Related Experiment Video

Updated: Jul 10, 2025

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The m7G Reader NCBP2 Promotes Pancreatic Cancer Progression by Upregulating MAPK/ERK Signaling

Jiancong Xie1, Taiwei Mo2,3, Ruibing Li3,4,5

  • 1Department of General Surgery (Pancreatic Hepatobiliary Surgery), The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou 510655, China.

Cancers
|November 25, 2023
PubMed

Insights

The m7G binding protein NCBP2 is highly expressed in pancreatic ductal adenocarcinoma (PDAC) and promotes tumor progression. Targeting NCBP2 may offer a new therapeutic strategy for PDAC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • RNA Biology

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) presents significant diagnostic and therapeutic challenges globally.
  • N7-methylguanosine (m7G) RNA modification is crucial in tumor development, but its role in PDAC is not fully understood.

Purpose of the Study:

  • To investigate the role of m7G regulatory genes in pancreatic ductal adenocarcinoma (PDAC) progression.
  • To identify novel diagnostic and therapeutic targets for PDAC.

Main Methods:

  • Integrated analysis of gene expression and clinical data from TCGA and GEO cohorts.
  • Constructed stable NCBP2-knockdown and overexpression PDAC cell lines.
  • Performed in-vitro and in-vivo experiments to assess cell proliferation and tumor growth.

Main Results:

  • NCBP2, an m7G binding protein, was found to be highly expressed in PDAC patients, correlating with a worse prognosis.
  • NCBP2 knockdown inhibited PDAC cell proliferation, while overexpression promoted tumor growth.
  • NCBP2 enhances c-JUN translation, activating the MEK/ERK signaling pathway.

Conclusions:

  • NCBP2 promotes PDAC progression by activating the MEK/ERK pathway.
  • NCBP2 represents a potential novel therapeutic target for pancreatic ductal adenocarcinoma.
Keywords:
MEK/ERKNCBP2c-JUNm7G methylationpancreatic adenocarcinoma

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