ArticleBMC cancer2018
Ras-ERK1/2 signaling contributes to the development of colorectal cancer via regulating H3K9ac.
Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 5 papers.
What it found
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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.
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.
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Who cites it
5 citing papers in PubMed.
- Testis-specific protein Y-encoded 1 regulates androgen receptor expression through the MAPK/ERK pathway in male hepatocellular carcinoma.Saudi medical journal · 2022Article
- Article
- Chemerin Regulates the Proliferation and Migration of Pulmonary Arterial Smooth Muscle CellsFrontiers in pharmacology · 2022Article
- Article
- Aberrant gene expression induced by a high fat diet is linked to H3K9 acetylation in the promoter-proximal region.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021Article
Corrections and comments
- Retraction · 2021-05-24Duplication of/in Image · Investigation by Third Party · Manipulation of Images · Paper Mill · Unreliable Data · · see also: https://pubpeer.com/publications/5C14EEA7C8B48E6548C6190FDC0FE1;
- Retracted
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUNDS/
aimsRas is a control switch of ERK1/2 pathway, and hyperactivation of Ras-ERK1/2 signaling appears frequently in human cancers. However, the molecular regulation following by Ras-ERK1/2 activation is still unclear. This work aimed to reveal whether Ras-ERK1/2 promoted the development of colorectal cancer via regulating H3K9ac.
methodsA vector for expression of K-Ras mutated at G12 V and T35S was transfected into SW48 cells, and the acetylation of H3K9 was measured by Western blot analysis. MTT assay, colony formation assay, transwell assay, chromatin immunoprecipitation and RT-qPCR were performed to detect whether H3K9ac was contributed to K-Ras-mediated cell growth and migration. Furthermore, whether HDAC2 and PCAF involved in modification of H3K9ac following Ras-ERK1/2 activation were studied.
resultsK-Ras mutated at G12 V and T35S induced a significant activation of ERK1/2 signaling and a significant down-regulation of H3K9ac. Recovering H3K9 acetylation by using a mimicked H3K9ac expression vector attenuated the promoting effects of Ras-ERK1/2 on tumor cells growth and migration. Besides, H3K9ac can be deacetylated by HDAC2 and MDM2-depedent degradation of PCAF.
conclusionH3K9ac was a specific target for Ras-ERK1/2 signaling pathway. H3K9 acetylation can be modulated by HDAC2 and MDM2-depedent degradation of PCAF. The revealed regulation provides a better understanding of Ras-ERK1/2 signaling in tumorigenesis.
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