Related Experiment Video

Updated: Jul 10, 2026

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
06:51

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

PRRC2A-mediated m6A modification on NCOA4 promotes thymic epithelial tumor progression through PKM2-induced

Tao Wang1, Lang Xia1, Lei Zhang1

  • 1Department of Thoracic Surgery, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, China.

Cell Death & Disease
|July 8, 2026
PubMed

Insights

Proline-rich Coiled-coil 2a (PRRC2A) protein promotes thymic epithelial tumor growth by stabilizing NCOA4 and increasing glycolysis. Inhibiting PRRC2A shows therapeutic potential for advanced thymic epithelial tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Metabolic Pathways

Background:

  • Thymic epithelial tumors (TETs) present challenges in advanced stages due to limited treatment options and poor outcomes.
  • The metabolic reprogramming in TETs is not well understood, hindering therapeutic development.

Purpose of the Study:

  • To investigate the role of Proline-rich Coiled-coil 2a (PRRC2A), an m6A reader protein, in the metabolic regulation and progression of TETs.
  • To identify potential therapeutic targets within the PRRC2A-mediated metabolic pathway.

Main Methods:

  • Multi-omics analyses and molecular experiments were used to elucidate the function of PRRC2A in TETs.
  • In vivo studies assessed the effects of PRRC2A inhibition and combined therapies on tumor growth and metastasis.

Main Results:

  • PRRC2A is upregulated in TETs and linked to poor clinical outcomes.
  • PRRC2A stabilizes NCOA4 mRNA, increasing NCOA4 protein expression, which enhances glycolysis via interaction with PKM2, thus promoting TET progression.
  • Inhibition of PRRC2A suppressed tumor growth and metastasis; combined PRRC2A knockdown and PKM2 inhibition showed enhanced antitumor effects.

Conclusions:

  • The PRRC2A-NCOA4-PKM2 axis is a key regulator of glycolytic metabolism in TETs.
  • Targeting this axis, particularly PRRC2A, offers a promising therapeutic strategy for advanced or aggressive thymic epithelial tumors.

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...