Evidence map›Paper›PMID 24554412›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014

CGB activates ERK and AKT kinases in cancer cells via LHCGR-independent mechanism.

Aleksandra Głodek, Anna Jankowska

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 27% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. 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

2 authors at 1 institution in 1 country.

Aleksandra GłodekDepartment of Cell Biology, Poznan University of Medical Sciences, Rokietnicka Street 5d, Poznań, 60-806, Poland, glodek@ump.edu.pl.
Anna Jankowska
Poznan University of Medical Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Expression of human chorionic gonadotropin free beta subunit (hCGβ) and its hyperglycosylated variant (hCGβ-H) is a phenomenon confirmed for tumors of different origin. Despite numerous studies, the mechanism of hCGβ action in cancer remains unknown especially that not all tumors secreting hCGβ express the receptor for human chorionic gonadotropin (LHCGR). In the presented study, we verified the hypothesis of hCGβ potential to activate signaling pathways involving extracellular signal-regulated kinase (ERK) and protein kinase B (AKT) kinases with and without the contribution of LHCGR. To achieve this goal, human ovarian carcinoma cells OVCAR-3 expressing LHCGR and SKOV-3 not expressing LHCGR were either transfected with a vector coding for hCGβ or stimulated with recombinant hCGβ and the level of pERK and pAKT was measured. The results of the experiments showed that hCGβ action leads to the increase in ERK and AKT kinases phosphorylation in cancer cells and indicate that these biological effects can be achieved independently of LHCGR presence. The study also demonstrated that the presence of the receptor is a key factor influencing the magnitude of cells' response.

Indexed as

Cell Line, TumorChorionic Gonadotropin, beta Subunit, HumanExtracellular Signal-Regulated MAP KinasesFemaleHumansOvarian NeoplasmsPhosphorylationProto-Oncogene Proteins c-aktReceptors, LHSignal TransductionTransfectionChorionic Gonadotropin, beta Subunit, HumanExtracellular Signal-Regulated MAP KinasesProto-Oncogene Proteins c-aktReceptors, LH

Identifiers

PMID24554412
OpenAlexW2061882179

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.