Evidence map›Paper›PMID 30361686›Full record

ArticleOncogene2019

Adipose stromal cell targeting suppresses prostate cancer epithelial-mesenchymal transition and chemoresistance.

Fei Su, Songyeon Ahn, Achinto Saha, John DiGiovanni, Mikhail G Kolonin

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

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.1field-weighted citation impact, top 4% 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

57 citing papers in PubMed, 79 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Fei SuThe Brown Foundation Institute of Molecular Medicine for the Prevention of Disease, The University of Texas Health Sciences Center at Houston, Houston, TX, 77030, USA.
Songyeon AhnDivision of Pharmacology and Toxicology, Dell Pediatric Research Institute The University of Texas at Austin, Austin, TX, 78723, USA.
Achinto SahaDivision of Pharmacology and Toxicology, Dell Pediatric Research Institute The University of Texas at Austin, Austin, TX, 78723, USA.
John DiGiovanniDivision of Pharmacology and Toxicology, Dell Pediatric Research Institute The University of Texas at Austin, Austin, TX, 78723, USA.
Mikhail G KoloninThe Brown Foundation Institute of Molecular Medicine for the Prevention of Disease, The University of Texas Health Sciences Center at Houston, Houston, TX, 77030, USA. mikhail.g.kolonin@uth.tmc.edu.ORCID http://orcid.org/0000-0002-3743-7869
The University of Texas at Austin · USBrown Foundation · US

Funding

The Role of CXCL12 Signaling in Obesity-Induced Prostate Cancer ProgressionR01CA196259 · NCI · UNIVERSITY OF TEXAS AT AUSTIN · PI DIGIOVANNI, JOHN, KOLONIN, MIKHAIL G · 2015 to 2019
$2.0M
Adipose stromal cell targeting: a new approach to breast cancer treatmentR21CA216745 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI KOLONIN, MIKHAIL G, UENO, NAOTO T. · 2018 to 2019
$381k
NCI NIH HHS R01 CA196259NCI NIH HHS R21 CA216745U.S. Department of Health & Human Services | National Institutes of Health (NIH) R01CA196259
6 · The paper itself

Abstract

Fat tissue, overgrowing in obesity, promotes the progression of various carcinomas. Clinical and animal model studies indicate that adipose stromal cells (ASC), the progenitors of adipocytes, are recruited by tumors and promote tumor growth as tumor stromal cells. Here, we investigated the role of ASC in cancer chemoresistance and invasiveness, the attributes of tumor aggressiveness. By using human cell co-culture models, we demonstrate that ASC induce epithelial-mesenchymal transition (EMT) in prostate cancer cells. Our results for the first time demonstrate that ASC interaction renders cancer cells more migratory and resistant to docetaxel, cabazitaxel, and cisplatin chemotherapy. To confirm these findings in vivo, we compared cancer aggressiveness in lean and obese mice grafted with prostate tumors. We show that obesity promotes EMT in cancer cells and tumor invasion into the surrounding fat tissue. A hunter-killer peptide D-CAN, previously developed for targeted ASC ablation, suppressed the obesity-associated EMT and cancer progression. Importantly, cisplatin combined with D-CAN was more effective than cisplatin alone in suppressing growth of mouse prostate cancer allografts and xenografts even in non-obese mice. Our data demonstrate that ASC promote tumor aggressiveness and identify them as a target of combination cancer therapy.

Indexed as

Drug Resistance, NeoplasmEpithelial-Mesenchymal TransitionAdipose TissueAnimalsAntineoplastic Combined Chemotherapy ProtocolsAnti-Obesity AgentsCell MovementCells, CulturedHumansMaleMiceMolecular Targeted TherapyNeoplasm InvasivenessObesityPC-3 CellsProstatic NeoplasmsAnti-Obesity AgentsReactive Oxygen Species

Identifiers

PMID30361686
PMCPMC6417957
OpenAlexW2898210146

What OpenQuestion holds

Textmetadata
LicenceTDM
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.