Evidence map›Paper›PMID 32155915›Full record

ArticleCancers2020

Haprolid Inhibits Tumor Growth of Hepatocellular Carcinoma through Rb/E2F and Akt/mTOR Inhibition.

Jun Xing, Vikas Bhuria, Khac Cuong Bui, Mai Ly Thi Nguyen, Zexi Hu, Chih-Jen Hsieh, Kathrin Wittstein, Marc Stadler, Ludwig Wilkens, Jun Li and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 19 citations in OpenAlex.

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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

13 authors at 5 institutions in 2 countries.

Jun XingDepartment of Internal Medicine I, Medical University Hospital, Eberhard Karls Universität Tübingen, 72076 Tubingen, Germany.ORCID 0000-0002-2771-6725
Vikas BhuriaDepartment of Internal Medicine I, Medical University Hospital, Eberhard Karls Universität Tübingen, 72076 Tubingen, Germany.
Khac Cuong BuiDepartment of Internal Medicine I, Medical University Hospital, Eberhard Karls Universität Tübingen, 72076 Tubingen, Germany.
Mai Ly Thi NguyenDepartment of Internal Medicine I, Medical University Hospital, Eberhard Karls Universität Tübingen, 72076 Tubingen, Germany.
Zexi HuDepartment of Internal Medicine VIII, Medical University Hospital, 72076 Tübingen, Germany.
Chih-Jen HsiehDepartment of Internal Medicine I, Medical University Hospital, Eberhard Karls Universität Tübingen, 72076 Tubingen, Germany.
Kathrin WittsteinDepartment Microbial Drugs, Helmholtz Centre for Infection Research GmbH (HZI), 38124 Braunschweig, Germany.
Marc StadlerDepartment Microbial Drugs, Helmholtz Centre for Infection Research GmbH (HZI), 38124 Braunschweig, Germany.ORCID 0000-0002-7284-8671
Ludwig WilkensInstitute of Pathology, Hannover Regional Hospital, 30043 Hannover, Germany.
Jun LiInstitute of Organic Chemistry, Leibniz University of Hannover, 30167 Hannover, Germany.
Markus KalesseInstitute of Organic Chemistry, Leibniz University of Hannover, 30167 Hannover, Germany.
Przemyslaw BozkoDepartment of Internal Medicine I, Medical University Hospital, Eberhard Karls Universität Tübingen, 72076 Tubingen, Germany.ORCID 0000-0001-8126-3686
Ruben R PlentzDepartment of Internal Medicine I, Medical University Hospital, Eberhard Karls Universität Tübingen, 72076 Tubingen, Germany.
University of Tübingen · DEHelmholtz Centre for Infection Research · DELeibniz University Hannover · DEKlinikum Bremen-Mitte · DEUniversity of Science and Technology of China · CN

Funding

China Scholarship Council 201608080176
6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) represents a major health burden with limited curative treatment options. There is a substantial unmet need to develop innovative approaches to impact the progression of advanced HCC. Haprolid is a novel natural component isolated from myxobacteria. Haprolid has been reported as a potent selective cytotoxin against a panel of tumor cells in recent studies including HCC cells. The aims of this study are to evaluate the antitumor effect of haprolid in HCC and to understand its underlying molecular mechanisms.

methodsThe efficacy of haprolid was evaluated in human HCC cell lines (Huh-7, Hep3B and HepG2) and xenograft tumors (NMRI-Foxn1

resultshaprolid treatment significantly inhibited cell proliferation, migration and invasion in vitro. The epithelial-mesenchymal transition (EMT) was impaired by haprolid treatment and the expression level of N-cadherin, vimentin and Snail was downregulated. Moreover, growth of HCC cells in vitro was suppressed by inhibition of G1/S transition, and partially by induction of apoptosis. The drug induced downregulation of cell cycle regulatory proteins cyclin A, cyclin B and CDK2 and induced upregulation of p21 and p27. Further evidence showed that these effects of haprolid were associated with Rb/E2F downregulation and Akt/mTOR inhibition. Finally, in vivo nude mice experiments demonstrated significant inhibition of tumor growth upon haprolid treatment.

conclusionOur results show that haprolid inhibits the growth of HCC through dual inhibition of Rb/E2F and Akt/mTOR pathways

Indexed as

Akt/mTORapoptosiscell cycleEMThaprolidHCCRb/E2F

Identifiers

PMID32155915
PMCPMC7139901
OpenAlexW3010481352

What OpenQuestion holds

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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.