Evidence map›Paper›PMID 28515430›Full record

ArticleScientific reports2017

A microfluidic chip for screening individual cancer cells via eavesdropping on autophagy-inducing crosstalk in the stroma niche.

Hacer Ezgi Karakas, Junyoung Kim, Juhee Park, Jung Min Oh, Yongjun Choi, Devrim Gozuacik, Yoon-Kyoung Cho

Abstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Article
  2. Review
  3. Microphysiological systems as models for immunologically 'cold' tumors.Frontiers in cell and developmental biology · 2024
    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

7 authors.

Hacer Ezgi KarakasMolecular Biology, Genetics and Bioegineering Program, Sabanci University, Istanbul, 34956, Turkey.
Junyoung KimDepartment of Biomedical Engineering, School of Life Sciences, Ulsan National Institute of Science and Technology (UNIST), Ulsan, 44919, Republic of Korea.
Juhee ParkCenter for Soft and Living Matter, Institute for Basic Science (IBS), Ulsan, 44919, Republic of Korea.
Jung Min OhCenter for Soft and Living Matter, Institute for Basic Science (IBS), Ulsan, 44919, Republic of Korea.
Yongjun ChoiDepartment of Biomedical Engineering, School of Life Sciences, Ulsan National Institute of Science and Technology (UNIST), Ulsan, 44919, Republic of Korea.
Devrim GozuacikMolecular Biology, Genetics and Bioegineering Program, Sabanci University, Istanbul, 34956, Turkey. dgozuacik@sabanciuniv.edu.ORCID 0000-0001-7739-2346
Yoon-Kyoung ChoDepartment of Biomedical Engineering, School of Life Sciences, Ulsan National Institute of Science and Technology (UNIST), Ulsan, 44919, Republic of Korea. ykcho@unist.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a cellular homeostatic mechanism where proteins and organelles are digested and recycled to provide an alternative source of building blocks and energy to cells. The role of autophagy in cancer microenvironment is still poorly understood. Here, we present a microfluidic system allowing monitoring of the crosstalk between single cells. We used this system to study how tumor cells induced autophagy in the stromal niche. Firstly, we could confirm that transforming growth factor β1 (TGFβ1) secreted from breast tumor cells is a paracrine mediator of tumor-stroma interaction leading to the activation of autophagy in the stroma component fibroblasts. Through proof of concept experiments using TGFβ1 as a model factor, we could demonstrate real time monitoring of autophagy induction in fibroblasts by single tumor cells. Retrieval of individual tumor cells from the microfluidic system and their subsequent genomic analysis was possible, allowing us to determine the nature of the factor mediating tumor-stroma interactions. Therefore, our microfluidic platform might be used as a promising tool for quantitative investigation of tumor-stroma interactions, especially for and high-throughput screening of paracrine factors that are secreted from heterogeneous tumor cell populations.

Indexed as

AutophagyCell CommunicationMicrofluidicsTumor MicroenvironmentCancer-Associated FibroblastsCell Line, TumorHumansLab-On-A-Chip DevicesNeoplasmsParacrine CommunicationSingle-Cell AnalysisStromal Cells

Identifiers

PMID28515430
PMCPMC5435728

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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.