Evidence map›Paper›PMID 26464652›Full record

ArticleInternational journal of clinical and experimental pathology2015

The silence of p66(Shc) in HCT8 cells inhibits the viability via PI3K/AKT/Mdm-2/p53 signaling pathway.

Ling Zhang, Shengtao Zhu, Xuesen Shi, Weihong Sha

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

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. The p66International journal of molecular sciences · 2023
    Review
  4. Article
  5. 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 3 institutions in 1 country.

Ling ZhangSouthern Medical University Guangzhou, China ; Department of Gastroenterology and Hepatology, Guangdong General Hospital, Guangdong Academy of Medical Sciences Guangzhou, China.
Shengtao ZhuDepartment of Gastroenterology, Beijing Digestive Disease Center, Beijing Friendship Hospital Affiliated to Capital Medical University Beijing, China.
Xuesen ShiDepartment of Gastroenterology, Inner Mongolia Baotou Central Hospital Baotou, China.
Weihong ShaDepartment of Gastroenterology and Hepatology, Guangdong General Hospital, Guangdong Academy of Medical Sciences Guangzhou, China.
Guangdong General Hospital · CNBaotou Central Hospital · CNBeijing Friendship Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colon cancer is the second most common cause of cancer-related death, indicating that some of its cancer cells are not eradicated by current therapies. The previous studies demonstrated that p66(Shc) protein, a member of Shc family, is highly expressed in colon cancer cells, but the role of p66(Shc) in the progress of colon cancer still unknown. In this study, we found that p66(Shc) highly expressed in colon cancer tissue and colon cancer cell line SW620 cells, HCT8 cells, HCT116 cells and CaCO2 cells. The silence of p66(Shc) in HCT8 cells reduced the proliferation and accelerated the apoptosis, in addition, the expression of pro-apoptotic proteins caspase-3, caspase-9, Bax was enhanced and the expression of anti-apoptotic protein Bcl-2 was declined. Moreover, the cell cycle arrest in G0/G1 phase after HCT8 cells treated with p66(Shc) siRNA. Furthermore, after HCT8 cells treated with p66(Shc) siRNA, the phosphorylation of PI3K and AKT was significantly suppressed, and the expression of Mdm-2, a downstream of AKT, was obviously prohibited, while the expression of p53 was enhanced. These results indicate that the silence of p66(Shc) in HCT8 cells inhibits the viability via PI3K/AKT/Mdm-2/p53 signaling pathway, it may provide a promising approach to prevent the progress of colon cancer cell.

Indexed as

Apoptosisbcl-2-Associated X ProteinCaspase 3Caspase 9Cell CycleCell Line, TumorCell ProliferationColonic NeoplasmsHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-mdm2Shc Signaling Adaptor ProteinsSignal TransductionSrc Homology 2 Domain-Containing, Transforming Protein 1bcl-2-Associated X ProteinCaspase 3Caspase 9Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-mdm2SHC1 protein, humanShc Signaling Adaptor ProteinsSrc Homology 2 Domain-Containing, Transforming Protein 1Tumor Suppressor Protein p53apoptosisColon cancerHCT8 cellsp53p66ShcPI3K/AKT/Mdm-2

Identifiers

PMID26464652
PMCPMC4583884
OpenAlexW1765895388

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.