Related Experiment Video

Updated: May 12, 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

RBM15/IGF2BP2-PTPRH m6A regulatory axis in non-small cell lung cancer

Keyue Qiu1,2, Xiaoxiao Zheng3, Hongxiang Li1,2

  • 1Department of Thoracic Surgery, The Affiliated Lihuili Hospital of Ningbo University, Ningbo, Zhejiang, 315000, China.

Cellular Oncology (Dordrecht, Netherlands)
|May 11, 2026
PubMed
Abstract

Insights

This study reveals a new mechanism where RBM15 and IGF2BP2 stabilize PTPRH mRNA via m6A modification, driving non-small cell lung cancer (NSCLC) progression. This RBM15/IGF2BP2-PTPRH axis presents a potential therapeutic target for NSCLC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Non-small cell lung cancer (NSCLC) is a major global cancer-related mortality cause.
  • Identifying novel molecular drivers and therapeutic targets for NSCLC is critical.
  • This research focuses on protein tyrosine phosphatase receptor type H (PTPRH) and its epitranscriptomic regulation in NSCLC.

Purpose of the Study:

  • To investigate the role and regulation of PTPRH in NSCLC.
  • To elucidate the epitranscriptomic mechanism involving N6-methyladenosine (m6A) modification in PTPRH regulation.
  • To identify the RBM15/IGF2BP2-PTPRH axis as a potential therapeutic target.

Main Methods:

  • Integrated analysis of The Cancer Genome Atlas and Gene Expression Omnibus datasets.
  • Validation of PTPRH expression in clinical NSCLC specimens and correlation with clinicopathological features.
  • In vitro and in vivo functional assays to assess PTPRH effects on tumor progression.
  • Investigation of m6A modification, RBM15, and IGF2BP2 roles in PTPRH mRNA stability.

Main Results:

  • PTPRH is overexpressed in NSCLC and correlates with poor prognosis.
  • PTPRH promotes proliferation, migration, invasion, and angiogenesis, while inhibiting apoptosis.
  • RBM15-mediated m6A modification and IGF2BP2 binding stabilize PTPRH mRNA, driving oncogenic functions.

Conclusions:

  • A novel RBM15/IGF2BP2-PTPRH axis regulates PTPRH mRNA stability via m6A modification in NSCLC.
  • This axis promotes NSCLC progression and represents a potential therapeutic target.
  • The study enhances understanding of post-transcriptional regulation in lung cancer.
Keywords:
IGF2BP2N6-methyladenosine (m6A)Non-small cell lung cancer (NSCLC)PTPRHRBM15

Related Concept Videos

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...
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...
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...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...