Related Experiment Video

Updated: Jan 18, 2026

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain
08:32

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain

Published on: January 4, 2018

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Insulin signalling-associated cell fate promotes neoplastic invasiveness in non-functioning pituitary gonadotroph

Hongwei Liu1,2,3, Zhouyang Pan1,2,3, Qi Yang1,2,3

  • 1Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.

British Journal of Cancer
|September 11, 2025
PubMed
Abstract

Insights

Non-functioning pituitary gonadotroph adenomas (NFGA) become invasive via insulin signaling. Targeting insulin resistance offers a new therapeutic strategy for invasive NFGA, improving patient outcomes.

Area of Science:

  • Endocrinology
  • Genomics
  • Cancer Biology

Background:

  • Non-functioning pituitary gonadotroph adenoma (NFGA) is the most common pituitary tumor type.
  • NFGA often becomes invasive and refractory to treatment.
  • Understanding NFGA invasiveness mechanisms is crucial for developing effective therapies.

Purpose of the Study:

  • Investigate cellular heterogeneity in NFGA invasion.
  • Identify molecular drivers of NFGA invasiveness.
  • Evaluate the role of insulin signaling in NFGA tumor progression.

Main Methods:

  • Integrated single-cell RNA sequencing (scRNA-seq) and single-cell ATAC sequencing (scATAC-seq) from NFGA patients.
  • Analyzed an independent cohort of 210 patients and primary cell lines.
  • Performed in vitro assays and cis-co-accessible network analysis.

Main Results:

  • Identified five cellular states and three distinct cell fates in NFGA with epigenetic heterogeneity.
  • Discovered insulin signaling as a driver of tumor invasiveness, with invasive NFGAs showing insulin resistance.
  • Observed altered chromatin interactions at insulin signaling-related cis-regulatory elements (CREs) in invasive NFGA.

Conclusions:

  • Insulin signaling activation via CREs drives the invasive cell fate in NFGA.
  • Elevated insulin resistance is linked to NFGA invasiveness.
  • Targeting insulin signaling presents a potential therapeutic avenue for invasive NFGA.

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