Evidence map›Paper›PMID 27102295›Full record

ArticleOncotarget2016

Human growth hormone and human prolactin function as autocrine/paracrine promoters of progression of hepatocellular carcinoma.

Xiangjun Kong, Wenyong Wu, Yan Yuan, Vijay Pandey, Zhengsheng Wu, Xuefei Lu, Weijie Zhang, Yijun Chen, Mingming Wu, Min Zhang and 6 more

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

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  9. Investigation of Anti-Liver Cancer Activity of the Herbal Drug FDY003 Using Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2022
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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

16 authors at 6 institutions in 3 countries.

Xiangjun KongThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui, China.
Wenyong WuDepartment of General Surgery, First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
Yan YuanThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui, China.
Vijay PandeyCancer Science Institute of Singapore and Department of Pharmacology, National University of Singapore, Singapore.
Zhengsheng WuDepartment of Pathology, Anhui Medical University, Hefei, Anhui, China.
Xuefei LuThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui, China.
Weijie ZhangThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui, China.
Yijun ChenCancer Science Institute of Singapore and Department of Pharmacology, National University of Singapore, Singapore.
Mingming WuThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui, China.
Min ZhangThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui, China.
Gaopeng LiThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui, China.
Sheng TanThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui, China.
Pengxu QianThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui, China.
Jo K PerryLiggins Institute, University of Auckland, Auckland, New Zealand.
Peter E LobieCancer Science Institute of Singapore and Department of Pharmacology, National University of Singapore, Singapore.
Tao ZhuThe CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui, China.
University of Science and Technology of China · CNHefei National Center for Physical Sciences at Nanoscale · CNAnhui Medical University · CNNational University of Singapore · SGNational University Cancer Institute, Singapore · SGUniversity of Auckland · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The death rates of hepatocellular carcinoma (HCC) are extremely high due to the paucity of therapeutic options. Animal models and anecdotal clinical evidence indicate a potential role of hGH and hPRL in HCC. However, the prognostic relevance and the functional role of tumor expression of these hormones in human HCC are not defined. Herein, we analyzed the mRNA and protein expression of hGH and hPRL in histopathological samples of non-neoplastic liver and HCC by in situ hybridization, PCR and immunohistochemistry techniques. Increased mRNA and protein expression of both hormones was observed in HCC compared with non-neoplastic liver tissues. hGH expression was significantly associated with tumor size and tumor grade. No significant association was observed between the expression of hPRL and any histopathological features. Amplification of both hGH and hPRL genes in HCC was observed when compared to non-neoplastic tissue. Expression of both hGH and hPRL was associated with worse relapse-free and overall survival in HCC patients. In vitro and in vivo functional assays performed with HCC cell lines demonstrated that autocrine expression of hGH or hPRL in HCC cells increased STAT3 activation, oncogenicity and tumor growth while functional antagonism with hGH-G120R significantly reduced these parameters. Hence, tumor expression of hGH/hPRL is associated with a worse survival outcome for patients with HCC and hGH/hPRL function as autocrine/paracrine promoters of HCC progression.

Indexed as

AnimalsAutocrine CommunicationCarcinoma, HepatocellularCell Line, TumorDisease ProgressionHeterograftsHuman Growth HormoneHumansKaplan-Meier EstimateLiver NeoplasmsMiceMice, NudeParacrine CommunicationPrognosisProlactinHuman Growth HormoneProlactingrowth hormonehepatocellular carcinomaoncogenicityprolactinsurvival

Identifiers

PMID27102295
PMCPMC5045410
OpenAlexW2339977836

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.