Evidence map›Paper›PMID 23416975›Full record

ArticleOncogene2014

PTTG acts as a STAT3 target gene for colorectal cancer cell growth and motility.

C Zhou, Y Tong, K Wawrowsky, S Melmed

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 2 pooled it
4.1field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Prognostic Impact of IL6 Genetic Variants in Patients with Metastatic Colorectal Cancer Treated with Bevacizumab-Based Chemotherapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Trial
  4. AreFrontiers in endocrinology · 2025
    Article
  5. World journal of gastrointestinal surgery · 2024
    Article
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  20. Targeting theOncotarget · 2017
    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

4 authors at 1 institution in 1 country.

C ZhouDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Y TongDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
K WawrowskyDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
S MelmedDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Cedars-Sinai Medical Center · US

Funding

Mechanisms of Pituitary TumorigenesisR01CA075979 · NCI · CEDARS-SINAI MEDICAL CENTER · PI MELMED, SHLOMO · 1999 to 2012
$3.5M
PTTG1 regulates anti-cancer drug responseR00CA138914 · NCI · CEDARS-SINAI MEDICAL CENTER · PI TONG, YUNGUANG · 2012 to 2014
$725k
NCI NIH HHS CA75979NCI NIH HHS R00 CA138914NCI NIH HHS R01 CA075979
6 · The paper itself

Abstract

Pituitary tumor-transforming gene (PTTG), the index mammalian securin, is abundantly expressed in several tumors and regulates tumor growth and progression. Molecular mechanisms elucidating PTTG regulation and actions remain elusive. Here, we provide evidence that PTTG acts as a signal transducer and activator of transcription factor 3 (STAT3) target gene. Total STAT3 and Tyr705 phosphorylated STAT3 were concordantly expressed with PTTG in human colorectal tumors (n=97 and n=95, respectively, P<0.001). STAT3 specifically bound the human PTTG promoter and induced PTTG transcriptional activity (twofold) as assessed by chromatin immunoprecipitation and luciferase reporter assays. STAT3 transfection increased PTTG mRNA and protein abundance twofold in HCT116 human colon cancer cells, and induction was further enhanced (threefold) by constitutively active STAT3 (STAT3-C), whereas strongly abrogated by dominant-negative STAT3 (STAT3-DN). Attenuating PTTG expression by siRNA in STAT3 HCT116 stable transfectants suppressed cell growth and colony formation in vitro, and PTTG cell knockout also constrained activated STAT3-induced explanted murine tumor growth in vivo. STAT3 increased HCT116 cell migration and invasion up to fivefold, whereas cell mobility was abolished by STAT3-DN (>85%). Impairing PTTG expression by siRNA also strongly suppressed STAT3-faciliated cell migration and invasion by up to 90%. Knocking out PTTG in STAT3-C HCT116 stable transfectants strongly decreased tumor metastases in nude mice, indicating the requirement of PTTG for STAT3-promoted metastasis. These results elucidate a mechanism for tumor cell PTTG regulation, whereby STAT3 induces PTTG expression to facilitate tumor growth and metastasis, and further support the rationale for targeting PTTG to abrogate colorectal cancer growth.

Indexed as

Cell ProliferationGene Expression Regulation, NeoplasticAnimalsCarcinogenesisCell MovementColorectal NeoplasmsFemaleGene ExpressionHCT116 CellsHumansInterleukin-6Liver NeoplasmsMiceMice, NudeNeoplasm TransplantationPhosphoproteinsIL6 protein, humanInterleukin-6Phosphoproteinspituitary tumor-transforming protein 1, humanSecurinSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID23416975
PMCPMC3930149
OpenAlexW2018769559

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.