Evidence map›Paper›PMID 37116665›Full record

ArticleBiochemical pharmacology2023

Quassinoid analogs exert potent antitumor activity via reversible protein biosynthesis inhibition in human colorectal cancer.

Ning Wei, James Burnett, Desirae L Crocker, Yixian Huang, Song Li, Peter Wipf, Edward Chu, John C Schmitz

Open access · greenAbstract read
In one paragraph

Article in Biochemical pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. CDK9 inhibition sensitizes intrinsically resistantActa pharmaceutica Sinica. B · 2026
    Article
  2. Article
  3. Review
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

8 authors at 2 institutions in 1 country.

Ning WeiDivision of Hematology-Oncology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States; Cancer Therapeutics Program, UPMC Hillman Cancer Center, Pittsburgh, PA, United States; Montefiore Einstein Cancer Center, Cancer Therapeutics Program, Albert Einstein College of Medicine, Bronx, NY, United States. Electronic address: ning.wei@einsteinmed.edu.
James BurnettDepartment of Chemistry, University of Pittsburgh, Pittsburgh, PA, United States.
Desirae L CrockerDepartment of Chemistry, University of Pittsburgh, Pittsburgh, PA, United States.
Yixian HuangDepartment of Pharmaceutical Sciences, School of Pharmacy, University of Pittsburgh, Pittsburgh, PA, United States.
Song LiDepartment of Pharmaceutical Sciences, School of Pharmacy, University of Pittsburgh, Pittsburgh, PA, United States.
Peter WipfCancer Therapeutics Program, UPMC Hillman Cancer Center, Pittsburgh, PA, United States; Department of Chemistry, University of Pittsburgh, Pittsburgh, PA, United States.
Edward ChuDivision of Hematology-Oncology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States; Cancer Therapeutics Program, UPMC Hillman Cancer Center, Pittsburgh, PA, United States; Montefiore Einstein Cancer Center, Cancer Therapeutics Program, Albert Einstein College of Medicine, Bronx, NY, United States.
John C SchmitzDivision of Hematology-Oncology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States; Cancer Therapeutics Program, UPMC Hillman Cancer Center, Pittsburgh, PA, United States. Electronic address: schmitzjc@upmc.edu.
University of Pittsburgh · USUPMC Hillman Cancer Center · US

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JOHN C. BYRD · 1988 to 2026
$158.0M
NCI NIH HHS P30 CA047904
6 · The paper itself

Abstract

Cellular protein synthesis is accelerated in human colorectal cancer (CRC), and high expression of protein synthesis regulators in CRC patients is associated with poor prognosis. Thus, inhibition of protein synthesis may be an effective therapeutic strategy for CRC. We previously demonstrated that the quassinoid bruceantinol (BOL) had antitumor activity against CRC. Herein, potent tumor growth suppression (>80%) and STAT3 inhibition was observed in two different mouse models following BOL administration. Loss of body and spleen weight was observed but was eliminated upon nanoparticle encapsulation while maintaining strong antitumor activity. STAT3 siRNA knockdown exhibited modest suppression of cell proliferation. Surprisingly, STAT3 inhibition using a PROTAC degrader (SD-36) had little effect on cancer cell proliferation suggesting the possibility of additional mechanism(s) of action for quassinoids. BOL-resistant (BR) cell lines, HCT116

Indexed as

Colorectal NeoplasmsQuassinsAnimalsCell Line, TumorCell ProliferationHumansMiceSTAT3 Transcription FactorXenograft Model Antitumor AssaysbruceantinolQuassinsSTAT3 Transcription FactorColorectal cancerProtein synthesisQuassinoid analogs

Identifiers

PMID37116665
PMCPMC11225567
OpenAlexW4367043529

What OpenQuestion holds

Textmetadata
LicenceTDM
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.