Evidence map›Paper›PMID 28293855›Full record

ArticleHormones & cancer2017

Growth Hormone Receptor Knockdown Sensitizes Human Melanoma Cells to Chemotherapy by Attenuating Expression of ABC Drug Efflux Pumps.

Reetobrata Basu, Nicholas Baumgaertel, Shiyong Wu, John J Kopchick

Open access · bronzeAbstract read
In one paragraph

Article in Hormones & cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Growth Hormone, Not Simply Just a Hormone for Growth.Endocrinology and metabolism (Seoul, Korea) · 2026
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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

4 authors at 1 institution in 2 countries.

Reetobrata BasuEdison Biotechnology Institute, Konneker Research Laboratory 206, Ohio University, Athens, OH, 45701, USA.ORCID http://orcid.org/0000-0001-8415-1356
Nicholas BaumgaertelEdison Biotechnology Institute, Konneker Research Laboratory 206, Ohio University, Athens, OH, 45701, USA.
Shiyong WuEdison Biotechnology Institute, Konneker Research Laboratory 206, Ohio University, Athens, OH, 45701, USA.
John J KopchickEdison Biotechnology Institute, Konneker Research Laboratory 206, Ohio University, Athens, OH, 45701, USA. kopchick@ohio.edu.
Biotechnology Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melanoma remains one of the most therapy-resistant forms of human cancer despite recent introductions of highly efficacious targeted therapies. The intrinsic therapy resistance of human melanoma is largely due to abundant expression of a repertoire of xenobiotic efflux pumps of the ATP-binding cassette (ABC) transporter family. Here, we report that GH action is a key mediator of chemotherapeutic resistance in human melanoma cells. We investigated multiple ABC efflux pumps (ABCB1, ABCB5, ABCB8, ABCC1, ABCC2, ABCG1, and ABCG2) reportedly associated with melanoma drug resistance in different human melanoma cells and tested the efficacy of five different anti-cancer compounds (cisplatin, doxorubicin, oridonin, paclitaxel, vemurafenib) with decreased GH action. We found that GH treatment of human melanoma cells upregulates expression of multiple ABC transporters and increases the EC50 of melanoma drug vemurafenib. Also, vemurafenib-resistant melanoma cells had upregulated levels of GH receptor (GHR) expression as well as ABC efflux pumps. GHR knockdown (KD) using siRNA in human melanoma cells treated with sub-EC50 doses of anti-tumor compounds resulted in significantly increased drug retention, decreased cell proliferation and increased drug efficacy, compared to mock-transfected controls. Our set of findings identify an unknown mechanism of GH regulation in mediating melanoma drug resistance and validates GHR as a unique therapeutic target for sensitizing highly therapy-resistant human melanoma cells to lower doses of anti-cancer drugs.

Indexed as

Antineoplastic AgentsCell Line, TumorCell ProliferationDoxorubicinDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansIndolesMelanomaMultidrug Resistance-Associated Protein 2PaclitaxelReceptors, SomatotropinSulfonamidesVemurafenibABCC2 protein, humanAntineoplastic AgentsDoxorubicinIndolesMultidrug Resistance-Associated Protein 2PaclitaxelReceptors, SomatotropinSulfonamidesVemurafenib

Identifiers

PMID28293855
PMCPMC10355985
OpenAlexW2609422755

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.