Evidence map›Paper›PMID 22914324›Full record

ArticleCell death & disease2012

The antitumor natural compound falcarindiol promotes cancer cell death by inducing endoplasmic reticulum stress.

H R Jin, J Zhao, Z Zhang, Y Liao, C-Z Wang, W-H Huang, S-P Li, T-C He, C-S Yuan, W Du

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.7field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Comparative Phytochemistry of Polyacetylenes of the GenusMolecules (Basel, Switzerland) · 2025
    Review
  5. Article
  6. Article
  7. Alaska's Flora as a Treatment for Cancer.International journal of biopharmaceutical sciences · 2024
    Article
  8. Review
  9. Review
  10. Synergistic activity of the combination of falcarindiol and itraconazoleFrontiers in cellular and infection microbiology · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Bioactive CMolecules (Basel, Switzerland) · 2020
    Review
  16. Article
  17. Kurarinone fromMolecules (Basel, Switzerland) · 2019
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

H R JinBen May Department for Cancer Research, The University of Chicago, Chicago, IL 60637, USA.
J Zhao
Z Zhang
Y Liao
C-Z Wang
W-H Huang
S-P Li
T-C He
C-S Yuan
W Du
University of Chicago · USUniversity of Macau · MO

Funding

Center for Herbal Research on Colorectal CancerP01AT004418 · NCCIH · UNIVERSITY OF CHICAGO · PI YUAN, CHUN-SU · 2008 to 2012
$5.9M
Control of Cell Proliferation and Differentiation in the Developing RetinaR01GM074197 · NIGMS · UNIVERSITY OF CHICAGO · PI DU, WEI · 2006 to 2013
$2.4M
A novel approach to target Rb mutant cancersR01CA149275 · NCI · UNIVERSITY OF CHICAGO · PI DU, WEI · 2011 to 2015
$1.6M
NCCIH NIH HHS AT004418NCCIH NIH HHS P01 AT004418NCI NIH HHS CA149275NCI NIH HHS R01 CA149275NIGMS NIH HHS GM074197NIGMS NIH HHS R01 GM074197
6 · The paper itself

Abstract

Falcarindiol (FAD) is a natural polyyne with various beneficial biological activities. We show here that FAD preferentially kills colon cancer cells but not normal colon epithelial cells. Furthermore, FAD inhibits tumor growth in a xenograft tumor model and exhibits strong synergistic killing of cancer cells with 5-fluorouracil, an approved cancer chemotherapeutic drug. We demonstrate that FAD-induced cell death is mediated by induction of endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR). Decreasing the level of ER stress, either by overexpressing the ER chaperone protein glucose-regulated protein 78 (GRP78) or by knockout of components of the UPR pathway, reduces FAD-induced apoptosis. In contrast, increasing the level of ER stress by knocking down GRP78 potentiates FAD-induced apoptosis. Finally, FAD-induced ER stress and apoptosis is correlated with the accumulation of ubiquitinated proteins, suggesting that FAD functions at least in part by interfering with proteasome function, leading to the accumulation of unfolded protein and induction of ER stress. Consistent with this, inhibition of protein synthesis by cycloheximide significantly decreases the accumulation of ubiquitinated proteins and blocks FAD-induced ER stress and cell death. Taken together, our study shows that FAD is a potential new anticancer agent that exerts its activity through inducing ER stress and apoptosis.

Indexed as

AnimalsAntineoplastic Agents, PhytogenicApoptosisCell Line, TumorColorectal NeoplasmsDiynesDrug SynergismEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressFatty AlcoholsFluorouracilHCT116 CellsHeat-Shock ProteinsHumansMiceTransplantation, HeterologousAntineoplastic Agents, PhytogenicDiynesEndoplasmic Reticulum Chaperone BiPfalcarindiolFatty AlcoholsFluorouracilHeat-Shock ProteinsHSPA5 protein, humanHspa5 protein, mouse

Identifiers

PMID22914324
PMCPMC3434669
OpenAlexW1966725969

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.