Evidence map›Paper›PMID 17072338›Full record

ArticleOncogene2007

RACK1 inhibits colonic cell growth by regulating Src activity at cell cycle checkpoints.

V Mamidipudi, N K Dhillon, T Parman, L D Miller, K C Lee, C A Cartwright

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

48 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Role of Sam68 in different types of cancer (Review).International journal of molecular medicine · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Dual functions of Rack1 in regulating Hedgehog pathway.Cell death and differentiation · 2020
    Article
  10. Review
  11. Article
  12. Article
  13. RACK1 Acts as a Potential Tumor Promoter in Colorectal Cancer.Gastroenterology research and practice · 2019
    Article
  14. Article
  15. Article
  16. Rack1 maintains intestinal homeostasis by protecting the integrity of the epithelial barrier.American journal of physiology. Gastrointestinal and liver physiology · 2018
    Article
  17. 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

6 authors at 1 institution in 1 country.

V MamidipudiDepartment of Medicine, Stanford University School of Medicine, Stanford University, Stanford, CA 94305, USA.
N K Dhillon
T Parman
L D Miller
K C Lee
C A Cartwright
Stanford University · US

Funding

Proteomics/GenomicsP30DK056339 · NIDDK · STANFORD UNIVERSITY · PI GREENBERG, HARRY BERNARD · 2001 to 2010
$10.4M
INTESTINAL CELL GROWTH CONTROL: ROLE OF TYROSINE KINASESR01DK043743 · NIDDK · STANFORD UNIVERSITY · PI CARTWRIGHT, CHRISTINE ANN · 1996 to 2015
$4.3M
INTESTINAL CELL GROWTH CONTROL--ROLE OF TYROSINE KINASER29DK043743 · NIDDK · STANFORD UNIVERSITY · PI CARTWRIGHT, CHRISTINE ANN · 1991 to 1995
–
NIDDK NIH HHS DK43743NIDDK NIH HHS DK56339
6 · The paper itself

Abstract

Previously, we showed that Src tyrosine kinases are activated early in the development of human colon cancer and are suppressed as intestinal cells differentiate. We identified RACK1 as an endogenous substrate, binding partner and inhibitor of Src. Here we show (by overexpressing RACK1, depleting Src or RACK1 and utilizing cell-permeable peptides that perturb RACK1's interaction with Src) that RACK1 regulates growth of colon cells by suppressing Src activity at G(1) and mitotic checkpoints, and consequently delaying cell cycle progression. Activated Src rescues RACK1-inhibited growth of HT-29 cells. Conversely, inhibiting Src abolishes growth promoted by RACK1 depletion in normal cells. Two potential mechanisms whereby RACK1 regulates mitotic exit are identified: suppression of Src-mediated Sam68 phosphorylation and maintenance of the cyclin-dependent kinase (CDK) 1-cyclin B complex in an active state. Our results reveal novel mechanisms of cell cycle control in G(1) and mitosis of colon cells. The significance of this work lies in the discovery of a mechanism by which the growth of colon cancer cells can be slowed, by RACK1 suppression of an oncogenic kinase at critical cell cycle checkpoints. Small molecules that mimic RACK1 function may provide a powerful new approach to the treatment of colon cancer.

Indexed as

Cell ProliferationAdaptor Proteins, Signal TransducingCarcinomaCell CycleColonic NeoplasmsDNA-Binding ProteinsGenes, cdcGTP-Binding ProteinsHumansNeoplasm ProteinsProtein BindingProto-Oncogene Proteins pp60(c-src)Receptors, Cell SurfaceReceptors for Activated C KinaseRNA-Binding ProteinsTumor Cells, CulturedAdaptor Proteins, Signal TransducingDNA-Binding ProteinsGTP-Binding ProteinsKHDRBS1 protein, humanNeoplasm ProteinsProto-Oncogene Proteins pp60(c-src)RACK1 protein, humanReceptors, Cell SurfaceReceptors for Activated C KinaseRNA-Binding Proteins

Identifiers

PMID17072338
OpenAlexW1967934704

What OpenQuestion holds

Textmetadata
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.