Evidence map›Paper›PMID 30985981›Full record

ArticleFEBS open bio2019

CFTR interacts with Hsp90 and regulates the phosphorylation of AKT and ERK1/2 in colorectal cancer cells.

Kaisheng Liu, Hongtao Jin, Yaomin Guo, Ying Liu, Yong Wan, Pan Zhao, Zhifan Zhou, Jianhong Wang, Maolin Wang, Chang Zou and 3 more

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

Article in FEBS open bio, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

6 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. CFTR and Gastrointestinal Cancers: An Update.Journal of personalized medicine · 2022
    Review
  5. Article
  6. 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

13 authors at 4 institutions in 1 country.

Kaisheng LiuThe First Affiliated Hospital of Southern University of Science and Technology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Hongtao JinThe First Affiliated Hospital of Southern University of Science and Technology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Yaomin GuoThe First Affiliated Hospital of Southern University of Science and Technology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Ying LiuThe First Affiliated Hospital of Southern University of Science and Technology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Yong WanThe First Affiliated Hospital of Southern University of Science and Technology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Pan ZhaoThe First Affiliated Hospital of Southern University of Science and Technology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Zhifan ZhouThe First Affiliated Hospital of Southern University of Science and Technology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Jianhong WangThe First Affiliated Hospital of Southern University of Science and Technology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Maolin WangSchool of Medicine, Health Science Centre, Shenzhen University, Shenzhen, China.
Chang ZouThe First Affiliated Hospital of Southern University of Science and Technology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Weiqing WuThe First Affiliated Hospital of Southern University of Science and Technology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Zhiqiang ChengThe First Affiliated Hospital of Southern University of Science and Technology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Yong DaiThe First Affiliated Hospital of Southern University of Science and Technology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Southern University of Science and Technology · CNJinan University · CNChinese University of Hong Kong · CNShenzhen University Health Science Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cystic fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. CF cells and tissues exhibit various mitochondrial abnormalities. However, the underlying molecular mechanisms remain elusive. Here, we examined the mechanisms through which CFTR regulates Bcl-2 family proteins, which in turn regulate permeabilization of the mitochondrial outer membrane. Notably, inhibition of CFTR activated Bax and Bad, but inhibited Bcl-2. Moreover, degradation of phosphorylated extracellular signal-regulated kinase 1/2 (ERK1/2) and AKT increased significantly in CFTR-knockdown cells. Dysfunction of CFTR decreased heat-shock protein 90 (Hsp90) mRNA levels, and CFTR was found to interact with Hsp90. Inhibition of Hsp90 by SNX-2112 induced the degradation of phosphorylated AKT and ERK1/2 in Caco2 and HRT18 cells. These findings may help provide insights into the physiological role of CFTR in CF-related diseases.

Indexed as

MAP Kinase Signaling Systembcl-2-Associated X Proteinbcl-Associated Death ProteinCaco-2 CellsColorectal NeoplasmsCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorGene Knockdown TechniquesHeterocyclic Compounds, 4 or More RingsHSP90 Heat-Shock ProteinsHumansMitochondriaPhosphorylationProteolysisProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2BAD protein, humanBAX protein, humanbcl-2-Associated X ProteinBCL2 protein, humanbcl-Associated Death ProteinCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorHeterocyclic Compounds, 4 or More RingsHSP90 Heat-Shock ProteinsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2SNX 2112AKTcystic fibrosis transmembrane conductance regulatorextracellular signal-regulated kinase ½heat-shock protein 90mitochondria

Identifiers

PMID30985981
PMCPMC6551490
OpenAlexW2937714804

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.