Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

Induction of apoptosis by 4-(3-(tert-butylamino)imidazo[1,2-α]pyridine-2-yl) benzoic acid in breast cancer cells via upregulation of PTEN

Siddharth, Sumit ; Mohapatra, Purusottam LU ; Preet, Ranjan ; Das, Dipon ; Satapathy, Shakti Ranjan LU ; Choudhuri, Tathagata and Kundu, Chanakya Nath (2013) In Oncology research 21(1). p.1-13
Abstract

We have previously reported that 4-(3-(tert-butylamino)imidazo[1,2-α]pyridine-2-yl)benzoic acid, a bicyclic N-fused aminoimidazoles derivative (BNFA-D), possesses anticancer potentiality against breast and kidney cancer cells with minimal toxicities to corresponding normal cells. Here, we explored the mechanism of action of BNFA-D in breast cancer cells using multiple cell-based assays such as MTT, DAPI, FACS, Western blot, and immunoprecipitation. BNFA-D caused apoptosis by upregulating PTEN leading to inhibition of Wnt/TCF signaling cascade and arresting S phase in breast cancer cells. Expression levels of β-catenin, cyclin D1, C-MYC, and phospho-AKT (Ser(473)) decreased with simultaneous increase in the levels of GSK3β, CK1, and PTEN... (More)

We have previously reported that 4-(3-(tert-butylamino)imidazo[1,2-α]pyridine-2-yl)benzoic acid, a bicyclic N-fused aminoimidazoles derivative (BNFA-D), possesses anticancer potentiality against breast and kidney cancer cells with minimal toxicities to corresponding normal cells. Here, we explored the mechanism of action of BNFA-D in breast cancer cells using multiple cell-based assays such as MTT, DAPI, FACS, Western blot, and immunoprecipitation. BNFA-D caused apoptosis by upregulating PTEN leading to inhibition of Wnt/TCF signaling cascade and arresting S phase in breast cancer cells. Expression levels of β-catenin, cyclin D1, C-MYC, and phospho-AKT (Ser(473)) decreased with simultaneous increase in the levels of GSK3β, CK1, and PTEN in BNFA-D-treated MCF-7 cells. Interestingly, silencing of PTEN in breast cancer cells reversed the phenomenon of Wnt/TCF signaling cascade inhibition after BNFA-D treatment.

(Less)
Please use this url to cite or link to this publication:
author
; ; ; ; ; and
publishing date
type
Contribution to journal
publication status
published
keywords
Apoptosis/drug effects, Benzoates/pharmacology, Breast Neoplasms/enzymology, Cell Growth Processes/drug effects, Cell Line, Tumor, Female, Gene Knockdown Techniques, Glycogen Synthase Kinase 3/metabolism, Glycogen Synthase Kinase 3 beta, Humans, Imidazoles/pharmacology, MCF-7 Cells, PTEN Phosphohydrolase/genetics, Phosphatidylinositol 3-Kinases/metabolism, Pyridines/pharmacology, TCF Transcription Factors/metabolism, Transfection, Up-Regulation/drug effects, Wnt Signaling Pathway/drug effects
in
Oncology research
volume
21
issue
1
pages
1 - 13
publisher
Tech Science Press
external identifiers
  • scopus:84890963781
  • pmid:24330847
ISSN
0965-0407
DOI
10.3727/096504013X13786659070190
language
English
LU publication?
no
id
a03066ac-469e-4a3a-afd5-600b1e976820
date added to LUP
2025-01-30 10:32:25
date last changed
2025-04-25 10:14:52
@article{a03066ac-469e-4a3a-afd5-600b1e976820,
  abstract     = {{<p>We have previously reported that 4-(3-(tert-butylamino)imidazo[1,2-α]pyridine-2-yl)benzoic acid, a bicyclic N-fused aminoimidazoles derivative (BNFA-D), possesses anticancer potentiality against breast and kidney cancer cells with minimal toxicities to corresponding normal cells. Here, we explored the mechanism of action of BNFA-D in breast cancer cells using multiple cell-based assays such as MTT, DAPI, FACS, Western blot, and immunoprecipitation. BNFA-D caused apoptosis by upregulating PTEN leading to inhibition of Wnt/TCF signaling cascade and arresting S phase in breast cancer cells. Expression levels of β-catenin, cyclin D1, C-MYC, and phospho-AKT (Ser(473)) decreased with simultaneous increase in the levels of GSK3β, CK1, and PTEN in BNFA-D-treated MCF-7 cells. Interestingly, silencing of PTEN in breast cancer cells reversed the phenomenon of Wnt/TCF signaling cascade inhibition after BNFA-D treatment.</p>}},
  author       = {{Siddharth, Sumit and Mohapatra, Purusottam and Preet, Ranjan and Das, Dipon and Satapathy, Shakti Ranjan and Choudhuri, Tathagata and Kundu, Chanakya Nath}},
  issn         = {{0965-0407}},
  keywords     = {{Apoptosis/drug effects; Benzoates/pharmacology; Breast Neoplasms/enzymology; Cell Growth Processes/drug effects; Cell Line, Tumor; Female; Gene Knockdown Techniques; Glycogen Synthase Kinase 3/metabolism; Glycogen Synthase Kinase 3 beta; Humans; Imidazoles/pharmacology; MCF-7 Cells; PTEN Phosphohydrolase/genetics; Phosphatidylinositol 3-Kinases/metabolism; Pyridines/pharmacology; TCF Transcription Factors/metabolism; Transfection; Up-Regulation/drug effects; Wnt Signaling Pathway/drug effects}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{1--13}},
  publisher    = {{Tech Science Press}},
  series       = {{Oncology research}},
  title        = {{Induction of apoptosis by 4-(3-(tert-butylamino)imidazo[1,2-α]pyridine-2-yl) benzoic acid in breast cancer cells via upregulation of PTEN}},
  url          = {{http://dx.doi.org/10.3727/096504013X13786659070190}},
  doi          = {{10.3727/096504013X13786659070190}},
  volume       = {{21}},
  year         = {{2013}},
}