FOXP4-AS1 suppresses papillary thyroid carcinoma progression by binding to Lactate Dehydrogenase A and suppressing

Ning Ma1, Hai-Ying Tian2, Wei Zhao3

  • 1Department of Vascular and Thyroid Surgery, Guizhou Provincial People's Hospital, No 83, Zhongshan East Road, Guiyang 550000, China; Guizhou Medical University, No 9, Beijing Road, Guiyang 550004, China.

Insights

FOXP4-AS1 acts as a tumor suppressor in papillary thyroid cancer (PTC), inhibiting cell growth and metastasis. It represses Lactate Dehydrogenase A (LDHA) to reduce aerobic glycolysis, offering potential therapeutic strategies for PTC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Metabolism

Background:

  • Papillary thyroid cancer (PTC) progression involves complex molecular mechanisms.
  • The role of long non-coding RNAs like FOXP4-AS1 in PTC is not fully understood.
  • FOXP4-AS1 is known to have oncogenic roles in other cancers.

Purpose of the Study:

  • To investigate the function of FOXP4-AS1 in papillary thyroid cancer.
  • To elucidate the molecular mechanism by which FOXP4-AS1 regulates PTC progression.
  • To identify potential therapeutic targets related to the FOXP4-AS1/LDHA axis.

Main Methods:

  • In vitro experiments assessing cell proliferation, migration, and invasion.
  • In vivo tumorigenesis assays in nude mice.
  • Analysis of FOXP4-AS1 and Lactate Dehydrogenase A (LDHA) expression and localization.
  • Mechanistic studies involving gene knockdown and inhibition.

Main Results:

  • FOXP4-AS1 overexpression suppressed PTC cell proliferation, migration, and invasion.
  • FOXP4-AS1 knockdown promoted malignant phenotypes and enhanced tumor growth in vivo.
  • FOXP4-AS1 interacts with LDHA, a key enzyme in aerobic glycolysis.
  • FOXP4-AS1 knockdown led to increased LDHA expression, which was partially reversed by LDHA inhibition.

Conclusions:

  • FOXP4-AS1 functions as a tumor suppressor in papillary thyroid cancer.
  • The FOXP4-AS1/LDHA axis regulates aerobic glycolysis in PTC.
  • FOXP4-AS1 represses LDHA expression, attenuating aerobic glycolysis and PTC progression.
  • This study provides insights into PTC mechanisms and identifies potential therapeutic and diagnostic targets.

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