Tannic acid attenuate AKT phosphorylation to inhibit UMUC3 bladder cancer cell proliferation

Ming Cheng Chen, Selvaraj Annseles Rajula, V. Bharath Kumar, Chiung Hung Hsu, Cecilia Hsuan Day, Ray Jade Chen, Tso Fu Wang, Vijaya Padma Viswanadha, Chi Cheng Li, Chih Yang Huang

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)


Urothelial bladder cancer is rapidly spreading across Western countries, and therapy has shown little-to-moderate effects on bladder cancer. Thus, focusing on curbing cancer incidence has become crucial. The aim of the present study was to investigate the anticancer effects of Tannic acid (TA) in human bladder cancer. UMUC3 bladder cancer cells were treated with different concentrations of TA (0–100 µM) and tested for cell viability, colony formation, and apoptosis. The involvement of the phosphoinositide-3 kinase (PI3K)/Akt pathway in the action of TA was examined. TA treatment significantly inhibited the viability and increased percentage of apoptotic cells, thereby decreasing antiapoptotic proteins (BCL2, MCL-1, and BCL-XL) expression, resulting in the Caspase-3 activation. TA treatment decreased stem cell markers expression such as SOX2, OCT4, and NANOG. Additionally, TA treatment significantly reduced the phosphorylation levels of Akt in bladder cancer cells. Our study demonstrates the growth inhibitory effects of TA in bladder cancer cells, and highlights its potential as an anticancer agent for bladder cancer.

Original languageEnglish
Pages (from-to)2863-2869
Number of pages7
JournalMolecular and Cellular Biochemistry
Issue number12
Publication statusPublished - Dec 2022


  • Apoptosis
  • BCL2
  • Bladder cancer
  • Caspase
  • MCL-1
  • SOX2
  • Tannic acid

ASJC Scopus subject areas

  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology


Dive into the research topics of 'Tannic acid attenuate AKT phosphorylation to inhibit UMUC3 bladder cancer cell proliferation'. Together they form a unique fingerprint.

Cite this