Evidence map›Paper›PMID 41802536›Full record

ArticleCancer letters2026

A MUC1-ALIX complex regulates extracellular vesicle cargo loading with activated SRC to enhance pancreatic cancer progression.

Ying Huang, Kristine V Hoagstrom, Clara S Mundry, Tuo Hu, Heather C Jensen-Smith, Jacob Wragge, Phong Le, Amina Baniya, Kyle L McAndrews, Thomas C Caffrey and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Ying HuangThe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, USA. Electronic address: ying.huang@unmc.edu.
Kristine V HoagstromThe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, USA.
Clara S MundryThe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, USA.
Tuo HuThe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, USA.
Heather C Jensen-SmithThe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, USA; Department of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, NE, USA.
Jacob WraggeThe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, USA.
Phong LeDepartments of Microbiology and Immunology, Cancer Biology, Loyola University Chicago, Chicago, IL, USA.
Amina BaniyaThe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, USA.
Kyle L McAndrewsThe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, USA.
Thomas C CaffreyThe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, USA.
Kelly A O'ConnellThe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, USA.
Pankaj K SinghThe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, USA.
Aleata A TriplettThe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, USA.
Paul M GrandgenettThe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, USA.
Michael A HollingsworthThe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, USA. Electronic address: mahollin@unmc.edu.

Funding

UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Lynette M Smith · 1985 to 2026
$55.0M
Pancreatic Cancer Detection ConsortiumU01CA210240 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Michael A. Hollingsworth · 2017 to 2026
$12.9M
Tissue Core-UNMC Rapid Autopsy ProgramU54CA274329 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Jixin Dong · 2022 to 2026
$7.8M
Critical Resources Provided by UNMC Rapid Autopsy Program (RAP) Biorepository Stimulate Cancer ResearchR50CA211462 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Paul M Grandgenett · 2016 to 2026
$1.4M
NCI NIH HHS P30 CA036727NCI NIH HHS R50 CA211462NCI NIH HHS U01 CA210240NCI NIH HHS U54 CA274329
6 · The paper itself

Abstract

Extracellular vesicles (EVs) are critical mediators of intercellular communication in the tumor microenvironment and play an essential role in tumor growth and metastasis. MUC1 has been identified in tumor cell-derived EVs, but its function in that context has not been well investigated. We show that MUC1 is highly enriched in EVs derived from pancreatic cancer cell lines and patient tumors but not normal pancreas. Pretreatment of mice with tumor derived MUC1 positive EVs promoted tumor cell growth and metastasis in vivo. MUC1 positive EVs enhanced tumor cell growth, motility and invasion in vitro. Proteomic profiling revealed that MUC1-positive EVs contain protein cargo distinct from MUC1-negative EVs, which implicates MUC1 in selective EV cargo regulation. We demonstrate that the cytoplasmic tail of MUC1 expressed in pancreatic cancer cells interacts with programmed cell death 6-interacting protein (ALIX) and influences EV biogenesis and loading of specific oncogenic cargo (Phospho

Indexed as

Extracellular VesiclesMucin-1Pancreatic Neoplasmssrc-Family KinasesAnimalsCell Line, TumorCell MovementCell ProliferationDisease ProgressionHumansMiceMice, NudeNeoplasm InvasivenessSignal TransductionMUC1 protein, humanMucin-1src-Family KinasesExtracellular vesicle cargo sortingMUC1-ALIX direct interactionPancreatic cancer progression

Identifiers

PMID41802536
PMCPMC13317643

What Socratic holds

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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 Socratic graph.