Evidence map›Paper›PMID 31407387›Full record

ArticleJournal of cellular biochemistry2020

Hypoxia alters the release and size distribution of extracellular vesicles in pancreatic cancer cells to support their adaptive survival.

Mary C Patton, Haseeb Zubair, Mohammad Aslam Khan, Seema Singh, Ajay P Singh

Abstract read
In one paragraph

Article in Journal of cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing 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

88 citing papers in PubMed.

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  15. Application of engineered exosomes in tumor therapy.American journal of translational research · 2025
    Review
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28 more citing papers are in PubMed but not listed here.

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

5 authors.

Mary C PattonMitchell Cancer Institute, University of South Alabama, Mobile, Alabama.
Haseeb ZubairMitchell Cancer Institute, University of South Alabama, Mobile, Alabama.
Mohammad Aslam KhanMitchell Cancer Institute, University of South Alabama, Mobile, Alabama.
Seema SinghMitchell Cancer Institute, University of South Alabama, Mobile, Alabama.
Ajay P SinghMitchell Cancer Institute, University of South Alabama, Mobile, Alabama.ORCID 0000-0003-3492-6330

Funding

Targeting tumor-stromal interaction for pancreatic cancer therapyR01CA175772 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SINGH, AJAY PRATAP · 2014 to 2018
$1.9M
A novel molecular cross-talk driving pancreatic cancer progressionR01CA224306 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SINGH, AJAY PRATAP · 2018 to 2022
$1.7M
NCI NIH HHS R01 CA175772NCI NIH HHS R01 CA224306
6 · The paper itself

Abstract

Pancreatic tumors are highly desmoplastic and poorly-vascularized, and therefore must develop adaptive mechanisms to sustain their survival under hypoxic condition. Extracellular vesicles (EV) play vital roles in pancreatic tumor pathobiology by facilitating intercellular communication. Here we studied the effect of hypoxia on the release of EVs and examined their role in adaptive survival of pancreatic cancer (PC) cells. Hypoxia promoted the release of EV in PC cell lines, MiaPaCa and AsPC1, wherein former exhibited a far greater induction. Moreover, a time-dependent, measurable and significant increase was recorded for small EV (SEV) in both the cell lines with only minimal induction observed for medium (MEV) and large EVs (LEV). Similarly, noticeable changes in size distribution of SEV were also recorded with a shift toward smaller average size under extreme hypoxia. Thrombospondin (apoptotic bodies marker) was exclusively detected on LEVs, while Arf6 (microvesicles marker) was mostly present on MEV with some expression in LEV as well. However, CD9 and CD63 (exosome markers) were expressed in both SEV and MEVs with a decreased expression recorded under hypoxia. Among all subfractions, SEV was the most bioactive in promoting the survival of hypoxic PC cells and hypoxia-inducible factor-1α stabilization was involved in heightened EV release under hypoxia and for their potency to promote hypoxic cell survival. Altogether, our findings provide a novel mechanism for the adaptive hypoxic survival of PC cells and should serve as the basis for future investigations on broader functional implications of EV.

Indexed as

Cell SurvivalCell CommunicationCell ProliferationExtracellular VesiclesHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitPancreatic NeoplasmsTumor Cells, CulturedHIF1A protein, humanHypoxia-Inducible Factor 1, alpha Subunitexosomesextracellular vesiclesHIF-1αhypoxiapancreatic cancertumor microenvironment

Identifiers

PMID31407387
PMCPMC6878126

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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.