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Updated: May 12, 2026

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
09:29

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies

Published on: September 30, 2016

Vitexin inhibits renal cell carcinoma progression by targeting Galectin-1-mediated glycolytic metabolism

Xinjun Wang1,2, Yue Bu1, Zhangqun Li1

  • 1Department of Urology, Zhongshan Hospital Xiamen University, School of Medicine, Xiamen University, Xiamen, China.

Molecular Biology Reports
|May 11, 2026
PubMed
Abstract

Insights

Vitexin, a natural compound, inhibits renal cell carcinoma (RCC) progression by targeting Galectin-1. This action disrupts tumor cell metabolism and offers a potential new therapeutic strategy for RCC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Vitexin, a natural flavonoid, exhibits anti-tumor properties, but its mechanism in Renal Cell Carcinoma (RCC) is not fully understood.
  • Galectin-1, a lectin, is implicated in tumor progression via metabolic reprogramming.

Purpose of the Study:

  • To investigate the anti-tumor activity of vitexin against RCC.
  • To determine if vitexin targets Galectin-1 and its downstream metabolic pathways.

Main Methods:

  • Assessed vitexin's effects on RCC cell lines (viability, apoptosis, cell cycle, migration, invasion).
  • Manipulated Galectin-1 expression (overexpression/knockdown) to study its role.
  • Utilized transcriptomic and metabolomic profiling to identify pathway alterations.
  • Evaluated glycolytic metabolism and validated in vivo efficacy using xenograft models.

Main Results:

  • Vitexin inhibited RCC proliferation, induced apoptosis, and suppressed migration/invasion, correlating with decreased Galectin-1 expression.
  • Galectin-1 modulation affected PI3K-AKT pathways and key glycolytic genes, altering cellular metabolism.
  • Vitexin treatment suppressed tumor growth in vivo, reduced Galectin-1 and PI3K/AKT signaling, and increased apoptosis.

Conclusions:

  • Vitexin demonstrates anti-tumor effects in RCC by inhibiting Galectin-1, thereby disrupting glycolytic metabolism via PI3K-AKT signaling.
  • Targeting Galectin-1 with vitexin presents a promising therapeutic strategy for RCC.
Keywords:
Galectin-1Glycolytic metabolismRenal cell carcinomaTumor suppressionVitexin

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