenografts.

    • Main Results:

    • YME1L was significantly upregulated in NPC tissues and cells.
    • YME1L depletion impaired mitochondrial function (depolarization, ROS generation, reduced ATP) and inhibited NPC cell viability, proliferation, and migration, while promoting apoptosis.
    • YME1L overexpression enhanced NPC cell proliferation and migration.
    • YME1L positively regulated the Akt-mTOR pathway; its depletion inactivated Akt-S6K phosphorylation, which was rescued by a constitutively active Akt1 mutant.
    • In vivo, YME1L inhibition via AAV suppressed NPC xenograft growth, correlating with mitochondrial dysfunction, oxidative stress, Akt-mTOR inactivation, and apoptosis.

    Conclusions:

    • Overexpressed YME1L promotes NPC progression through enhanced mitochondrial function and Akt-mTOR activation.
    • Targeting YME1L represents a potential therapeutic strategy for nasopharyngeal carcinoma.