Evidence map›Paper›PMID 26411369›Full record

ArticleOncogene2016

INPP4B is an oncogenic regulator in human colon cancer.

S T Guo, M N Chi, R H Yang, X Y Guo, L K Zan, C Y Wang, Y F Xi, L Jin, A Croft, H-Y Tseng and 14 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. [Preliminary Study of the Role of INPP4B in Promoting Colorectal Cancer Metastasis and the Mechanisms Involved].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024
    Article
  5. Article
  6. Article
  7. Review
  8. Phosphoinositides in New Spaces.Cold Spring Harbor perspectives in biology · 2023
    Review
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  10. Article
  11. Article
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  14. Article
  15. Article
  16. Review
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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

24 authors at 6 institutions in 3 countries.

S T GuoDepartment of Molecular Biology, Shanxi Cancer Hospital and Institute, Affiliated Hospital of Shanxi Medical University, Shanxi, China.
M N ChiSchool of Medicine and Public Health, University of Newcastle, Newcastle, New South Wales, Australia.
R H YangDepartment of Molecular Biology, Shanxi Cancer Hospital and Institute, Affiliated Hospital of Shanxi Medical University, Shanxi, China.
X Y GuoDepartment of Molecular Biology, Shanxi Cancer Hospital and Institute, Affiliated Hospital of Shanxi Medical University, Shanxi, China.
L K ZanDepartment of Pathology, Shanxi Cancer Hospital and Institute, Shanxi, China.
C Y WangDepartment of Molecular Biology, Shanxi Cancer Hospital and Institute, Affiliated Hospital of Shanxi Medical University, Shanxi, China.
Y F XiDepartment of Pathology, Shanxi Cancer Hospital and Institute, Shanxi, China.
L JinSchool of Medicine and Public Health, University of Newcastle, Newcastle, New South Wales, Australia.
A CroftDepartment of Medical Oncology, Calvary Mater Newcastle Hospital, Newcastle, New South Wales, Australia.
H-Y TsengSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia.
X G YanSchool of Medicine and Public Health, University of Newcastle, Newcastle, New South Wales, Australia.
M FarrellySchool of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia.
F H WangDepartment of Molecular Biology, Shanxi Cancer Hospital and Institute, Affiliated Hospital of Shanxi Medical University, Shanxi, China.
F LaiSchool of Medicine and Public Health, University of Newcastle, Newcastle, New South Wales, Australia.
J F WangDepartment of Pathology, Shanxi Cancer Hospital and Institute, Shanxi, China.
Y P LiDepartment of Colorectal Surgery, Shanxi Cancer Hospital and Institute, Shanxi, China.
S AcklandDepartment of Medical Oncology, Calvary Mater Newcastle Hospital, Newcastle, New South Wales, Australia.
R ScottSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia.
I U AgoulnikDepartment of Cellular Biology and Pharmacology, Herbert Wertheim College of Medicine, Miami, FL, USA.
H HondermarckSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia.
R F ThorneSchool of Environmental and Life Sciences, University of Newcastle, Callaghan, New South Wales, Australia.
T LiuChildren's Cancer Institute Australia for Medical Research, University of New South Wales, Sydney, New South Wales, Australia.
X D ZhangSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia.
C C JiangSchool of Medicine and Public Health, University of Newcastle, Newcastle, New South Wales, Australia.
University of Newcastle Australia · AUShanxi Medical University · CNShanxi Provincial Cancer Hospital · CNCalvary Mater Newcastle Hospital · AUChildren's Cancer Institute Australia · AUDr. Herbert & Nicole Wertheim Family Foundation · US

Funding

Regulation of metastases by tumor suppressor INPP4BR15CA179287 · NCI · FLORIDA INTERNATIONAL UNIVERSITY · PI AGOULNIK, IRINA · 2014 to 2014
$418k
NCI NIH HHS R15 CA179287
6 · The paper itself

Abstract

Inositol polyphosphate 4-phosphatase type II (INPP4B) negatively regulates phosphatidylinositol 3-kinase signaling and is a tumor suppressor in some types of cancers. However, we have found that it is frequently upregulated in human colon cancer cells. Here we show that silencing of INPP4B blocks activation of Akt and serum- and glucocorticoid-regulated kinase 3 (SGK3), inhibits colon cancer cell proliferation and retards colon cancer xenograft growth. Conversely, overexpression of INPP4B increases proliferation and triggers anchorage-independent growth of normal colon epithelial cells. Moreover, we demonstrate that the effect of INPP4B on Akt and SGK3 is associated with inactivation of phosphate and tensin homolog through its protein phosphatase activity and that the increase in INPP4B is due to Ets-1-mediated transcriptional upregulation in colon cancer cells. Collectively, these results suggest that INPP4B may function as an oncogenic driver in colon cancer, with potential implications for targeting INPP4B as a novel approach to treat this disease.

Indexed as

Cell Line, TumorCell ProliferationColonic NeoplasmsHumansImmunohistochemistryPhosphoric Monoester Hydrolasesphosphatidylinositol-3,4-bisphosphate 4-phosphatasePhosphoric Monoester Hydrolases

Identifiers

PMID26411369
PMCPMC4908438
OpenAlexW2205934982

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.